Mitochondrial Electron Transport

Mitochondria generate ROS during normal oxidative phosphorylation and ATP synthesis through electron leak [25]. ROS production by the organelle, however, can be enhanced in response to numerous stimuli or alterations in the cellular environment, resulting in pathologic consequences.

Studies performed by Brownlee and coworker [26] suggest that hyperglycemia-induced oxidative stress from mitochondria is the earliest event in the development of diabetic vascular complications. However, in part because mitochondrial inhibitors are toxic and no experimental animal models are available, the role of excess ROS from mitochondria during in vivo pathologies is poorly understood [27]. The role of mitochondria-derived superoxide in ED has not been investigated.

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