Oxidative stress in aging: Important or overtaken

When getting older, the body changes because of an accumulation of chronological and multifactor processes. A characteristic process of aging is a decreased homeostasis by a progressive physio-pathological deterioration with time. This decrease leads to a deteriorated physiological capacity, and a decreased environmental tolerance. This inability to respond to environmental stimuli increases the chance of age-related diseases by mitochondrial changes, inactive proteins stuck in the cytosol, somatic mutations, a lack of transcription ability and chemical damage to macromolecules. These processes of the human body are thought to be mediated by damage of the reactive oxygen species (ROS) originated in mitochondria. ROS are intermediates or products of the metabolism, such as unstable superoxide radical, hydroxyl radical or hydrogen peroxide. ROS are constantly produced in the metabolic pathways by aerobic cells. These reactive oxygen species are used as signaling molecules to maintain homeostasis. It can cause oxidative molecular damage to lipids, proteins and DNA when their production is overwhelming the capacity of antioxidant systems. (1) A molecular defect (superoxide dismutases, SOD) that leads to a change in expression of the mitochondrial DNA(mtDNA) or to damage in the biogenesis of mitochondria, provides a loss of energy metabolism in the affected tissue cells. (2) (9) The life span of an organism can also be associated with antioxidants capacity. Antioxidants are capable of inhibiting the oxidation of other molecules. Because of the decrease of activity and capacity of antioxidants in aging, the balance of pro/antioxidants will lead to an accumulation of oxidative damage in the aging process. (1) Two theories emerged. One by Raymond Pearl, the so called “Rate of living theory”, where he suggested that the metabolic rate determines the longevity and life span of an organism. (3). And the “Mitochondrial free-radical theory of aging” by Harman, where he suggests that aging and death were the consequences of the effect of free radicals produced during aerobic respiration, on cell components and connective tissues causing cumulative damage over time. (7)(8). By focusing on relations between ROS mechanisms and ageing in species with markedly different life spans, we evaluated these theories and tried to produce a new light on these theories.