Aging and oxidative stress alter DNA repair mechanisms in male germ cells of superoxide dismutase-1 null mice

In this study, we evaluated the effects of aging and removing SOD1 (in male germ cells of SOD1-null (Sod1-/-) mice) in order to determine the potential mechanism(s) of DNA damage in these cells. Immunohistochemical analysis showed an increase in lipid peroxidation and DNA damage in the germ cells of aged wild-type (WT) and Sod1-/- mice of all age. Immunostaining of OGG1, a marker of base excision repair (BER), increased in aged WT and young Sod1-/- mice. In contrast, immunostaining intensity of LIGIV and RAD51, markers of non-homologous end-joining (NHEJ) and homologous recombination (HR), respectively, decreased in aged and Sod1-/- mice. Gene expression analysis showed similar results with altered mRNA expression of these key DNA repair transcripts in pachytene spermatocytes and round spermatids of aged and Sod1-/- mice. Our study indicates that DNA repair pathway markers of BER, NHEJ, and HR are differentially regulated as a function of aging and oxidative stress in spermatocytes and spermatids, and aging enhances the repair response to increased oxidative DNA damage, whereas impairments in other DNA repair mechanisms may contribute to the increase in DNA damage caused by aging and the loss of SOD1.PMID:34098580 | DOI:10.1093/biolre/ioab114
Source: Biology of Reproduction - Category: Reproduction Medicine Authors: Source Type: research