Heat-related illnesses are known to involve mitochondrial damage leading to the production of elevated levels of reactive oxygen species. The primary source of reactive oxygen species involves the electron transport chain and nicotinamide adenine dinucleotide phosphate (NADPH) oxidase. Skeletal muscle is highly susceptible to heat stress, but little is known of the mechanisms involved in the responses and whether an antioxidant might mitigate the effects. A study involving cells and isolated muscle fibers was conducted by Yu and colleagues in order to add to our understanding of these pathways. The results of their study are published in the September 2020 issue of The Journal of Nutrition.
Mouse C2C12 myoblasts and isolated rat primary flexor digitorum brevis myofibers were cultured in media containing 0 or 5 µM curcumin and held at 37 or 43°C. Mice were also allocated to treatments of: 1) control/non-heat, 2) curcumin/non-heat, 3) control/heat, or 4) curcumin/heat. Curcumin treatment levels were 15, 50, or 100 mg/kg body weight, which was provided by gavage for 10 days prior to heat exposure (39.5°C for 3 hours).
Heat-induced mitochondrial fragmentation, ROS overproduction and apoptosis were prevented by curcumin treatment of the C2C12 myoblasts. ROS levels and NADPH oxidase protein levels were elevated by 2 and 4 hours of curcumin treatment of cells incubated at 37°C, which was inhibited by reducing NADPH oxidase levels. Curcumin mitigated changes in mitochondrial morphology and function caused by heat stress in rat myofibers and mouse muscles, as well as heat-induced mitochondrial ROS overproduction. These data led the authors to conclude that curcumin was able to regulate ROS levels, which helped preserve mitochondrial function in skeletal muscle.
References Yu T, Dohl J, Wang L, Chen Y, Gasier HG, Deuster PA. Curcumin ameliorates heat-induced injury through NADPH oxidase-dependent redox signaling and mitochondrial preservation in C2C12 myoblasts and mouse skeletal muscle. Journal of Nutrition, Volume 150, Issue 9, 1 September 2020, Pages 2257–2267, https://doi.org/10.1093/jn/nxaa201.
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