Mitochondria, as the center for energy production, perform the biochemical transformation of glycolysis products to generate usable energy in the form of ATP. Mitochondrial malfunction can lead to senescence and aging phenotypes. Theory predicts degenerative phenotypes and metabolic diseases associated with mitochondria may occur more frequently in males than females due to the matrilineal inheritance pattern of mitochondrial DNA (mtDNA). Mitochondrially driven senescence may be caused by the overproduction of reactive oxygen species generated by oxidative phosphorylation inefficiencies which may damage both mtDNA and nuclear DNA, exacerbating the aging phenotype. Here we estimate sex-specific longevity for parental and reciprocal F1 hybrid crosses between two allopatric Tigriopus californicus populations which display over 20% mtDNA divergence. T. californicus is an emerging model system used to estimate the mitochondrial contribution to sex-specific aging because disparate populations have high divergence, yet remain viable when crossed, and they lack sex chromosomes allowing for more direct testing of mitochondria in sex-specific aging. Along with estimating sex-specific longevity, we estimate aging and damage related phenotypes including mtDNA content and 8-OH-dG DNA damage 28 and 56 days post-hatch. Overall, males live longer than females yet the sex-difference depends on the mitochondrial genotype. Males have lower mtDNA content which decreases with age. Interestingly, males show an increase in 8-OH-dG DNA damage with age while females do not. Hormetic effects in males where an intermediate amount of cellular stress or damage is beneficial may help to explain the relationship between increased DNA damage and increased lifespan when compared to females.