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We hypothesized, therefore, that the ROS from hyperglycemic mitochondria directly reacts with and consumes the intracellular H 2 S, which then creates additional mitochondrial dysfunction, possibly by oxidative modification to mitochondrial proteins and proposed that such a positive feed-forward cycle may then culminate in a dysfunctional mitochondrial state where molecular oxygen is utilized to produce ROS (as opposed to ATP), and where mitochondrial efficacy is diminished (58)

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Injection(s):Eight

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