There is a link between mitochondrial dysfunction resulting in increased ROS production, however is the reverse relationship possible where ROS causes mitochondrial dysfunction?..How would this occur?
ROS contribute significantly to the regulation of activity of various signal transduction pathways and transcription factors. ROS activates members of the MAP kinase pathway & play a role in growth factor receptor activation through oxidative deactivation of protein tyrosine phosphatases that maintain the growth factor receptors in an inactive state.So if eg. Complex I is underactive then there would be no spare free electrons.Accumulated non-oxidised electrons interact with molecular oxygen to generate reactive oxygen species. Maintaining a healthy mitochondrial membrane potential through calorific reduction and increasing OXPHOS through exercise thus ensuring adequate cytoplasmic ADP can alleviate stress in mitochondria. So in a normal well balanced environment the excess substrate (accumulated electrons) wouldn't initiate an increased mito membrane potential causing reduced H+ re entry because they woule be employed in the generation of ATP
Oxidative phosphorylation takes place in the mitochondria. Leakages from the intermembrane space in the course of electron transport even cause damages to the membrane structure and compromise membrane integrity. ROS has been implicated in mitochondrial dysfunctions leading to mtDNA damages and manifestations in mitochondrial disorders. So yes, excessive ROS generation can precipitate mitochondrial dysfunction.
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