The etiologies of DNA abnormalities in male infertility: An assessment and review

S. Pourmasumi, P. Sabeti, T. Rahiminia, E. Mangoli, N. Tabibnejad, A. Talebi
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引用次数: 33

Abstract

The sperm DNA damage may occur in testis, genital ducts, and also after ejaculation. Mechanisms altering chromatin remodeling are abortive apoptosis and oxidative stress resulting from reactive oxygen species. Three classifications of intratesticular, post-testicular, and external factors have been correlated with increased levels of human sperm DNA damage which can affect the potential of fertility. Lifestyle, environment, medical, and iatrogenic factors might be considered to cause dysmetabolism to make distracting interactions and endocrine disrupting compounds. As a result, these may induce chromatin/DNA alteration in germ cells, which may be transmitted across generations with phenotypic consequences. Alcohol consumption may not increase the rate of sperm residual histones and protamine deficiency; however, it causes an increase in the percentage of spermatozoa with DNA fragmentation and apoptosis. In a medical problem as spinal cord injury, poor semen parameters and sperm DNA damage were reported. Infection induces reactive oxygen species production, decreases the total antioxidant capacity and sperm DNA fragmentation or antigen production that lead to sperm dysfunctions and DNA fragmentation. While reactive oxygen species generation increases with age, oxidative stress may be responsible for the age-dependent sperm DNA damage. The exposing of reproductive organs in older men to oxidative stress for a long time may produce more DNA-damaged spermatozoa than youngers. Examining the sperm chromatin quality in testicular cancer and Hodgkin’s lymphoma patients prior to chemotherapy demonstrated the high incidence of DNA damage and low compaction in spermatozoa at the time of the diagnosis. In chemotherapy cycle with genotoxic agents in cancer patients, an increase in sperm DNA damage was shown after treatment. In overall, those factors occurring during the prenatal or the adult life alter the distribution of proteins associated with sperm chromatin induce changes in germ cells which can be detected in infertile patients.
男性不育症DNA异常的病因:评估和回顾
精子DNA损伤可能发生在睾丸、生殖道,也可能发生在射精后。改变染色质重塑的机制是由活性氧引起的凋亡流产和氧化应激。三种类型的睾丸内、睾丸后和外部因素与人类精子DNA损伤水平的增加有关,这可能影响生育的潜力。生活方式、环境、医学和医源性因素均可引起代谢障碍,产生分散注意力的相互作用和内分泌干扰化合物。因此,这些可能会诱导生殖细胞的染色质/DNA改变,这可能会通过表型后果跨代传播。饮酒可能不会增加精子残留组蛋白和鱼精蛋白缺乏率;然而,它会导致精子DNA断裂和细胞凋亡的比例增加。在脊髓损伤等医学问题中,有精液参数差和精子DNA损伤的报道。感染诱导活性氧产生,降低总抗氧化能力和精子DNA断裂或抗原产生,导致精子功能障碍和DNA断裂。虽然活性氧的产生随着年龄的增长而增加,但氧化应激可能是造成年龄依赖性精子DNA损伤的原因。老年男性的生殖器官长期暴露于氧化应激下,可能比年轻人产生更多dna受损的精子。在化疗前检查睾丸癌和霍奇金淋巴瘤患者的精子染色质质量表明,在诊断时,DNA损伤的发生率高,精子压实度低。在基因毒性药物化疗周期中,癌症患者治疗后精子DNA损伤增加。总的来说,在产前或成年期发生的这些因素改变了与精子染色质相关的蛋白质的分布,导致了生殖细胞的变化,这些变化可以在不育患者中检测到。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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93
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6-12 weeks
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