Mitochondria are evolved remnants of symbiotic bacteria within our cells. They produce chemical energy stores used to power cellular operations, but that process also produces damaging oxidative molecules, and the mitochondria themselves bear the brunt of that. Unfortunately some rare forms of the resulting damage sabotage mitochondrial machinery in ways that propagate throughout a cell's herd of mitochondria, turning the entire cell into a malfunctioning exporter of harmful oxidative molecules. The growing numbers of such cells in the body cause increasing harm, and this is one of the contributing causes of degenerative aging.
There are natural antioxidants present in mitochondria, such as forms of superoxide dismutase, and the situation would - in theory - be far worse without them. Researchers have shown that boosting the levels of some of these antioxidants can be beneficial in mice, and targeting designed antioxidant molecules to the mitochondria can similarly produce benefits to health and life span.
Interestingly it is possible to extend life in some cases by reducing the level of natural antioxidants in the mitochondria. In this case it is thought that increased levels of oxidants produce a hormetic response in cells, driving more housekeeping and maintenance activities to create a net benefit. The inner workings of mitochondria are both very complex and very important to metabolism and aging, and the results of any change to these mechanisms can be counterintuitive:
The processes that control aging remain poorly understood. We have exploited mutants in the nematode, Caenorhabditis elegans, that compromise mitochondrial function and scavenging of reactive oxygen species (ROS) to understand their relation to lifespan.
We discovered unanticipated roles and interactions of the mitochondrial superoxide dismutases (mtSODs): SOD-2 and SOD-3. Both SODs localize to mitochondrial supercomplex I:III:IV. Loss of SOD-2 specifically (i) decreases the activities of complexes I and II, complexes III and IV remain normal; (ii) increases the lifespan of animals with a complex I defect, but not the lifespan of animals with a complex II defect, and kills an animal with a complex III defect; (iii) induces a presumed pro-inflammatory response. Knockdown of a molecule that may be a pro-inflammatory mediator very markedly extends lifespan and health of certain mitochondrial mutants.
The relationship between the electron transport chain, ROS, and lifespan is complex, and defects in mitochondrial function have specific interactions with ROS scavenging mechanisms. We conclude that mtSODs are embedded within the supercomplex I:III:IV and stabilize or locally protect it from reactive oxygen species (ROS) damage.