astaxanthine and Muscular-Diseases

This study aimed to: 1) investigate sex differences in heat-induced mitochondrial dysfunction, ROS production, and skeletal muscle injury in mice; 2) evaluate whether curcumin and astaxanthin, alone or together, would prevent those heat-induced changes.. Male and female C57BL/6J mice were treated with curcumin and astaxanthin for 10 days, then exposed to 39.5 °C heat for up to 3 h. Heat-induced hyperthermia, changes in mitochondrial morphology and function, and oxidative damage to skeletal muscle were evaluated.. Although female mice had a slightly higher basal core body temperature (Tc) than male mice, peak Tc during heat exposure was significantly lower in females than in males. Heat increased ROS levels in skeletal muscle in both sexes; interestingly, the increases in ROS were greater in females than in males. Despite the above-mentioned differences, heat induced similar levels of mitochondrial fragmentation and membrane potential depolarization, caspase 3/7 activation, and injury in male and female skeletal muscle. Individual treatment of curcumin or astaxanthin did not affect basal and peak Tc but prevented heat-induced mitochondrial dysfunction, ROS increases, and apoptosis in a dose-dependent manner. Moreover, a low-dose combination of curcumin and astaxanthin, which individually showed no effect, reduced the heat-induced oxidative damage to skeletal muscle.. Both male and female mice can develop mitochondrial dysfunction and oxidative stress in skeletal muscle when exposed to heat stress. High doses of either curcumin or astaxanthin limit heat-induced skeletal muscle injury, but a low-dose combination of these ingredients may increase their efficacy.

Topics: Animals; Anti-Inflammatory Agents, Non-Steroidal; Curcumin; Diet; Female; Heat-Shock Response; Hyperthermia, Induced; Male; Mice; Mice, Inbred C57BL; Muscle, Skeletal; Muscular Diseases; Oxidative Stress; Protective Agents; Reactive Oxygen Species; Xanthophylls

Heat stress causes mitochondrial dysfunction and increases mitochondrial production of reactive oxygen species (ROS), both of which contribute to heat-induced skeletal muscle injury. In this study, we tested whether either astaxanthin or quercetin, two dietary antioxidants, could ameliorate heat-induced skeletal muscle oxidative injury. In mouse C2C12 myoblasts exposed to 43°C heat stress, astaxanthin inhibited heat-induced ROS production in a concentration-dependent manner (1-20 μM), whereas the ROS levels remained high in cells treated with quercetin over a range of concentrations (2-100 µM). Because mitochondria are both the main source and a primary target of heat-induced ROS, we then tested the effects of astaxanthin and quercetin on mitochondrial integrity and function, under both normal temperature (37°C) and heat stress conditions. Quercetin treatment at 37°C induced mitochondrial fragmentation and decreased membrane potential (ΔΨ

Topics: Animals; Caspase 3; Caspase 7; Cell Line; Cell Survival; Hot Temperature; Membrane Potential, Mitochondrial; Mice; Mitochondria; Muscular Diseases; Myoblasts; Oxidative Stress; Quercetin; Rats; Reactive Oxygen Species; Xanthophylls