Ribose and stress management -
Additionally, it can cause low blood sugar levels, so it is important to monitor blood sugar levels while taking this supplement.
Finally, it can cause allergic reactions in some people, so it is important to be aware of any potential allergic reactions before taking this supplement. D-Ribose is regulated differently across the world. In the United States, it is regulated as a dietary supplement by the Food and Drug Administration FDA.
In the European Union, it is regulated as a food supplement by the European Food Safety Authority EFSA.
In Canada, it is regulated as a natural health product by Health Canada. In Australia, it is regulated as a therapeutic good by the Therapeutic Goods Administration TGA.
In India, it is regulated as a food supplement by the Food Safety and Standards Authority of India FSSAI. Tags: Energy. Get the most up-to-date information about D-Ribose with SGS Digicomply.
Stay informed about current regulations, incident monitoring, risk prevention, scientific insights, mentions in the media, and relevant updates. Smart GPT-like search, customizable dashboard, and comprehensive guides tailored to your specific area, product, and target market.
Dietary Supplements Database D-Ribose December 1 Where is D-Ribose used? How is D-Ribose used in the food industry? Health benefits of D-Ribose? What are the dangers of D-Ribose? Example products containing D-Ribose : Energy drinks, Protein bars, Sports drinks, Supplements, Powders, Capsules.
How is D-Ribose regulated across the world? Upcoming Free Webinar Regulatory Change Management in Another pathway activates the breakdown of glucose through glycolysis, harnessing the released energy to form ATP through other processes.
D-ribose supplementation provides the body with more building blocks for ATP. The more ATP molecules that are synthesized in a cell, the more energy is available for cellular functions. This process occurs in every cell in your body—including the cells that comprise the adrenal glands, muscles, and brain—powering all the processes that are required to keep you alive.
Since ATP creation occurs within the mitochondria, diseases affecting the mitochondria often cause body-wide disturbances, including hormone and neurotransmitter imbalances, muscle weakness, gastrointestinal disorders, neurologic issues, and sensory impairment.
A mitochondrial dysfunction may therefore manifest as one or many of these symptoms. In the case of muscle cells, a lack of ATP production leads to muscle weakness. In the case of adrenal cells, reduced ATP leads to a decrease in cortisol production.
In the hypothalamus, in the levels of a cortico-releasing hormone are reduced, and so on. Eventually, such dysfunctions can lead to cell death, causing serious issues throughout the body.
Ribose supplements can alleviate the symptoms of mitochondrial dysfunction and thus help alleviate fatigue and revitalize cells. Collagen is also affected as we age. Collagen is a crucial protein in the body, found in connective tissue such as skin, bone, joints, and muscle.
Therefore, taken together with D-ribose, collagen could be a significant step towards Adrenal Fatigue recovery, aiding the body in healing and slowing some of the effects of aging. In addition, just as ribose is the building block for ATP, collagen is a building block for many proteins in our body.
Collagen contains many amino acids that the human body cannot generate itself. These amino acids must be consumed by eating protein, especially meat, or through proper supplementation.
Collagen supplementation is thought to particularly help with inflammation, joint pain, and muscle function, all of which are often affected by Adrenal Fatigue. Thus, ribose and collagen can work together in your muscles to decrease pain, help increase your energy levels, and get you up and moving again.
To recover from Adrenal Fatigue, proper functioning of the adrenal glands must be restored. As this happens, the neuroendometabolic NEM stress response system —which is responsible for handling stress in the body—can then rebalance itself and bring the many processes in your body back into sync.
The adrenals are a vital part of the NEM system, so an essential part of recovery is ensuring that the adrenal glands have enough energy. Some of these essential functions include creating hormones such as cortisol clearing waste out of cells, and detoxifying the cell matrix.
All of this requires energy from ATP. When ribose is present at sufficient levels in the cell, it stimulates the formation of the ATP. When this occurs, there is plenty of ATP to perform cell functions.
In normal, healthy cells, enough ribose is present because the pentose shunt from glucose is able to keep up with the demand. In some cases, however, as in those with chronic stress, the cells cannot keep up with the demand.
This is when cells begin to fatigue. This is why ribose supplementation can be beneficial. Ribose is not directly available in the diet; it can only be created in the body when it is broken down from glucose. This breakdown process takes energy.
Therefore, the supplement is a quicker way to provide your body with ribose, so that it can then build ATP, activate it through the mitochondria, and use this energy for the cell's functions.
Adrenal Fatigue occurs because the body is under constant stress. This chronic stress can be due to a work situation, a relationship, or even a previous injury or illness. Sometimes the stress is itself caused by an underlying condition such as an autoimmune disease or a mitochondrial disorder.
This stress on the body triggers the hypothalamic-pituitary-adrenal axis HPA axis , which acts on the adrenal glands to generate more cortisol. When the body has responded sufficiently, cortisol acts on the hypothalamus to turn the HPA axis off.
In those suffering from Adrenal Fatigue, however, the HPA does not function properly. The adrenal glands cannot keep up with the demand for cortisol.
Cortisol levels start to drop, which means that the HPA axis cannot be turned off, and the body keeps pushing for more cortisol. Eventually, there is not enough material or energy to create cortisol. Ribose supplementation provides more energy to the adrenal glands, which gives them a boost in making cortisol.
Ideally, this helps in the later stages of Adrenal Fatigue, when cortisol levels have dropped because of the long-term demand. Ribose will also help if the cause of Adrenal Fatigue and hormone imbalance is actually a mitochondrial deficiency.
If a dysfunction in the mitochondria is the underlying cause of the symptoms, D-ribose will help to bringing the body back into balance.
The body responds holistically to stress. This means that usually more than one pathway is affected, as in the case of Adrenal Fatigue.
The mitochondria are extremely important to the overall function of the body, especially when dealing with stress. One component is the HPA axis, as discussed above.
