Exercise causes oxidative damage to rat skeletal muscle microsomes while increasing cellular sulfhydryls

Rajguru, Shailesh U.; Yeargans, George S; Seidler, Norbert W.

doi:10.1016/0024-3205(94)00584-2

Cited by 63 publications

(36 citation statements)

References 17 publications

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“…Repetitive muscle contractions, as occur in strenuous exercise, produce reactive oxygen species (6,15,28,30,34) that oxidize GSH to increase in intracellular GSSG, resulting in a shift of the intracellular redox balance toward an oxidative state. It has been reported that skeletal muscle dysfunction may occur after intense exercise (29,30). The activation of RyR channels through the shift in the myoplasmic redox potential might also be involved in the pathophysiological changes of skeletal muscles.…”

Section: Discussionmentioning

confidence: 99%

Redox states of type 1 ryanodine receptor alter Ca²⁺ release channel response to modulators

Ôba

Murayama

Ogawa

2002

American Journal of Physiology-Cell Physiology

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The type 1 ryanodine receptor (RyR1) from rabbit skeletal muscle displayed two distinct degrees of response to cytoplasmic Ca2+ [high- and low-open probability ( P o) channels]. Here, we examined the effects of adenine nucleotides and caffeine on these channels and their modulations by sulfhydryl reagents. High- P o channels showed biphasic Ca2+ dependence and were activated by adenine nucleotides and caffeine. Unexpectedly, low- P o channels did not respond to either modulator. The addition of a reducing reagent, dithiothreitol, to the cis side converted the high- P o channel to a state similar to that of the low- P o channel. Treatment with p-chloromercuriphenylsulfonic acid (pCMPS) transformed low- P o channels to a high- P o channel-like state with stimulation by β,γ-methylene-ATP and caffeine. In experiments under redox control using glutathione buffers, shift of the cis potential toward the oxidative state activated the low- P ochannel, similar to that of the high- P o or the pCMPS-treated channel, whereas reductive changes inactivated the high- P o channel. Changes in transredox potential, in contrast, did not affect channel activity of either channel. In all experiments, channels with higher P o were stimulated to a great extent by modulators, but ones with lower P o were unresponsive. These results suggest that redox states of critical sulfhydryls located on the cytoplasmic side of the RyR1 may alter both gating properties of the channel and responsiveness to channel modulators.

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Section: Discussionmentioning

confidence: 99%

Redox states of type 1 ryanodine receptor alter Ca²⁺ release channel response to modulators

Ôba

Murayama

Ogawa

2002

American Journal of Physiology-Cell Physiology

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“…In contrast, lipid peroxidation is frequently used as an index of oxidative stress during exercise because polyunsatured fatty acids are especially susceptible to ROS attack and byproducts of lipid peroxidation are easily measured. Several studies have shown an increased lipid peroxidation in various tissues, such as skeletal [16,[26][27][28][29] and cardiac [28][29][30] muscle, liver [16,26,28,29], brain [31] and in erythrocytes [30] of untrained rats after acute exercise. However, not all studies have found evidence of oxidative stress following exercise, and contradictory data do exist.…”

