Naked mole‐rats (NMRs) are mouse‐sized mammals that exhibit an exceptionally long lifespan (>30 vs. <4 years for mice), and resist aging‐related pathologies such as cardiovascular and pulmonary diseases, cancer, and neurodegeneration. However, the mechanisms underlying this exceptional longevity and disease resistance remain poorly understood. The oxidative stress theory of aging posits that (a) senescence results from the accumulation of oxidative damage inflicted by reactive oxygen species (ROS) of mitochondrial origin, and (b) mitochondria of long‐lived species produce less ROS than do mitochondria of short‐lived species. However, comparative studies over the past 28 years have produced equivocal results supporting this latter prediction. We hypothesized that, rather than differences in ROS generation, the capacity of mitochondria to consume ROS might distinguish long‐lived species from short‐lived species. To test this hypothesis, we compared mitochondrial production and consumption of hydrogen peroxide (H2O2; as a proxy of overall ROS metabolism) between NMR and mouse skeletal muscle and heart. We found that the two species had comparable rates of mitochondrial H2O2 generation in both tissues; however, the capacity of mitochondria to consume ROS was markedly greater in NMRs. Specifically, maximal observed consumption rates were approximately two and fivefold greater in NMRs than in mice, for skeletal muscle and heart, respectively. Our results indicate that differences in matrix ROS detoxification capacity between species may contribute to their divergence in lifespan.
CONCLUSION
Our finding of increased capacity for H2O2 consumption in NMR mitochondria has multiple implications. First, it reconciles the biology of the NMR with the mitochondrial oxidative stress hypothesis of aging: macromolecules of the matrix suffer lesser basal oxidant insult in long‐lived NMRs than in short‐lived mice. Second, it offers a potential explanation for the lack of consistency across previous comparative studies of aging. If long‐lived species mostly differ from short‐lived ones for enhanced matrix antioxidants capacities, then past studies using traditional measures of H2O2 efflux might have struggled to identify an inverse relationship with longevity simply because H2O2 efflux is a poor (and indirect) means of estimating matrix antioxidants. Third, the possibility that the evolution of long lifespan proceeds through upregulation of matrix antioxidants and not by modifying sites of ROS production has profound implications for the medical domain. For instance, such a finding may foster additional interest in developing synthetic antioxidants targeted to mitochondria for the postponement of aging‐related diseases (Shabalina et al., 2017; Skulachev et al., 2009). Future studies are required at this point to investigate whether greater mitochondrial capacity to consume H2O2 is a generalized trait across long‐lived species relative to their shorter‐lived counterparts, which would represent a major paradigm shift in the field of aging.
SOURCE: https://onlinelibrar...1111/acel.12916
. So, tunt01, in your wise hands is to wipe it out at once. 