Managemment are High GI foods that act nonspecifically to combat stress by regulating the key elements managemfnt in stress-induced pathologies. D-Ribose-L-cysteine DRLCa potent Fueling for youth team sports Strsss booster, nanagement been Ribose and stress management for relief of stress. Ribose and stress management, we investigated its adaptogenic-like effect in mice subjugated to unpredictable chronic mild stress UCMS. The animals in groups were subjugated to UCMS 30 min later, daily for 21 days and afterwards, tested for memory and anxiety. Blood glucose, serum corticosterone concentrations and adrenal weight were determined. The brain tissues were processed for estimation of malondialdehyde MDAGSH, superoxide-dismutase SODcatalase, tumor necrosis factor-alpha TNF-αinterleukin-6, acetyl-cholinesterase, and caspase-3 activities. The histomorphologic features and neuronal viability of the hippocampus, amygdala and prefrontal cortex were also determined.Journal of the International Mental relaxation techniques of Sports Nutrition volume 14Article number: 47 Cite this article. Metrics Ribose and stress management. Skeletal muscle adenosine triphosphate ATP levels are severely mabagement during strsss following prolonged high intensity exercise.
Recovery from these lower ATP levels can take Rinose, which can affect performance on subsequent days of Ribosse.
Untrained an often suffer Ribise stress Supporting regulated blood sugar levels consequences of acute, repeated bouts of exercise Gut health essentials not having the ability to perform or recovery sufficiently to exercise on subsequent strsss.
Conversely, trained individuals may be able to recover more quickly due to their enhanced metabolic strsss. D-Ribose DR has managemen shown to enhance the recovery in ATP; however, it is not known if recovery and performance can be managemwnt with DR ingestion.
Therefore, this study was designed to determine what influence DR might have on muscular performance, recovery, and metabolism during and following a multi-day exercise mabagement.
Subjects were Refillable health supplements into two groups based on peak VO 2 results, lower VO 2 Wtress 2 and higher peak VO 2 HVO Riboss.
Mean and strdss PO increased significantly from day 1 to day 3 for the IRbose trial compared to DEX in managemet LVO 2 group. Riobse of perceived exertion RPE and creatine kinase CK were Riboee lower for DR than DEX in the LVO 2 group. No differences in PO, RPE, heart managemnt, CK, blood urea nitrogen, or glucose were found between either supplement for the HVO 2 group.
DR supplementation in the lower VO 2 max group resulted in maintenance in Brown rice for cholesterol management performance, manayement well as lower managemment of RPE and Mansgement.
Unlike no observed znd with DEX supplementation. It has been well established that exercise mnagement leads to many physiological and biochemical adaptations. Proper training leads to increased ajd synthesis, greater muscular strress of glucose, attenuation in insulin resistance, improved redox status, and improved fat oxidation capacity qnd trained individuals compared to the Fueling for youth team sports Ribode 123456 Citrus fruit production, 7 Ribose and stress management.
Because of their fitness level, Ribose and stress management sttress suffer stresss stress and consequences of acute, Blood circulation and smoking bouts of exercise Detox not having the ability Ribose and stress management perform or Ribose and stress management sufficiently to Ribkse on subsequent days streas 89 ].
Additionally, the trained manxgement has the capacity to oxidize significantly Fueling for youth team sports fat at the same exercise intensity compared to the mangement. This, by managdment, should provide an improved recovery pattern, provided janagement are adequate substrates streds facilitate recovery, for the trained individual due to the sparing of muscle Targeted weight loss supplements and Riboae providing a greater manqgement producing potential.
Every cell requires adequate levels of Fueling for youth team sports triphosphate ATP Ribose and stress management maintain its energy level and function. During and following prolonged, repeated high intensity manqgement, reaching or exceeding anaerobic Ribose and stress management, ATP levels are depleted severely in skeletal Homeopathic remedies for allergies. Previous mahagement have demonstrated that the recovery of ATP levels can take days, which ultimately can affect Leafy green supply chain and potentially the ability to exercise Glucose monitoring devices a full manaegment day after anc [ 101112 ].
The recovery of ATP levels in skeletal muscle involves the adenine salvage pathway or de mangement ATP synthesis. The strese to replenish this ATP deficiency following high intensity exercise Ribose and stress management important in maintaining both the biochemical an physical cellular managment following strdss [ 1314 Liver detoxification for improved nutrient absorption. Therefore, it managemdnt important mansgement the recovery of stres ATP levels following anv should be as quick as possible.
Various manatement have been investigated to maangement to enhance mnaagement recovery in ATP levels. D-ribose DRa naturally occurring pentose carbohydrate, has shown promise by Ribosw the recovery in depressed ATP levels following stress.
Due Resveratrol and respiratory health low levels of ribose in habitual daily diets, Fueling for youth team sports of DR may be beneficial to produce the necessary levels of Internal body cleanse energy, i.
Manayement, during and following high intensity exercise. D-ribose plays Ribosf important role as a building block for nucleotides, coenzymes, nicotinate adenine dinucleotide phosphate, nucleic acids, and ATP. Even with this ability to enhance the recovery in ATP levels, its role in aiding muscular performance following high intensity exercise and endurance has revealed mixed results [ 15161718 ].
The purpose of this project was to investigate the influence of supplementing DR ingesting on muscular performance, recovery, and exercise metabolism during and following a consecutive days of high intensity exercise.
To our knowledge, this is the first study assessing the effects of DR on both high and low intensity consecutive exercise sessions. Based on the work of Barr et al. It is also hypothesized that the trained subjects will not gain a benefit from the supplementation of DR.
After obtaining Institutional Review Board approval at Montana State University in Bozeman, MT, written informed consent was obtained from 26, healthy subjects Table 1.
The 26 subjects were divided into two equal-numbered groups based on their peak oxygen uptake VO 2 results, lower peak VO 2 LVO 2 and higher peak VO 2 HVO 2. This group was involved in minimal exercise training throughout the week.
The HVO 2 group consisted of individuals who were consistently exercising. Each subject was required to maintain their normal diet during this study, as well as performing their normal daily activities without performing any additional separate exercise sessions not designated in this study.
Five grams of either supplement was mixed with their food or in a self-selected beverage with lunch and an additional 5 g was ingested with dinner for 2 days as a loading dose prior to exercise.
On the following 3 days of exercise, subjects ingested a standardized pre-exercise snack along with 5 g of the supplement 2 h before their exercise session.
Following exercise, subjects ingested their final daily dose of 5 g before leaving the laboratory along with a snack which consisted of g of yogurt and two granola bars.