Section: Lipid Peroxidationmentioning

confidence: 99%

Mitochondria in Exercise-Induced Oxidative Stress

Meo

Venditti²

2001

Biol Signals Recept

163

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In recent years it has been suggested that reactive oxygen species (ROS) are involved in the damage to muscle and other tissues induced by acute exercise. Despite the small availability of direct evidence for ROS production during exercise, there is an abundance of literature providing indirect support that oxidative stress occurs during exercise. The electron transport associated with the mitochondrial respiratory chain is considered the major process leading to ROS production at rest and during exercise. It is widely assumed that during exercise the increased electron flow through the mitochondrial electron transport chain leads to an increased rate of ROS production. On the other hand, results obtained by in vitro experiments indicate that mitochondrial ROS production is lower in state 3 (ADP-stimulated) than in state 4 (basal) respiration. It is possible, however, that factors, such as temperature, that are modified in vivo during intense physical activity induce changes (uncoupling associated with loss of cytochrome oxidase activity) leading to increased ROS production. The mitochondrial respiratory chain could also be a potential source of ROS in tissues, such as liver, kidney and nonworking muscles, that during exercise undergo partial ischemia because of reduced blood supply. Sufficient oxygen is available to interact with the increasingly reduced respiratory chain and enhance the ROS generation. At the cessation of exercise, blood flow to hypoxic tissues resumes leading to their reoxygenation. This mimics the ischemia-reperfusion phenomenon, which is known to cause excessive production of free radicals. Apart from a theoretical rise in ROS, there is little evidence that exercise-induced oxidative stress is due to its increased mitochondrial generation. On the other hand, if mitochondrial production of ROS supplies a remarkable contribution to exercise-induced oxidative stress, mitochondria should be a primary target of oxidative damage. Unfortunately, there are controversial reports concerning the exercise effects on structural and functional characteristics of mitochondria. However, the isolation of mitochondrial fractions by differential centrifugation has shown that the amount of damaged mitochondria, recovered in the lightest fraction, is remarkably increased by long-lasting exercise.

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“…Neutrophil activation infiltrating the muscle after injury by exercise may also produce ROS (12). ROS may cause oxidative tissue damage (13), e.g., DNA injury (14), lipid peroxidation (15) and protein oxidation (16)(17)(18). These processes are associated with the appearance of and increase in the severity of many diseases (19,20).…”

mentioning

confidence: 99%

Plasma antioxidant status and cell injury after severe physical exercise

Chevion

Moran

Heled

et al. 2003

Proc. Natl. Acad. Sci. U.S.A.

220

137

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Strenuous exercise leads to an increase in metabolic rate, increased production of reactive oxygen species, and compromised antioxidant defense systems. To study the effects of oxidative stress during strenuous exercise, a homogeneous group of 31 male subjects participated in a 6-month, 5 days͞week training schedule involving two extreme marches of 50 km and 80 km at sea level, separated by 2 weeks of regular training. Each participant carried 35 kg of extra weight. Blood samples were drawn imediately before and after each march. Twenty-nine subjects completed the 50-km march, and only 16 completed the 80-km march. Plasma levels of reduced ascorbic acid, total ascorbate, and dehydroascorbate did not undergo significant changes during either march. However, the 50-and 80-km marches led to 25% and 37% increases, respectively, in plasma levels of uric acid; due presumably to increases in the metabolic rate and consequent pyrimidine nucleotide metabolism. Both marches led to Ϸ10-fold increase leakage of creatine phosphokinase into the plasma. Likewise, plasma levels of aspartate transaminase, a characteristic marker of liver injury, increased Ϸ4-fold. Plasma levels of bilirubin, creatine, urea, and glucose also increased. Plasma protein carbonyl content, a marker of protein oxidative damage, decreased significantly during each march. These results are discussed with respect to the consideration that elevation of the respiration rate during exercise leads to production of more reactive oxygen species than the antioxidant systems can scavenge. Plausible explanations for leakage of molecules into the plasma are discussed.

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Exercise causes oxidative damage to rat skeletal muscle microsomes while increasing cellular sulfhydryls

Cited by 63 publications

References 17 publications

Redox states of type 1 ryanodine receptor alter Ca²⁺ release channel response to modulators

Redox states of type 1 ryanodine receptor alter Ca²⁺ release channel response to modulators

Mitochondria in Exercise-Induced Oxidative Stress

Plasma antioxidant status and cell injury after severe physical exercise

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Exercise causes oxidative damage to rat skeletal muscle microsomes while increasing cellular sulfhydryls

Cited by 63 publications

References 17 publications

Redox states of type 1 ryanodine receptor alter Ca2+ release channel response to modulators

Redox states of type 1 ryanodine receptor alter Ca2+ release channel response to modulators

Mitochondria in Exercise-Induced Oxidative Stress

Plasma antioxidant status and cell injury after severe physical exercise

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Redox states of type 1 ryanodine receptor alter Ca²⁺ release channel response to modulators

Redox states of type 1 ryanodine receptor alter Ca²⁺ release channel response to modulators