Sex differences in survival and mitochondrial bioenergetics during aging inDrosophila

Abstract

SummaryThe goal of this study is to test the role of mitochondria and of mitochondrial metabolism in determining the processes that influence aging of female and male Drosophila . We observe that Drosophila simulans females tended to have shorter lifespan, higher levels of hydrogen peroxide production and significantly lower levels of catalase but not superoxide dismutase compared to males. In contrast, mammalian females tend to be longer lived, have lower rates of reactive oxygen species production and higher antioxidant activity. In both Drosophila and mammals, mitochondria extracted from females consume a higher quantity of oxygen when provided with adenosine diphosphate and have a greater mtDNA copy number than males. Combined, these data illustrate important similarities between the parameters that influence aging and mitochondrial metabolism in Drosophila and in mammals but also show surprising differences.

High sucrose consumption promotes obesity whereas its low consumption induces oxidative stress in Drosophila melanogaster

“…Only male flies showed positive association between enzymatic activities and transcript levels of SOD and catalase which may indicate tight regulation of these enzymes on transcriptional level. Similar sex-specificity of antioxidant response was observed in previous studies (Ballard et al, 2007;Lushchak et al, 2011;Lozinsky et al, 2012Lozinsky et al, , 2013. Strong dependence of catalase activity on fly gender might be explained by different expression of catalase isoforms (CG6871 and CG9314) in males and females.…”

Condition Dependence of Male Mortality Drives the Evolution of Sex Differences in Longevity

“…Although the mother's curse hypothesis has enjoyed experimental support [36], and mtDNA mutations are likely to increase variance in male aging, neither of these two hypotheses is likely to provide a general explanation for the evolution of sex differences in longevity and aging because males live longer than females in many taxa [7,12,37,38]. Our results show that selection on males, and in a broad sense, sex-limited selection in either sex, is sufficient to generate sexual dimorphism in aging and longevity, whereas the interaction between the rate and the source of mortality (i.e., whether mortality is random or condition dependent, with respect to whole-organism performance) can determine which sex will live the longest.…”

Depleted Leukocyte Mitochondrial DNA Copy Number in Metabolic Syndrome

“…Age and sex were reported as two confounding factors related to alteration of the mtDNA copy number 5,11) .Then we applied the partial correlation to process the analysis in Table 2 under age and sex control. MtDNA copy number of leukocytes from subjects with MetS was found to correlate positively with the HDL-cholesterol concentration and negatively with blood pressure, HOMA-IR and triglyceride concentration; however, the mtDNA copy number was not significantly correlated with waist circumference, smoking index, fasting glucose, insulin, BUN, creatinine, total cholesterol, or LDL-cholesterol concentration.…”