During the first visit to the laboratory, each subject signed the informed consent and completed a health history questionnaire. Thereafter, each subject underwent a maximal oxygen uptake test and practiced the 2 min power test assessment using a cycle ergometer Monark E, Sweden.
Cycling resistance was then increased by 0. Heart rate HRVO 2 and a blood lactate Lac sample were collected at of each stage. This assessment established exercise workloads during the two treatment sessions. The exercise session consisted of six, 10 min intervals of exercise on a cycle ergometer.
At the end of the 60 min exercise session, each subject completed a 2 min performance task. This performance task required the subject to produce as much power as possible during this 2 min interval. Peak power PO and average power was assessed during this 2 min task trial.
A minimum of 4 day washout period was employed between crossover arms of the study to allow adequate recovery. Venous blood samples were drawn via a venipuncture 15 min before exercise and 24 h post exercise.
Finger stick techniques at 10 min before exercise, 20 min, 40 min, and 60 min during exercise. The finger stick blood samples collected during exercise were assayed for blood glucose. Creatine kinase CK and blood urea nitrogen BUN concentrations were measured at pre-exercise and 24 h post exercise following the last exercise session.
Subjects ingested ml of water at 20 and 40 min during exercise to minimize any effects of dehydration. Rating of perceived exertion RPE was recorded every 20 min during exercise using the Borg scale.
Heart rate was recorded using a Polar HR monitor RC3; Polar, Inc. Blood glucose Gluc concentration were measured using a Bayer Gluc monitor Bayer Medical, NJ. Blood lactate levels were measured by an AccuSport Lactate Analyzer Akira, Japan.
Creatine kinase and BUN were measured utilizing an Abaxis Piccolo analyzer Princeton, NJ. Power data from the time trial performance test was assessed with the Sports Medicine Industries SMI software package St.
Cloud, MN. Statistical analyses of performance, physiological measurements, and laboratory values during and following intense exercise provides evidence of what specific role DR can play in a untrained or trained athlete.
Data was analyzed with SPSS statistical software using a 2-way ANOVA with repeated measures with time and treatments as independent variables.
Heart rate, RPE, blood Gluc, serum CK, serum BUN and power data were dependent measures. All 26 subjects completed the study without any adverse events. Data are presented as main effects as there were no interactions. No statistical differences were observed for the dependent measures when data were analyzed from 26 subjects.
Therefore, subjects were divided into two equal groups based on their VO 2 max values. Relative and absolute mean power data can be found in Table 2. The average changes in relative and absolute peak power from Day 1 to Day 3 were 0.
Relative and absolute mean PO were not different between DR and DEX treatments for the HVO 2 group. The average changes in relative and absolute peak PO from Day 1 to Day 3 were 0.
Analysis of serum CK data indicated that DR ingestion led to lower change in the LVO 2 group. Creatine kinase levels increased by an average of No differences for change in CK and BUN levels were observed between DR No differences were observed for blood Gluc and remained stable for all treatments and within both groups Table 3.
No difference between treatments was found for HR in the LVO 2 group. The purpose of this project was to investigate the influence of DR on muscular performance and recovery during and following a multi-day high intensity exercise regimen in LVO 2 and HVO 2 groups.
The pertinent results indicate that DR ingestion improved performance and recovery for the LVO 2 group during a multi-day exercise study, but not in the HVO 2 group.
The role in which DR could play on performance during intense exercise has been uncertain. Due to this uncertainty, this study has demonstrated that DR supplementation provided a performance benefit undergoing repeated days of high intensity exercise.
The rate of ATP utilization during high intensity exercise may exceed ATP production and a considerable amount of time is required for these deficient levels to recover [ 1019 ]. Hellsten et al.
A decrease in cellular high energy phosphates can affect muscular function besides producing symptoms of soreness and fatigue, which can affect subsequent exercise sessions [ 21 ]. Studies have revealed mixed results in replenishing muscular energy levels, maintaining or enhancing performance and alleviating post-exercise symptoms with substrate supplementation [ 22 ].
Alternatives to metabolic pathways can play important roles in ATP generation, such as the pentose phosphate pathway. The pentose phosphate pathway is critical for the formation of 5-phosphyl-ribosepyrophosphate PRPPan intermediate in the production of ATP, and plays a role in ATP de novo synthesis which is dependent on a rate limiting enzyme, glucose 6-phosphte dehydrogenase G6PDH [ 21 ].
However, DR is unique in that it bypasses this rate limiting enzymatic step in the formation of PRPP [ 23 ]. This enhanced production of ATP by DR replenishes the cellular energy deficiency and can shorten the energy recovery period following high intensity exercise. On the other hand, subjects in the LVO 2 group may not have had the ability to fully utilize other pathways i.
PRPP to assist in recovery. Thus, DR gave them extra substrate to bypass the G6PDH step and, potentially, increase the efficiency of the recovery, reflecting a potential increase in muscle ATP levels. This study did not measure muscle ATP levels, which could have provided additional supporting data for both the trained and untrained athlete.
The measurement of muscle ATP levels could provide a more in-depth metabolic explanation. The effect of DR on performance has provided mixed results.
