학술논문

Diphenyl diselenide blunts swimming training on mitochondrial liver redox adaptation mechanisms of aged animals
Document Type
Original Paper
Source
Sport Sciences for Health: Founded by the Faculty of Exercise Science - University of Milan, official journal of the Italian Society of Exercise and Sport Sciences. 16(2):281-290
Subject
Exercise
Supplement
Hepatic damage
Oxidative stress
Aging
Language
English
ISSN
1824-7490
1825-1234
Abstract
Background: Studies about antioxidant supplementation and exercises combined, especially at hepatic liver tissue, are rare and still controversial. In this study, we aimed to evaluate if the association between a recognized antioxidant compound—Diphenyl Diselenide ([(PhSe)2])—and training can reduce homogenate liver and liver mitochondria oxidative stress in old rats.Methods: Old male Wistar rats were divided into four groups (six animals per group): old-sedentary, old-sedentary [(PhSe)2] supplemented, old-trained, and old-trained [(PhSe)2] supplemented. Trained groups were submitted to swimming training sessions (3% of body weight, 20 min/day during 4 weeks); animals were fed daily with standard feed or standard feed supplemented with 1 ppm of [(PhSe)2] during 4 weeks.Results: Trained and trained + [(PhSe)2] groups decreased reactive oxygen species (ROS) generation, while only the trained group reduces GSSG production and increased GSH/GSSG ratio when compared to trained + [(PhSe)2]. Mitochondrial ROS production was elevated in control sedentary group, but only swimming training prevented its elevation. However, MnSOD activity was found elevated at trained + [(PhSe)2] rats when compared to the trained and [(PhSe)2] supplementation groups. Mitochondrial Δψm in trained + [(PhSe)2] was decreased compared to trained group, while ratio (III/IV states) was increased when compared to control sedentary.Conclusions: We conclude that the combination of [(PhSe)2] and swimming training did not manifest synergic effect since it does not prevent the aging-induced hepatic oxidative stress generation, but blunted the induced-exercise adaptations, including at mitochondrial mechanisms.