[Paper introduction] Cystine attenuates mitochondrial dysfunction in C2C12 myotubes under moderate oxidative stress induced by hydrogen peroxide exposure

Moderate oxidative stress induces a temporary functional impairment of mitochondrial ATP production. Glutathione (GSH) concentration is decreased by the removal of oxidative stress through redox reactions, and intracellular GSH content is crucial for maintaining mitochondrial function under oxidative stress. GSH precursors such as N-acetylcysteine ​​and cysteine ​​are known to suppress oxidative stress by providing cysteine ​​residues, which are rate-limiting for GSH synthesis. However, it is unclear whether cystine reduces mitochondrial dysfunction under oxidative stress. Therefore, we investigated whether cystine reduces mitochondrial dysfunction under moderate oxidative stress without scavenging reactive oxygen species (ROS) in the medium. C2C12 myotube cells were incubated in cystine-supplemented medium for 120 min, followed by hydrogen peroxide (H₂O₂) were exposed to oxidative stress. The changes in heme oxygenase-1 (HO-1) gene expression, intracellular cysteine ​​and GSH levels, intracellular ATP levels, and mitochondrial maximum respiratory capacity, which are all responsive to oxidative stress, were evaluated. The results showed that cystine supplementation significantly increased GSH levels in a dose-dependent manner. In addition, cystine supplementation reduced H₂O₂The HO-1 gene expression induced by exposure to H₂O₂The amount of GSH was reduced by exposure to 500 μg/ml of sucrose, but was improved by the addition of cystine. These results suggest that the addition of cystine attenuates oxidative stress-induced mitochondrial dysfunction by maintaining the amount of GSH under moderate oxidative stress without scavenging ROS in the medium.

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https://link.springer.com/article/10.1007/s00726-022-03176-y