Effects Of Sleep Deprivation On Histopathological Changes And Oxidative Damage In Different Type Muscle Fibers

Doxorubicin (Dox) is a potent antitumor agent used in cancer treatment. Unfortunately, Dox is myotoxic and results in significant reductions in skeletal muscle mass and function. Complete knowledge of the mechanism(s) by which Dox induces toxicity in skeletal muscle is incomplete, but it is established that Dox-induced toxicity is associated with increased generation of reactive oxygen species and oxidative damage within muscle fibers. Since muscular exercise promotes the expression of numerous cytoprotective proteins (e.g., antioxidant enzymes, heat shock protein 72), we hypothesized that muscular exercise will attenuate Dox-induced damage in exercise-trained muscle fibers. To test this postulate, Sprague-Dawley rats were randomly assigned to the following groups: sedentary, exercise, sedentary with Dox, or exercise with Dox. Our results show increased oxidative stress and activation of cellular proteases (calpain and caspase-3) in skeletal muscle of animals treated with Dox. Importantly, our findings reveal that exercise can prevent the Dox-induced oxidative damage and protease activation in the trained muscle. This exercise-induced protection against Dox-induced toxicity may be due, at least in part, to an exercise-induced increase in muscle levels of antioxidant enzymes and heat shock protein 72. Together, these novel results demonstrate that muscular exercise is a useful countermeasure that can protect skeletal muscle against Dox treatment-induced oxidative stress and protease activation in skeletal muscles.

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Trichloroethylene induced cutaneous irritation in BALB/c hairless mice: Histopathological changes and oxidative damage

Toxicology ◽

10.1016/j.tox.2008.03.016 ◽

2008 ◽

Vol 248 (2-3) ◽

pp. 113-120 ◽

Cited By ~ 18

Author(s):

Tong Shen ◽

Qi-Xing Zhu ◽

Sen Yang ◽

Chang-Hao Wu ◽

Hong-Fu Zhang ◽

...

Keyword(s):

Oxidative Damage ◽

Histopathological Changes ◽

Hairless Mice

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Oxidative damage and histopathological changes in lung of rat chronically exposed to nicotine alone or associated to ethanol

Pathologie Biologie ◽

10.1016/j.patbio.2015.10.001 ◽

2015 ◽

Vol 63 (6) ◽

pp. 258-267 ◽

Cited By ~ 11

Author(s):

H. Dhouib ◽

M. Jallouli ◽

M. Draief ◽

S. Bouraoui ◽

S. El-Fazâa

Keyword(s):

Oxidative Damage ◽

Histopathological Changes

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Improved Physical Performance and Decreased Muscular and Oxidative Damage With Postlunch Napping After Partial Sleep Deprivation in Athletes

International Journal of Sports Physiology and Performance ◽

10.1123/ijspp.2019-0308 ◽

2020 ◽

Vol 15 (6) ◽

pp. 874-883 ◽

Cited By ~ 1

Author(s):

Mohamed Romdhani ◽

Nizar Souissi ◽

Yassine Chaabouni ◽

Kacem Mahdouani ◽

Tarak Driss ◽

...

Keyword(s):

Reaction Time ◽

Glutathione Peroxidase ◽

Oxidative Damage ◽

Sleep Deprivation ◽

Aspartate Aminotransferase ◽

Epworth Sleepiness Scale ◽

Mean Power ◽

Test Reaction ◽

Before And After ◽

Partial Sleep Deprivation

Purpose: To investigate the effects of napping after partial sleep deprivation (PSD) on reaction time, mood, and biochemical response to repeated-sprint exercise in athletes. Methods: Nine male judokas performed 4 test sessions in a counterbalanced and randomized order. Participants accomplished 1 control session after a normal sleep night (NSN) and 3 after PSD with (1) no nap, (2) ∼20-min nap (N20), and (3) ∼90-min nap (N90) opportunities. Test sessions included the running-based anaerobic sprint test, reaction time, Hooper index, and Epworth Sleepiness Scale. Muscle-damage biomarkers and antioxidant status were evaluated before and after exercise. Results: PSD decreased maximum (P < .001, d = 1.12), mean (P < .001, d = 1.33), and minimum (P < .001, d = 1.15) powers compared with NSN. However, N20 and N90 enhanced maximum power compared with PSD (P < .05, d = 0.54; P < .001, d = 1.06, respectively). Minimum power and mean power increased only after N90 (P < .001, d = 1.63; P < .001, d = 1.16, respectively). Epworth Sleepiness Scale increased after PSD (P < .001, d = 0.86) and decreased after N20 (P < .001, d = 1.36) and N90 (P < .001, d = 2.07). N20 reduced multiple-choice reaction time (P < .001, d = 0.61). Despite performance decrement, PSD increased postexercise aspartate aminotransferase (P < .001, d = 4.16) and decreased glutathione peroxidase (P < .001, d = 4.02) compared with NSN. However, the highest performances after N90 were accompanied with lesser aspartate aminotransferase (P < .001, d = 1.74) and higher glutathione peroxidase (P < .001, d = 0.86) compared with PSD. Conclusions: Napping could be preventive against performance degradation caused by sleep loss. A short nap opportunity could be more beneficial when the subsequent effort is brief and requires frequent decision making. However, a longer nap opportunity could be preventive against muscle and oxidative damage, even for higher performances.

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