The impact of XXXX and hydrogen peroxide on muscle cell plasticity shows a dose-dependent interaction.

@entity274 @entity1184 @entity4222 @entity26 @entity19490 @entity9703 @entity4025
While reactive @entity26 species (ROS) play a role in muscle repair, excessive amounts of ROS for extended periods may lead to oxidative stress. Antioxidants, as @entity4025 (RS), may reduce oxidative stress, restore mitochondrial function and promote myogenesis and @entity1184 . However, RS dose-effectiveness for muscle plasticity is unclear. Therefore, we investigated RS dose-response on C2C12 myoblast and myotube plasticity 1. in the presence and 2. absence of different degrees of oxidative stress. Low RS concentration (10    M) stimulated myoblast cell cycle arrest, @entity4222 and sprouting, which were inhibited by higher doses (40-60    M). RS did not increase oxidative capacity. In contrast, RS induced mitochondria loss, reduced cell viability and ROS production, and activated stress response pathways [Hsp70 and pSer36- @entity19490 ( @entity9703 ) proteins]. However, the deleterious effects of @entity274 (1000     M) on cell @entity4222 were alleviated after preconditioning with 10     M-RS. This dose also enhanced cell motility mediated by 100     M- @entity274 , while higher RS-doses augmented the @entity274 -induced impaired myoblast regeneration and mitochondrial dehydrogenase activity. In conclusion, low @entity4025 doses promoted in vitro muscle regeneration and attenuated the impact of ROS, while high doses augmented the reduced plasticity and metabolism induced by oxidative stress. Thus, the effects of @entity4025 depend on its dose and degree of oxidative stress.