: Ribose and stress management| Top bar navigation | CAS PubMed Google Scholar Berardi J, Ziegenfuss T, Hall B. Diabetes has a number of complications over time, of which macrovasculopathy is very important. When the feet touch the ground, the legs are used to cushion the impact of landing Fig. However, as shown in Figure 2 , reduced NADPH is, in turn, needed by these reductases for their continuous action. Melatonin in the Promotion of Health , 2nd Edn. Aoyama K, Nakaki T Impaired glutathione synthesis in neurodegeneration. Murr, C. |
| Background | D-Ribose is a type of sugar molecule that is found naturally in the body and is used as a dietary supplement to help improve energy levels, reduce fatigue, and improve athletic performance. Please Note: The articles on this database are automatically generated by our AI system. While we strive for accuracy, these articles may not contain verified information and should be used for informational purposes only. We recommend consulting verified sources or experts for accurate and reliable information. D-Ribose is a dietary supplement that is used to help improve energy levels, reduce fatigue, and improve exercise performance. It is also used to help improve symptoms of fibromyalgia, chronic fatigue syndrome, and other conditions. D-Ribose is a dietary supplement that is used in the food industry as an energy booster. It is often added to energy drinks, sports drinks, and other beverages to provide a quick boost of energy. It can also be used as an ingredient in baked goods, cereals, and other food products to provide a natural source of energy. Additionally, D-Ribose is used as a sweetener in some food products, as it has a low glycemic index and is a natural sugar. D-Ribose is a naturally occurring sugar that has been found to have a number of health benefits. It has been shown to improve energy levels, reduce fatigue, and improve exercise performance. It may also help to reduce inflammation, improve heart health, and reduce symptoms of fibromyalgia. Additionally, D-Ribose may help to improve cognitive function, reduce stress, and improve sleep quality. D-Ribose is a naturally occurring sugar found in the body and is used as a dietary supplement to increase energy levels. However, it can cause side effects such as nausea, vomiting, diarrhea, and abdominal pain. It can also interact with certain medications, such as those used to treat diabetes, so it is important to consult with a doctor before taking this supplement. Additionally, it can cause low blood sugar levels, so it is important to monitor blood sugar levels while taking this supplement. Finally, it can cause allergic reactions in some people, so it is important to be aware of any potential allergic reactions before taking this supplement. D-Ribose is regulated differently across the world. This includes systematically determination of SG components that are PARylated or PAR-bound under different stresses. Different groups have used diverse approaches to identify PARylated vs. PAR-binding proteins Daniels et al. For example, in a recently published paper, hundreds of novel PAR-binding proteins were identified using photoaffinity-based proteomics, which provides us with a valuable resource for exploring proteins involved in LLPS and SG formation Dasovich et al. Moreover, innovative approaches are needed to systematically identify the modified sites on SG components and even the PAR chain length and structure on each site. It would be beneficial for identifying SG scaffold proteins and their binding partners, and building the overall PAR-mediated interaction networks in SGs. However, there are studies that failed to identify PARPs in SGs Markmiller et al. Therefore, whether the initiation and dynamic maintenance of diverse SGs absolutely require PAR? Up to now, the mechanism of SG formation is not fully resolved, and the diversity of SG is stress or cell-type dependent. Does SG formation under different stress conditions have different requirements for PAR? The other remaining question is what are the individual roles played by various PARPs in SGs, and whether or not they affect each other. Six reported SG-localized PARPs might have their own specific targets and functions. They might specifically regulate the localization, LLPS behavior, and interaction network of their substrates. Therefore, determination of which PARP responsible for the specific modification of different SG components could help in the development of novel therapeutic avenues, which could specifically regulate the formation and composition of pathogenic SGs. Moreover, what are the links between ADP-ribosylation and other PTMs. Do they work together synergistically or compete with each other on substrates via conjunction on the same or adjacent motifs in SG regulation? A previous study indicated that PAR-dependent anchoring of TDP to SGs inhibits its disease-associated phosphorylation. If TDP were to accumulate excessively in the cytoplasm and become excluded from SGs, it could become phosphorylated and form irreversible aggregates McGurk et al. Therefore, as a single SG component may be modified by multiple PTMs, there might be interplays between ADP-ribosylation and other PTMs. PAR synthesis and degradation is a highly dynamic process, whose timely regulation ensures proper formation and dynamics of SGs. But how do cells finely regulate these processes? Should other PTMs such as phosphorylation block continued ADP-ribosylation on same substrate to ensure that the high levels of PAR are transient, preventing PARylated or PAR-binding proteins from transformation into pathogenic aggregates under long-term stress. Thus, more details of the mechanism of interplay between ADP-ribosylation and other PTMs need to be revealed. Poly ADP-ribose as an important novel regulator of SG formation and dynamics, in-depth investigations on the remaining questions discussed above will help us to acquire a clear mechanistic view on global PAR-mediated interaction networks, specific functions of PARPs and links between ADP-ribosylation and other PTMs in SGs. This will eventually contribute on the development of novel therapeutic approaches targeting the aberrant pathogenic SG formation and further pave the way for effective SG-related neurodegenerative disease treatments. XJ, XC, and BL contributed to the design and wrote the manuscript. BL and SL supervised the overall direction, planning, and editing of the manuscript. All authors contributed to the article and approved the submitted version. The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest. Ahel, D. Poly ADP-ribose -dependent regulation of DNA repair by the chromatin remodeling enzyme ALC1. Science , — doi: PubMed Abstract CrossRef Full Text Google Scholar. Alberti, S. Liquid-liquid phase separation in disease. A Systematic Survey Identifies Prions and Illuminates Sequence Features of Prionogenic Proteins. Cell , — Altmeyer, M. Liquid demixing of intrinsically disordered proteins is seeded by poly ADP-ribose. Ando, Y. ELTA: enzymatic labeling of terminal ADP-ribose. Cell 73, — Bai, P. Biology of poly ADP-ribose polymerases: the factotums of cell maintenance. Cell 58, — Bonfiglio, J. Mass spectrometry for serine ADP-ribosylation? Think o-glycosylation!. Nucleic Acids Res. Buchan, J. Eukaryotic stress granules: the ins and outs of translation. Cell 36, — Cao, X. The involvement of stress granules in aging and aging-associated diseases. Aging Cell e Catara, G. PARP1-produced poly-ADP-ribose causes the PARP12 translocation to stress granules and impairment of Golgi complex functions. Cheruiyot, A. Poly ADP-ribose -binding promotes Exo1 damage recruitment and suppresses its nuclease activities. DNA Repair 35, — Corda, D. Functional aspects of protein mono-ADP-ribosylation. EMBO J. Crawford, K. Specificity of reversible ADP-ribosylation and regulation of cellular processes. Daniels, C. The promise of proteomics for the study of ADP-ribosylation. Dasovich, M. Identifying poly ADP-ribose -binding proteins with photoaffinity-based proteomics. Deiana, A. Intrinsically disordered proteins and structured proteins with intrinsically disordered regions have different functional roles in the cell. PLoS One e Duan, Y. PARylation regulates stress granule dynamics, phase separation, and neurotoxicity of disease-related RNA-binding proteins. Cell Res. Eckei, L. The conserved macrodomains of the non-structural proteins of Chikungunya virus and other pathogenic positive strand RNA viruses function as mono-ADP-ribosylhydrolases. Fahrer, J. Quantitative analysis of the binding affinity of poly ADP-ribose to specific binding proteins as a function of chain length. High-affinity interaction of poly ADP-ribose and the human DEK oncoprotein depends upon chain length. Biochemistry 49, — Falahati, H. Thermodynamically driven assemblies and liquid-liquid phase separations in biology. Soft Matter 15, — Fischbach, A. The C-terminal domain of p53 orchestrates the interplay between non-covalent and covalent poly ADP-ribosyl ation of p53 by PARP1. Geuens, T. The hnRNP family: insights into their role in health and disease. Gomes, E. The molecular language of membraneless organelles. Grimaldi, G. PARPs and PAR as novel pharmacological targets for the treatment of stress granule-associated disorders. Guillén-Boixet, J. RNA-induced conformational switching and clustering of G3BP drive stress granule assembly by condensation. Gupte, R. PARPs and ADP-ribosylation: recent advances linking molecular functions to biological outcomes. Genes Dev. Hyman, A. Liquid-liquid phase separation in biology. Cell Dev. Isabelle, M. Quantitative proteomics and dynamic imaging reveal that G3BP-mediated stress granule assembly is poly ADP-ribose -dependent following exposure to MNNG-induced DNA alkylation. Cell Sci. Jankevicius, G. A family of macrodomain proteins reverses cellular mono-ADP-ribosylation. Jayabalan, A. Stress granule formation, disassembly, and composition are regulated by alphavirus ADP-ribosylhydrolase activity. Kam, T. Science eaat Karras, G. The macro domain is an ADP-ribose binding module. Kedersha, N. Stress granules and cell signaling: more than just a passing phase?. Trends Biochem. Stress granules and processing bodies are dynamically linked sites of mRNP remodeling. Cell Biol. Kim, D. Activation of PARP-1 by snoRNAs controls ribosome biogenesis and cell growth via the RNA helicase DDX Cell 75, — Kim, H. Mutations in prion-like domains in hnRNPA2B1 and hnRNPA1 cause multisystem proteinopathy and ALS. Nature , — Krietsch, J. Reprogramming cellular events by poly ADP-ribose -binding proteins. Aspects Med. Leslie Pedrioli, D. Comprehensive ADP-ribosylome analysis identifies tyrosine as an ADP-ribose acceptor site. EMBO Rep. Leung, A. Poly ADP-ribose : an organizer of cellular architecture. Poly ADP-ribose : a dynamic trigger for biomolecular condensate formation. Trends Cell Biol. Poly ADP-ribose regulates stress responses and microRNA activity in the cytoplasm. Cell 42, — Li, G. Structure and identification of ADP-ribose recognition motifs of APLF and role in the DNA damage response. Liu, C. New insights of poly ADP-ribosylation in neurodegenerative diseases: a focus on protein phase separation and pathologic aggregation. Luscher, B. ADP-ribosylation, a multifaceted posttranslational modification involved in the control of cell physiology in health and disease. Markmiller, S. Context-dependent and disease-specific diversity in protein interactions within stress granules. Mastrocola, A. The RNA-binding protein fused in sarcoma FUS functions downstream of poly ADP-ribose polymerase PARP in response to DNA damage. McGurk, L. Poly ADP-ribose prevents pathological phase separation of TDP by promoting liquid demixing and stress granule localization. Cell 71, — Poly ADP-ribose engages the TDP nuclear-localization sequence to regulate granulo-filamentous aggregation. Biochemistry 57, — Poly ADP-ribosylation in age-related neurological disease. Trends Genet. Mohagheghi, F. TDP functions within a network of hnRNP proteins to inhibit the production of a truncated human SORT1 receptor. Molliex, A. Phase separation by low complexity domains promotes stress granule assembly and drives pathological fibrillization. Emerging roles of eraser enzymes in the dynamic control of protein ADP-ribosylation. Otto, H. In silico characterization of the family of PARP-like poly ADP-ribosyl transferases pARTs. BMC Genomics 6:e Palazzo, L. ADP-ribosylation: new facets of an ancient modification. FEBS J. Patel, A. A liquid-to-solid phase transition of the als protein fus accelerated by disease mutation. Perina, D. Distribution of protein poly ADP-ribosyl ation systems across all domains of life. DNA Repair 23, 4— Pleschke, J. Poly ADP-ribose binds to specific domains in DNA damage checkpoint proteins. Popp, O. Site-specific noncovalent interaction of the biopolymer poly ADP-ribose with the Werner syndrome protein regulates protein functions. ACS Chem. Prasad, A. Molecular mechanisms of TDP misfolding and pathology in amyotrophic lateral sclerosis. Protter, D. Principles and properties of stress granules. Qi, H. Multiple roles for mono- and Poly ADP-ribose in regulating stress responses. Rosenthal, F. Macrodomain-containing proteins are new mono-ADP-ribosylhydrolases. Schwartz, J. |
