Exercise and diet modulate cardiac lipid peroxidation and antioxidant defenses

Kim, Jong Dai; Yu, Byung Pal; McCarter, Roger; Lee, Sang Young; Herlihy, Jeremiah T.

doi:10.1016/0891-5849(95)02023-3

Cited by 91 publications

(49 citation statements)

References 24 publications

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“…Studies performed thus far, in which food intake was carefully controlled, have only been able to show an increase in mean lifespan, with no change in maximum lifespan (23,24). Furthermore, only a handful of studies using long-term wheel running (Ͼ18 mo) have measured any parameters of oxidative stress (29,30,33); to our knowledge, none has determined the effects on oxidant production. We determined whether longterm voluntary wheel running could reduce oxidant production, enhance antioxidant defenses, and reduce oxidative damage in two populations of heart mitochondria with distinct metabolic demands.…”

Section: Discussionmentioning

confidence: 99%

“…Voluntary wheel running increases mean lifespan (23,24), and survival is significantly enhanced in wheel-running rats compared with treadmilltrained rats (40). There is also evidence that exercise may reduce oxidative damage and increase antioxidant enzyme activities in a variety of tissues (29,30,33); more recently, it has been shown that long-term voluntary exercise can attenuate many age-related changes in gene expression (inflammatory response, stress response, signal transduction, and energy metabolism) (10). However, little is known regarding the specific effects of long-term voluntary wheel running on mitochondrial function and oxidative stress in the heart.…”

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confidence: 99%

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Exercise by lifelong voluntary wheel running reduces subsarcolemmal and interfibrillar mitochondrial hydrogen peroxide production in the heart

Judge

Jang²,

Smith³

et al. 2005

American Journal of Physiology-Regulatory, Integrative and Comp

122

114

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-Evidence suggests that mitochondrial dysfunction and oxidant production, in association with an accumulation of oxidative damage, contribute to the aging process. Regular physical activity can delay the onset of morbidity, increase mean lifespan, and reduce the risk of developing several pathological states. No studies have examined age-related changes in oxidant production and oxidative stress in both subsarcolemmal (SSM) and interfibrillar (IFM) mitochondria in combination with lifelong exercise. Therefore, we investigated whether long-term voluntary wheel running in Fischer 344 rats altered hydrogen peroxide (H 2O2) production, antioxidant defenses, and oxidative damage in cardiac SSM and IFM. At 10 -11 wk of age, rats were randomly assigned to one of two groups: sedentary and 8% food restriction (sedentary; n ϭ 20) or wheel running and 8% food restriction (runners; n ϭ 20); rats were killed at 24 mo of age. After the age of 6 mo, running activity was maintained at an average of 1,145 Ϯ 248 m/day. Daily energy expenditure determined by doubly labeled water technique showed that runners expended on average ϳ70% more energy per day than the sedentary rats. Long-term voluntary wheel running significantly reduced H 2O2 production from both SSM (Ϫ10.0%) and IFM (Ϫ9.6%) and increased daily energy expenditure (kJ/day) significantly in runners compared with sedentary controls. Additionally, MnSOD activity was significantly lowered in SSM and IFM from wheel runners, which may reflect a reduction in mitochondrial superoxide production. Activities of the other major antioxidant enzymes (glutathione peroxidase and catalase) and glutathione levels were not altered by wheel running. Despite the reduction in mitochondrial oxidant production, no significant differences in oxidative stress levels (4-hydroxy-2-nonenal-modified proteins, protein carbonyls, and malondialdehyde) were detected between the two groups. The health benefits of chronic exercise may be, at least partially, due to a reduction in mitochondrial oxidant production; however, we could not detect a significant reduction in several selected parameters of oxidative stress.

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Section: Discussionmentioning

confidence: 99%

mentioning

confidence: 99%

Exercise by lifelong voluntary wheel running reduces subsarcolemmal and interfibrillar mitochondrial hydrogen peroxide production in the heart

Judge

Jang²,

Smith³

et al. 2005

American Journal of Physiology-Regulatory, Integrative and Comp

122

114

View full text Add to dashboard Cite

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“…26 There is also evidence that exercise may reduce oxidative damage and increase antioxidant enzyme activities in a variety of tissues. [27][28][29] Conversely Judge etal.reported that voluntary exercise resulted in a significant reduction in MnSOD activity although there was no effect of wheel running on GPX and CAT activity in the heart. Moreover there were no changes in cytosolic SOD, GPX, or CAT activities.…”

Section: Discussionmentioning

confidence: 99%

Voluntary Exercise Protects Heart from Oxidative Stress in Diabetic Rats

et al. 2015

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“…One major mechanism by which dietary restriction retards the aging process is its remarkable ability to reduce ox idative damages (5-10). For example, Kim et al (11) have shown that dietary restriction decreases the mal ondialdehyde content of cardiac mitochondria, indicat ing a decrease in lipid peroxidation. Restricted feeding regimens enhance the organism's ability to attenuate levels of harmful reactive-free radicals in various organs (12,13).…”

Section: Discussionmentioning

confidence: 99%

Dietary Restriction Downregulates Free Radical and Lipid Peroxide Production: Plausible Mechanism for Elongation of Life Span.

Lim

Sugano

2002

Journal of Nutritional Science and Vitaminology, J Nutr Sci Vit

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SummaryDietary restriction elongates life span by suppressing age-related diseases in experimental animals. It has received a great deal of attention in connection with the rela tionship between aging, nutrition, and oxidative stress because oxidative injury in several tissues is a prominent feature in the aging process. Although the oxidative stress theory of aging has currently gained popularity, the premise from which this hypothesis was derived is paradoxical because the same oxygen, that supports life in one hand threatens survival and promotes aging in the other. Until recently, no single experimental paradigm could offer satisfactory mechanistic explanations for this complex issue. Recent investigations using the life-extending dietary restriction regimen could offer satisfactory mechanistic explanations for this apparent self contradiction to life. The modulation of free radical-induced oxidative stress provided sufficient data to support the notion that dietary restriction's antiaging ef fect may come from its ability to tightly regulate the oxidative status of an organism. The re sult is the maintenance of cellular homeostasis, a hallmark of dietary restriction's action in the extension of life span. To date, we reported that dietary restriction (maintained on 60% of ad libitum feeding) suppresses age-related oxidative damage by modulating the amount as well as the fatty acid composition of tissue phospholipids. These remarkable findings have been incorporated into the new "membrane peorxidation cycle" concept. The intervention of this cycle appears to be an evolutionary process that the dietary restricted rats have adapted as a strategy to protect the membrane in an oxidative environment.

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Exercise and diet modulate cardiac lipid peroxidation and antioxidant defenses

Cited by 91 publications

References 24 publications

Exercise by lifelong voluntary wheel running reduces subsarcolemmal and interfibrillar mitochondrial hydrogen peroxide production in the heart

Exercise by lifelong voluntary wheel running reduces subsarcolemmal and interfibrillar mitochondrial hydrogen peroxide production in the heart

Voluntary Exercise Protects Heart from Oxidative Stress in Diabetic Rats

Dietary Restriction Downregulates Free Radical and Lipid Peroxide Production: Plausible Mechanism for Elongation of Life Span.

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