Noblanc Anaīs, Klaassen Alicia, Robaire Bernard
Department of Pharmacology and Therapeutics, McGill University, Montreal, QC, H3G 1Y6, Canada.
Department of Obstetrics and Gynecology, McGill University, Montreal, QC H4A 3J1, Canada.
Antioxidants (Basel). 2020 Feb 11;9(2):151. doi: 10.3390/antiox9020151.
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 () antioxidant gene results in impaired mechanisms of repairing DNA damage in the testis in young mice. In this study, we examined the effects of aging and the 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 mice. These findings indicate that lack of SOD1 results in an exacerbation of the oxidative damage accumulation-related aging phenotype.
越来越多的证据表明，精子质量会随着年龄的增长而下降，而且父亲年龄较大时生育的子女出现出生缺陷和基因突变的几率更高。衰老的自由基理论认为，衰老带来的变化是由于暴露于过量活性氧物种所诱导的损伤积累所致。我们之前发现，超氧化物歧化酶1（SOD1）抗氧化基因缺失会导致年轻小鼠睾丸中DNA损伤修复机制受损。在本研究中，我们检测了衰老和SOD1突变对小鼠附睾组织学以及氧化损伤标志物表达的影响。我们发现，氧化核酸损伤（通过8-羟基鸟苷检测）和脂质过氧化（通过4-羟基壬烯醛检测）均随年龄增长以及SOD1基因敲除小鼠的出现而增加。这些发现表明，缺乏SOD1会导致与氧化损伤积累相关的衰老表型加剧。
