Abstract
Glutathione (GSH) is an abundant thiol that is critical in cellular redox status. Reduced cellular antioxidant capacity has been shown to increase cellular damage and apoptosis. In this study we investigated the effect of GSH depletion, by L‐buthionine‐[S,R]‐sulfoximine (BSO), on redox status and apoptotic signaling in rat quadriceps muscle. BSO treatment significantly (p<0.05) reduced whole muscle and mitochondrial GSH content by 95% and 84%, respectively. Whole muscle reactive oxygen species (ROS) generation was also found to be significantly (p<0.05) elevated in BSO‐treated animals compared to controls. In addition, CuZnSOD protein content was significantly (p<0.05) increased in BSO‐treated animals compared to controls. Flow cytometric analysis also revealed that membrane potential was significantly (p<0.05) reduced in isolated mitochondria of BSO‐treated animals. Interestingly, the activity of caspase‐3 and ‐9 in skeletal muscle was not significantly different between groups. This data suggests that glutathione depletion significantly alters muscle/mitochondrial redox status as well as mitochondrial membrane potential but not basal apoptotic signaling. It remains to be determined if these changes influence apoptotic signaling/susceptibility to additional cellular stressors. Research supported by NSERC of Canada.
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