Damaging reactive oxygen species (ROS) and other free radicals are generated within your cells, largely as a result of the day to day operations of mitochondria, the power plants of the cell that produce chemical energy stores used by cellular processes. Too many free radicals produce the state called oxidative stress, in which a cell struggles to keep up with the repair of its protein machinery. Oxidative stress increases with age: this is thought to be due to increasing dysfunction in mitochondria, and to be a root cause of degenerative aging.
It's not quite so simple, however, as the presence of oxidative molecules in our biology is vital to life. Evolution eagerly uses and reuses every cog, nut, and bolt that happens to be to hand, and so ROS are involved in a range of essential cellular mechanisms. Low levels of ROS are usually beneficial and necessary, while high levels are usually damaging and bad. (Unless you are a naked mole rat, in which case high levels seem to be business as usual and something to be shrugged off in the course of living for an exceedingly long time). Biology is a complex business, and it is always the case that the details matter: you can't just talk about ROS levels, but have to talk about where, when, how they change, and their interaction with other processes.
Under normal physiological conditions, reactive oxygen species (ROS) serve as 'redox messengers' in the regulation of intracellular signalling, whereas excess ROS may induce irreversible damage to cellular components and lead to cell death by promoting the intrinsic apoptotic pathway through mitochondria. In the aging process, accumulation of mitochondria DNA mutations, impairment of oxidative phosphorylation as well as an imbalance in the expression of antioxidant enzymes result in further overproduction of ROS. This mitochondrial dysfunction-elicited ROS production axis forms a vicious cycle, which is the basis of mitochondrial free radical theory of aging. In addition, several lines of evidence have emerged recently to demonstrate that ROS play crucial roles in the regulation of cellular metabolism, antioxidant defence and posttranslational modification of proteins.
We first discuss the oxidative stress responses, including metabolites redistribution and alteration of the acetylation status of proteins, in human cells with mitochondrial dysfunction and in aging. On the other hand, autophagy and mitophagy eliminate defective mitochondria and serve as a scavenger and apoptosis defender of cells in response to oxidative stress during aging. These scenarios mediate the restoration or adaptation of cells to respond to aging and age-related disorders for survival.
In the natural course of aging, the homeostasis in the network of oxidative stress responses is disturbed by a progressive increase in the intracellular level of the ROS generated by defective mitochondria. Caloric restriction, which is generally thought to promote longevity, has been reported to enhance the efficiency of this network and provide multiple benefits to tissue cells. In this review, we emphasize the positive and integrative roles of mild oxidative stress elicited by mitochondria in the regulation of adaptation, anti-aging and scavenging pathway beyond their roles in the vicious cycle of mitochondrial dysfunction in the aging process.