can occur with lack of decreases or even increases in o2 consumption is often inferred as opposing the mitochondrial free radical theory of aging. according to a study by g. barja, significant decreases in mitochondrial oxygen radical production (per unit of o2 consumed) occur during dietary restriction, aerobic exercise, chronic exercise, and hyperthyroidism. additionally, mitochondrial oxygen radical generation is lower in long-lived birds than in short-lived mammals of comparable body size and metabolic rate. thus, mitochondrial ros production must be regulated independently of o2 consumption in a variety of species, tissues and physiologic states. challenges to the theory naked mole-rat the naked mole-rat is a long-lived (32 years) rodent. as reviewed by lewis et al., (2013), levels of ros production in the naked mole rat are similar to that of another rodent, the relatively short-lived mouse (4 years). they concluded that it is not oxidative stress that modulates health-span and longevity in these rodents, but rather other cytoprotective mechanisms that allow animals to deal with high levels of oxidative damage and stress. in the naked mole-rat, a likely important cytoprotective mechanism that could provide longevity assurance is elevated expression of dna repair genes involved in several key dna repair pathways. (see dna damage theory of aging.) compared with the mouse, the naked mole rat had significantly higher expression levels of genes essential for the dna repair pathways of dna mismatch repair, non-homologous end joining and base excision repair. birds among birds, parrots live about five times longer than quail. ros production in heart, skeletal muscle, liver and intact erythrocytes was found to be similar in parrots and quail and showed no correspondence with longevity difference. these findings were concluded to cast doubt on the robustness of the oxidative stress theory of aging.