| The influence of D-ribose ingestion and fitness level on performance and recovery | Cell , — Altmeyer, M. Liquid demixing of intrinsically disordered proteins is seeded by poly ADP-ribose. Ando, Y. ELTA: enzymatic labeling of terminal ADP-ribose. Cell 73, — Bai, P. Biology of poly ADP-ribose polymerases: the factotums of cell maintenance. Cell 58, — Bonfiglio, J. Mass spectrometry for serine ADP-ribosylation? Think o-glycosylation!. Nucleic Acids Res. Buchan, J. Eukaryotic stress granules: the ins and outs of translation. Cell 36, — Cao, X. The involvement of stress granules in aging and aging-associated diseases. Aging Cell e Catara, G. PARP1-produced poly-ADP-ribose causes the PARP12 translocation to stress granules and impairment of Golgi complex functions. Cheruiyot, A. Poly ADP-ribose -binding promotes Exo1 damage recruitment and suppresses its nuclease activities. DNA Repair 35, — Corda, D. Functional aspects of protein mono-ADP-ribosylation. EMBO J. Crawford, K. Specificity of reversible ADP-ribosylation and regulation of cellular processes. Daniels, C. The promise of proteomics for the study of ADP-ribosylation. Dasovich, M. Identifying poly ADP-ribose -binding proteins with photoaffinity-based proteomics. Deiana, A. Intrinsically disordered proteins and structured proteins with intrinsically disordered regions have different functional roles in the cell. PLoS One e Duan, Y. PARylation regulates stress granule dynamics, phase separation, and neurotoxicity of disease-related RNA-binding proteins. Cell Res. Eckei, L. The conserved macrodomains of the non-structural proteins of Chikungunya virus and other pathogenic positive strand RNA viruses function as mono-ADP-ribosylhydrolases. Fahrer, J. Quantitative analysis of the binding affinity of poly ADP-ribose to specific binding proteins as a function of chain length. High-affinity interaction of poly ADP-ribose and the human DEK oncoprotein depends upon chain length. Biochemistry 49, — Falahati, H. Thermodynamically driven assemblies and liquid-liquid phase separations in biology. Soft Matter 15, — Fischbach, A. The C-terminal domain of p53 orchestrates the interplay between non-covalent and covalent poly ADP-ribosyl ation of p53 by PARP1. Geuens, T. The hnRNP family: insights into their role in health and disease. Gomes, E. The molecular language of membraneless organelles. Grimaldi, G. PARPs and PAR as novel pharmacological targets for the treatment of stress granule-associated disorders. Guillén-Boixet, J. RNA-induced conformational switching and clustering of G3BP drive stress granule assembly by condensation. Gupte, R. PARPs and ADP-ribosylation: recent advances linking molecular functions to biological outcomes. Genes Dev. Hyman, A. Liquid-liquid phase separation in biology. Cell Dev. Isabelle, M. Quantitative proteomics and dynamic imaging reveal that G3BP-mediated stress granule assembly is poly ADP-ribose -dependent following exposure to MNNG-induced DNA alkylation. Cell Sci. Jankevicius, G. A family of macrodomain proteins reverses cellular mono-ADP-ribosylation. Jayabalan, A. Stress granule formation, disassembly, and composition are regulated by alphavirus ADP-ribosylhydrolase activity. Kam, T. Science eaat Karras, G. The macro domain is an ADP-ribose binding module. Kedersha, N. Stress granules and cell signaling: more than just a passing phase?. Trends Biochem. Stress granules and processing bodies are dynamically linked sites of mRNP remodeling. Cell Biol. Kim, D. Activation of PARP-1 by snoRNAs controls ribosome biogenesis and cell growth via the RNA helicase DDX Cell 75, — Kim, H. Mutations in prion-like domains in hnRNPA2B1 and hnRNPA1 cause multisystem proteinopathy and ALS. Nature , — Krietsch, J. Reprogramming cellular events by poly ADP-ribose -binding proteins. Aspects Med. Leslie Pedrioli, D. Comprehensive ADP-ribosylome analysis identifies tyrosine as an ADP-ribose acceptor site. EMBO Rep. Leung, A. Poly ADP-ribose : an organizer of cellular architecture. Poly ADP-ribose : a dynamic trigger for biomolecular condensate formation. Trends Cell Biol. Poly ADP-ribose regulates stress responses and microRNA activity in the cytoplasm. Cell 42, — Li, G. Structure and identification of ADP-ribose recognition motifs of APLF and role in the DNA damage response. Liu, C. New insights of poly ADP-ribosylation in neurodegenerative diseases: a focus on protein phase separation and pathologic aggregation. Luscher, B. ADP-ribosylation, a multifaceted posttranslational modification involved in the control of cell physiology in health and disease. Markmiller, S. Context-dependent and disease-specific diversity in protein interactions within stress granules. Mastrocola, A. The RNA-binding protein fused in sarcoma FUS functions downstream of poly ADP-ribose polymerase PARP in response to DNA damage. McGurk, L. Poly ADP-ribose prevents pathological phase separation of TDP by promoting liquid demixing and stress granule localization. Cell 71, — Poly ADP-ribose engages the TDP nuclear-localization sequence to regulate granulo-filamentous aggregation. Biochemistry 57, — Poly ADP-ribosylation in age-related neurological disease. Trends Genet. Mohagheghi, F. TDP functions within a network of hnRNP proteins to inhibit the production of a truncated human SORT1 receptor. Molliex, A. Phase separation by low complexity domains promotes stress granule assembly and drives pathological fibrillization. Emerging roles of eraser enzymes in the dynamic control of protein ADP-ribosylation. Otto, H. The present study demonstrates that subject selection criterion i. fitness level has a significant influence in the results. When data were analyzed by treatment DR vs. DEX , regardless of fitness level, no statistical differences were observed. In fact, values were comparable between the treatments. Untrained individuals appear to suffer the consequences of acute, repeated bouts of exercise by not having the ability to perform or recovery sufficiently to exercise on subsequent days [ 8 , 9 ]. The potential beneficial role of DR also depends upon the dosage and timing of dosing, type of exercise, degree of intensity and duration of exercise. We designed a high-intensity exercise protocol where cellular anaerobic metabolism commences; thereby stressing the metabolic activity in these exercising muscles and to see what role DR may play on recovery and performance. In evaluating performance in the LVO 2 group, we found that mean and peak PO increased significantly with DR from day 1 to 3, which was not observed in the DEX treatment. Multiple factors can account for the performance benefits with DR. For example, differences in muscular CK levels might shed light on this beneficial difference in performance by indicating a maintenance, or lack thereof, of cell membrane integrity. The