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Aging in mammals leads to reduction in genes encoding the 45-subunit mitochondrial electron transport chain complex I. It has been hypothesized that normal aging and age-related diseases such as Parkinson’s disease are in part due to modest decrease in expression of mitochondrial complex I subunits. By contrast, diminishing expression of mitochondrial complex I genes in lower organisms increases lifespan. Furthermore, metformin, a putative complex I inhibitor, increases healthspan in mice and humans. In the present study, we investigated whether loss of one allele of  Ndufs2 , the catalytic subunit of mitochondrial complex I, impacts healthspan and lifespan in mice. Our results indicate that  Ndufs2  hemizygous mice ( Ndufs2  +/− ) show no overt impairment in aging-related motor function, learning, tissue histology, organismal metabolism, or sensitivity to metformin in a C57BL6/J background. Despite a significant reduction of  Ndufs2  mRNA, the mice do not demonstrate a significant decrease in complex I function. However, there are detectable transcriptomic changes in individual cell types and tissues due to loss of one allele of  Ndufs2 . Our data indicate that a 50% decline in mRNA of the core mitochondrial complex I subunit  Ndufs2  is neither beneficial nor detrimental to healthspan.

Reduced expression of mitochondrial complex I subunit Ndufs2 does not impact healthspan in mice