Abstract
There is growing evidence that the quality of spermatozoa decreases with age and that children of older fathers have a higher incidence of birth defects and genetic mutations. The free radical theory of aging proposes that changes with aging are due to the accumulation of damage induced by exposure to excess reactive oxygen species. We showed previously that absence of the superoxide dismutase 1 (Sod1) antioxidant gene results in impaired mechanisms of repairing DNA damage in the testis in young Sod1−/− mice. In this study, we examined the effects of aging and the Sod−/− mutation on mice epididymal histology and the expression of markers of oxidative damage. We found that both oxidative nucleic acid damage (via 8-hydroxyguanosine) and lipid peroxidation (via 4-hydroxynonenal) increased with age and in Sod1−/− mice. These findings indicate that lack of SOD1 results in an exacerbation of the oxidative damage accumulation-related aging phenotype.
Highlights
Reactive oxygen species (ROS) generate chain reactions that can affect numerous biomolecules, including lipids, RNA, DNA, proteins [1,2,3,4]
In old (18 months) superoxide dismutase 1 (Sod1)−/− and WT mice distinctive features included an increase in the tubule diameter all along the epididymis, a decrease in the height of epididymal cells, as well as an accumulation of spermatozoa in the initial segments, where they are usually absent
The thickening of the myoid layer was greater in old Sod1−/− mice than in old WT mice, but this is visible in cauda epididymidis of young Sod1−/− mice
Summary
Reactive oxygen species (ROS) generate chain reactions that can affect numerous biomolecules, including lipids, RNA, DNA, proteins [1,2,3,4]. The consequences of these biochemical reactions are part of the normal cellular function but, in excess, they can be deleterious and severely damage major cellular processes. The major characteristics of aging in the epididymis are a thickening of the basement membrane along the epididymis, a decreased integrity and functionality of the blood-epididymis barrier [9], a segment-dependent variation of each cell type distribution; in particular a decrease in the proportion of principal, clear, and basal cells and an increase in the number of halo cells in the entire epididymis was found [10]. Halo cells are immune cells and their increased number in the epididymal epithelium may reflect a lack of balance of the immune steady-state of the epididymis, in accordance with the proposed general hallmarks of aging [11]
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