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The complicated pathogenesis of PD involves oxidative stress, mitochondrial dysfunction, neuroinflammation, impaired autophagy, and proteostasis imbalance, altogether contributing to neuronal vulnerability

Except for cytochrome oxidase which retains the reduced form of oxygen intermediates to their active site, all the other elements of the mitochondrial respiratory chain transfer the electrons directly to oxygen and do not retain any reduced intermediate of oxygen at their active site to protect the cell against oxidative damages

So, for example, during expression and purification of a recombinant protein, it may have a disulfide bond form, which wouldnt normally form in the proteins natural context