Aging reduces responsiveness to BSO- and heat stress-induced perturbations of glutathione and antioxidant enzymes

Morrison, Joanna; Coleman, Mitchell C.; Aunan, Elizabeth S; Walsh, Susan A.; Spitz, Douglas R.; Kregel, Kevin C.

doi:10.1152/ajpregu.00254.2005

Cited by 22 publications

(13 citation statements)

References 56 publications

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“…The activation of SOD is usually caused by increased superoxide radical formation (Ji 1993). SOD is a free radical-chain breaking enzyme that catalyzes the dismutation of superoxide radical into oxygen and H 2 O 2 (Halliwell and Chirico 1993), and while it is an important antioxidant defense mechanism in aerobic organisms it can be affected by changes in temperature, as demonstrated by previous studies using animal models (Oztürk and Gümüslü 2004;Morrison et al 2005). In the present study, SOD activity was not affected by heat stress at rest but was reduced when heat stress was superimposed with exercise.…”

Section: Discussionmentioning

confidence: 96%

Separate and combined effects of heat stress and exercise on circulatory markers of oxidative stress in euhydrated humans

et al. 2010

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Combined heat stress, dehydration, and exercise is associated with enhanced oxidative stress in humans, but the separate and combined effects of heat stress and exercise on circulatory markers of oxidative stress without the influence of dehydration remain uncertain. The purpose of this study was to determine the effects of whole body heat stress alone and in combination with exercise on blood markers of oxidative stress in euhydrated humans. Eight males wore a water-perfused suit at rest and during 6 min of one-legged knee extensor exercise under control and heat stress conditions while maintaining euhydration. Following the control trial and a 15 min resting period, hot water was perfused through the suit in order to increase core, skin, and mean body temperatures by ~1, ~6, and ~2°C, respectively. Blood samples were taken to measure reduced glutathione (GSH), oxidized glutathione (GSSG), superoxide dismutase (SOD) and plasma isoprostanes. Heat stress alone did not alter GSH, SOD activity, or plasma isoprostanes, but increased GSSG leading to a reduction in the GSH/GSSG ratio. No changes in these variables were observed with exercise alone. Conversely, combined heat stress and exercise increased both GSH and GSSG, decreased SOD activity, but did not alter GSH/GSSG ratio or isoprostanes. In conclusion, these findings suggest that heat stress, independently of dehydration, induces non-radical oxidative stress at rest but not during moderate exercise because an increase in antioxidant defense compensates the heat stress-induced non-radical oxidative stress.

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Section: Discussionmentioning

confidence: 96%

Separate and combined effects of heat stress and exercise on circulatory markers of oxidative stress in euhydrated humans

et al. 2010

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“…Heat stress was also shown to decrease or inhibit SOD expression and activities [52][53][54]. This inhibition can be attributed to thermal/oxidative inactivation of the enzyme [55].…”

Section: Mitochondrial Antioxidant System and Thermal Sensitivitymentioning

confidence: 97%

Reactive oxygen species, heat stress and oxidative-induced mitochondrial damage. A review

Slimen¹,

Najar

Ghram

et al. 2014

International Journal of Hyperthermia

617

248

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In recent years there has been enormous interest in researching oxidative stress. Reactive oxygen species (ROS) are derived from the metabolism of oxygen as by-products of cell respiration, and are continuously produced in all aerobic organisms. Oxidative stress occurs as a consequence of an imbalance between ROS production and the available antioxidant defence against them. Nowadays, a variety of diseases and degenerative processes such as cancer, Alzheimer's and autoimmune diseases are mediated by oxidative stress. Heat stress was suggested to be an environmental factor responsible for stimulating ROS production because of similarities in responses observed following heat stress compared with that occurring following exposure to oxidative stress. This manuscript describes the main mitochondrial sources of ROS and the antioxidant defences involved to prevent oxidative damage in all the mitochondrial compartments. It also deals with discussions concerning the cytotoxic effect of heat stress, mitochondrial heat-induced alterations, as well as heat shock protein (HSP) expression as a defence mechanism.

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“…In this direction Morrison et al (2005) showed that CAT activity significantly decreases with aging, while the activity of GPx remains unchanged during aging. This outcome was not observed in our study and we found that CAT activity does not change and the GPx activity decreases with aging of rats, in both the liver and kidney.…”

Section: Discussionmentioning

confidence: 87%

l-2-oxothiazolidine-4-carboxylate influence on age- and heat exposure-dependent peroxidation in rat's liver and kidney

Hadzi‐Petrushev

Јankulovski

Milev

et al. 2012

Journal of Thermal Biology

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Aging reduces responsiveness to BSO- and heat stress-induced perturbations of glutathione and antioxidant enzymes

Cited by 22 publications

References 56 publications

Separate and combined effects of heat stress and exercise on circulatory markers of oxidative stress in euhydrated humans

Separate and combined effects of heat stress and exercise on circulatory markers of oxidative stress in euhydrated humans

Reactive oxygen species, heat stress and oxidative-induced mitochondrial damage. A review

l-2-oxothiazolidine-4-carboxylate influence on age- and heat exposure-dependent peroxidation in rat's liver and kidney

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