change in CK level from day 1 to day 3 was about 3 times greater for the DEX treatment compared to DR in the LVO 2 group. Besides the impact of high intensity exercise on cellular metabolism, additional factors may also play a role, such as reactive oxygen species. High intensity exercise may result in oxidative damage in both the blood and skeletal muscle [ 25 ]; however, high intensity exercise is superior to low intensity exercise in upregulating the muscle to produce superoxide dismutase and GSH peroxidase [ 26 ]. Seifert et al. The biochemical mechanisms responsible for these symptoms remain unclear; however, the production of free radicals could play an important role as mediators of muscular damage. Sjodin et al. The metabolic stress during exercise alters the biochemical state of the cell, which ultimately enhances the rate of oxygen free radical production from semiquinone and xanthine oxidase. It is therefore, plausible that if mitochondrial function is altered during exercise, performance may be inhibited. This study did not measure produced products of oxidative stress, which could have provided additional interesting and supporting data during and following high intensity exercise. The delivery and utilization of oxygen to exercising muscle is a major factor in assessing fitness and maximal VO 2 levels [ 28 ]. Upon further assessment of our subjects in this study into LVO 2 and HVO 2 groups, revealed significant differences when consuming DR during the high intensity exercise sessions for the LVO 2 group. These findings appear to suggest that individuals that have not consistently performed exercise above the Lac threshold level do not fair equally with individuals that exercise or train on a more intense regimen schedule. The rise in CK levels observed in the LVO 2 group appears to imply that a strenuous, anaerobic exercise produced cellular stress in which enzymatic leaking occurs, which can not only effect cellular homeostasis, but performance and recovery as well. In conclusion, high intensity, anaerobic exercise decreases muscular ATP levels and a considerable amount of time is required for these lower energy levels to recover. Some studies have reported mixed performance benefits with DR, probably reflecting protocol differences, dosing of DR, timing of the DR dosage, intensity of exercise, and subject specificity. For this last reason we developed a protocol that induced a level of high intensity, anaerobic exercise in two fitness level groups. The analysis revealed that the LVO 2 value subjects had a significant improvement in performance, lower changes in CK, and lower RPE with DR compared to DEX. Assessment of metabolic serum parameters did not reflect any appreciable differences between the treatments, not clearly demonstrating a potential mechanism accounting for this benefit. A limitation of this study would be dietary control. While subjects were instructed to maintain their dietary habits as usual during the study, an in depth analysis of intakes was not performed. It is possible that some members of the LVO2 group had an insufficient diet that would have benefitted from supplementation. In summary, DR demonstrated a performance, perceptual, and serum benefits in the lower fitness adult subjects undergoing high intensity exercise. The stress of high intensity exercise has the potential to be benefited with supplementation of DR around these exercise sessions. Future studies are needed to elucidate the mechanism s of action of DR ingestion and exercise. Roedde S, MacDougall JD, Sutton JR, Green HJ. Supercompensation of muscle glycogen in trained and untrained subjects. Can J Appl Sport Sci. CAS PubMed Google Scholar. Dela F, Mikines KJ, von Linstow M, Secher NH, Galbo H. Effect of training on insulin-mediated glucose uptake in human muscle. Am J Phys. Google Scholar. Phielix E, Meex R, Ouwens DM, Sparks L, Hoeks J, Schaart G, Moonen-Kornips E, Hesselink MK, Schrauwen P. High oxidative capacity due to chronic exercise training attenuates lipid-induced insulin resistance. Article CAS PubMed PubMed Central Google Scholar. Lewis NA, Howatson G, Morton K, Hill J, Pedlar CR. Alterations in redox homeostasis in the elite endurance athlete. Sports Med. Article PubMed Google Scholar. Stisen AB, Stougaard O, Langfort J, Helge JW, Sahlin K, Madsen K. Maximal fat oxidation rates in endurance trained and untrained women. Eur J Appl Physiol. Article CAS PubMed Google Scholar. Coggan AR, Raguso CA, Gastaldelli A, Sidossis LS, Yeckel CW. Fat metabolism during high-intensity exercise in endurance-trained and untrained men. Sidossis LS, Wolfe RR, Coggan AR. Regulation of fatty acid oxidation in untrained vs. trained men during exercise. CAS Google Scholar. Darr KC, Bassett DR, Morgan BJ, Thomas DP. Effects of age and training status on heart rate recovery after peak exercise. Am J Physiol Heart Circ Physiol. Tomlin DL, Wenger HA. The relationship between aerobic fitness and recovery from high intensity intermittent exercise. Hellsten-Westing Y, Balsom PD, Norman B, Sjodin B. The effect of high-intensity training on purine metabolism in man. Acta Physiol Scand. Hellsten-Westing Y, Norman B, Balsom PD, Sjodin B. Decreased resting levels of adenine nucleotides in human skeletal muscle after high-intensity training. J Appl Physiol. Stathis CG, Febbraio MA, Carey MF, Snow RJ. Influence of sprint training on human skeletal muscle purine nucleotide metabolism. Hargreaves M, McKenna MJ, Jenkins DG, Warmington SA, Li JL, Snow RL, Febbraio MA. Muscle metabolites and performance during high-intensity, intermittent exercise. Tullson PC, Bangsbo J, Hellsten Y, Richter EA. IMP metabolism in human skeletal muscle after exhaustive exercise. Eijnde BO, Van Leemputte M, Brouns F, Van Der Vuss GJ, Labarque V, Ramaekers M, Schuylenberg R, Verbessem P, Wijnen LT, Hespel P. No effects of oral ribose supplementation on repeated maximal exercise and de novo ATP resynthesis. Kreider RB, Melton C, Greenwood M, Rasmussen C, Lundberg J, Earnest C, Almada A. Effects of oral D-ribose supplementation on anaerobic capacity and selected metabolic markers in healthy males. Int J Sport Nutr Exerc Metab. Van Gammeren D, Falk D, Antonio J. The effects of four weeks of ribose supplementation on body composition and exercise performance in healthy, young, male recreational bodybuilders: a double blind, placebo controlled trial. Curr Ther Res. Article Google Scholar. Raue U, Gallagher PM, Williamson DL, Trappe SW. Effects of ribose supplementation on performance during repeated high-intensity cycle sprints. Med Sci Sport Exerc. Sjordin B, Hellsten-Westing Y, Apple FS. Biochemical mechanisms for oxygen free radical formation during exercise. Hellsten