Protective effects of atromid-S in vivo on mitochondrial stability in tissues of aged hamsters.
Atromid-S and nicotinic acid (hypocholesterolemic agents) were tested in vivo for their effects on mitochondrial yields and oxidative phosphorylation in tissues of aging hamsters. It was observed that atromid-S increased mitochondrial yields from both heart and skeletal muscle (39 and 64%, respectively), while nicotinic acid increased the yield only from skeletal muscle (97%). Efficiency (P:0 ratios) and rates of oxidative phosphorylation remained unchanged by drug treatment. Atromid-S treatment only partially protected against loss of controlled phosphorylation on prolonged storage of heart and skeletal muscle mitochondria of aging hamsters. It appeared that atromid-S may produce its effects on mitochondrial yields by decreasing the fragility of the mitochondria from the aging animals. The effects of the drug were not permanent, and values returned to control levels after 3 weeks from cessation of treatment.
D000375:Aging; D000818:Animals; D002994:Clofibrate / Q000494:pharmacology*; D006224:Cricetinae; D008099:Liver / Q000378:metabolism; D008297:Male; D008930:Mitochondria, Liver / Q000187:drug effects*; D008931:Mitochondria, Muscle / Q000187:drug effects*; D009132:Muscles / Q000378:metabolism; D009206:Myocardium / Q000378:metabolism; D009539:Nicotinic Acids / Q000494:pharmacology; D010085:Oxidative Phosphorylation / Q000187:drug effects; D013385:Succinate Dehydrogenase / Q000032:analysis
D009539:Nicotinic Acids; D013385:Succinate Dehydrogenase; D002994:Clofibrate