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

Biology of Reproduction
Paulina Nguyen-Powanda, Bernard Robaire

Abstract

The efficiency of antioxidant defense system decreases with aging, thus resulting in high levels of reactive oxygen species and DNA damage in spermatozoa. This damage can lead to genetic disorders in the offspring. There are limited studies investigating the effects of the total loss of antioxidants, such as superoxide dismutase-1 (SOD1), in male germ cells as they progress through spermatogenesis. 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 8-oxoguanine DNA glycosylase, a marker of base excision repair (BER), increased in aged WT and young Sod1-/- mice. In contrast, immunostaining intensity of DNA ligase 4 and RAD51 Recombinase, markers of nonhomologous 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 sperm...Continue Reading

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