Y, Skadhauge L, Bangsbo J. Effect of ribose supplementation on resynthesis of adenine nucleotides after intense intermittent training in humans. Am J Physiol Regul Integr Comp Physiol. Dodd SL, Johnson CA, Fernholz K, St. Cyr JA. The role of ribose in human skeletal muscle metabolism. Med Hypotheses. Shecterle LM, St. Myocardial ischemia: alterations in myocardial cellular energy and diastolic function, a potential role for D-ribose. In: Lakshmanadoss U, editor. Novel strategies in ischemic heart disease. Croatia: In Tech; Brault JJ, Terjung RL. Purine salvage to adenine nucleotides in different skeletal muscle fiber types. Berardi J, Ziegenfuss T, Hall B. Cell Death Differ — Dash PK, Blum S, Moore AN Caspase activity plays an essential role in long-term memory. NeuroReport — Khalil H, Peltzer N, Walicki J, Yang J, Dubuis G, Gardiol N, Held W, Bigliardi P, Marsland B, Liaudet L, Widmann C Caspase-3 protects stressed organs against cell death. Mol Cell Biol — Fernando P, Brunette S, Megeney LA Neural stem cell differentiation is dependent upon endogenous caspase 3 activity. FASEB J — Download references. Authors thank the technical staff of the Department of Pharmacology and Therapeutics as well as Dr T. Aina of the Department of Veterinary Pathology of the University of Ibadan for their assistance in the biochemical and histological studies during the course of the research. This research did not receive any specific grant from funding agencies in the public, commercial, or not-for-profit sectors. Neuropharmacology Unit, Department of Pharmacology and Therapeutics, Faculty of Basic Medical Sciences, College of Medicine, University of Ibadan, Ibadan, Nigeria. Love Okoh, Abayomi M. Department of Pharmacology, Faculty of Basic Medical Sciences, PAMO University of Medical Sciences, Port Harcourt, River States, Nigeria. Department of Pharmacology and Therapeutics, College of Medicine and Health Sciences, Afe Babalola University, Ado Ekiti, Ekiti State, Nigeria. You can also search for this author in PubMed Google Scholar. Correspondence to Solomon Umukoro. Springer Nature remains neutral with regard to jurisdictional claims in published maps and institutional affiliations. Reprints and permissions. Okoh, L. et al. d -Ribose— l -cysteine exhibits adaptogenic-like activity through inhibition of oxido-inflammatory responses and increased neuronal caspase-3 activity in mice exposed to unpredictable chronic mild stress. Mol Biol Rep 47 , — Download citation. Received : 17 June Accepted : 15 September Published : 21 September Issue Date : October Anyone you share the following link with will be able to read this content:. Sorry, a shareable link is not currently available for this article. Provided by the Springer Nature SharedIt content-sharing initiative. Abstract Adaptogens are substances that act nonspecifically to combat stress by regulating the key elements involved in stress-induced pathologies. Access this article Log in via an institution. Scheme 1. Abbreviations GSH: Glutathione DRLC: d -Ribose— l -cysteine UCMS: Unpredictable chronic mild stress MDA: Malondialdehyde SOD: Superoxide-dismutase TNF-α: Tumor necrosis factor-alpha IL Interleukin-6 AChE: Acetyl-cholinesterase HPA: Hypothalamic—pituitary—adrenal IOAA: Index of open arm avoidance. References Panossian A, Wikman G Effects of adaptogens on the central nervous system and the molecular mechanisms associated with their stress-protective activity. Pharmaceuticals — Article CAS Google Scholar Panossian A Understanding adaptogenic activity: specificity of the pharmacological action of adaptogens and other phytochemicals. Ann NY Sci —67 Article CAS Google Scholar McEwen BS, Gray JD, Nasca C Recognizing resilience: learning from the effects of stress on the brain. Neurobiol Stress —11 Article Google Scholar Panossian A, Seo E, Efferth T Novel molecular mechanisms for the adaptogenic effects of herbal extracts on isolated brain cells using systems biology. Phytomedicine — Article Google Scholar Wiegant FAC, Limandjaja G, de Poot SAH Plant adaptogens activate cellular adaptive mechanisms by causing mild damage. Narosa Publishing House Pvt Ltd, New Delhi, pp — Google Scholar Hovhannisyan AS, Nylander M, Panossian AG Efficacy of adaptogenic supplements on adapting to stress: a randomized, controlled trial. J Athlet Enhanc Article Google Scholar Chakravarty S, Reddy BR, Sudhakar SR, Saxena S, Das T, Meghah V, BrahmendraSwamy CV, Kumar A, Idris MM Chronic unpredictable stress CUS -induced anxiety and related mood disorders in a Zebra fish model: altered brain proteome profile implicates mitochondrial dysfunction. PLoS ONE Article Google Scholar Willner P, Mitchell PJ The validity of animal models of predisposition to depression. Behav Pharmacol — Article CAS Google Scholar Anisman H, Matheson K Stress, depression, and anhedonia: caveats concerning animal models. Neurosci Biobehav Rev — Article Google Scholar Umukoro S, Aluko OM, Eduviere AT, Owoeye O Evaluation of adaptogenic-like property of methyl jasmonate in mice exposed to unpredictable chronic mild stress. Brian Res Bull — Article CAS Google Scholar Roberts JC, Francetic DJ Mechanisms of chemoprotection by ribo-cysteine, a thiazolidineprodrug of L-cysteine. Med Chem Resp — CAS Google Scholar KaderT PCM, Williams MJ, Gieseg SP, McCormick SP Ribose-cysteine increases glutathione-based antioxidant status and reduces LDL in human lipoprotein a mice. Atherosclerosis — Article Google Scholar Aoyama K, Nakaki T Impaired glutathione synthesis in neurodegeneration. Int J Mol Sci — Article Google Scholar Falana B, Adeleke O, Orenolu M, Osinubi A, Oyewopo A Effect of D-ribose-L-cysteine on aluminum induced testicular damage in male Sprague-Dawley rats. JBRA Assisted Reproduction — Article Google Scholar Omran H, Illien S, MacCarter D D-Ribose improves diastolic function and quality of life in congestive heart failure patients: a prospective feasibility study. Eur J Heart Fail — Article CAS Google Scholar Teitelbaum JE, Johnson C, St. J Altern Complemen Med — Article Google Scholar Emokpae O, Ben-Azu B, Ajayi AM, Umukoro S D-Ribose- l -cysteine attenuates lipopolysaccharide-induced memory deficits through inhibition of oxidative stress, release of proinflammatory cytokines, and nuclear factor-kappa B expression in mice. Naunyn-Schmied Arch Pharm — Article CAS Google Scholar Moron MS, Depierre JW, Mannervik B Levels of glutathione, glutathionereductase and glutathione S-transferase activities in rat lung and liver. Biochem Biophys Acta —78 Article CAS Google Scholar Okhawa H, Ohishi N, Yagi K Assay for lipid peroxides in animal tissues by thiobarbituric acid reaction. |
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