One important reason for male infertility is oxidative stress and its destructive effects on sperm structures and functions. The particular composition of the sperm membrane, rich in polyunsaturated fatty acids, and the easy access of sperm DNA to oxidative damage due to sperm cell specific cytologic and metabolic features (no cytoplasm left and cells unable to mount stress responses) make it the cell type in metazoans most susceptible to oxidative damage. In particular, oxidative damage to the spermatozoa genome is an important issue and a cause of male infertility, usually associated with single- or double-strand paternal DNA breaks. Various methods of detecting sperm DNA fragmentation have become important diagnostic tools in the prognosis of male infertility and such assays are available in research laboratories and andrology clinics. However, to date, there is not a clear consensus in the community as to their respective prognostic value. Nevertheless, it is important to understand that the effects of oxidative stress on the sperm genome go well beyond DNA fragmentation alone. Oxidation of paternal DNA bases, particularly guanine and adenosine residues, the most sensitive residues to oxidative alteration, is the starting point for DNA damage in spermatozoa but is also a danger for the integrity of the embryo genetic material independently of sperm DNA fragmentation. Due to the lack of a spermatozoa DNA repair system and, if the egg is unable to correct the sperm oxidized bases, the risk of de novo mutation transmission to the embryo exists. These will be carried on to every cell of the future individual and its progeny. Thus, in addition to affecting the viability of the pregnancy itself, oxidation of the DNA bases in sperm could be associated with the development of conditions in young and future adults. Despite these important issues, sperm DNA base oxidation has not attracted much interest among clinicians due to the lack of simple, reliable, rapid and consensual methods of assessing this type of damage to the paternal genome. In addition to these technical issues, another reason explaining why the measurement of sperm DNA oxidation is not included in male fertility is likely to be due to the lack of strong evidence for its role in pregnancy outcome. It is, however, becoming clear that the assessment of DNA base oxidation could improve the efficiency of assisted reproductive technologies and provide important information on embryonic developmental failures and pathologies encountered in the offspring. The objective of this work is to review relevant research that has been carried out in the field of sperm DNA base oxidation and its associated genetic and epigenetic consequences.

中文翻译：

---

精子DNA的氧化与男性不育

男性不育的重要原因之一是氧化应激及其对精子结构和功能的破坏作用。精子细胞膜的特殊组成，富含多不饱和脂肪酸，并且由于精子细胞特有的细胞学和代谢特征（没有细胞质，细胞无法承受应激反应）而使精子DNA容易受到氧化损伤。在后生动物中最容易受到氧化损伤。特别地，对精子基因组的氧化损伤是重要的问题，并且是男性不育的原因，通常与单链或双链父系DNA断裂有关。在男性不育症的预后中，检测精子DNA片段化的各种方法已成为重要的诊断工具，这种检测方法可用于研究实验室和男科诊所。然而，迄今为止，社区对其各自的预后价值尚无明确共识。然而，重要的是要了解氧化应激对精子基因组的影响远不止DNA片段化。父系DNA碱基的氧化，特别是鸟嘌呤和腺苷残基（对氧化变化最敏感的残基）的氧化，是精子DNA损伤的起点，但也对胚胎遗传物质的完整性构成威胁，而与精子DNA片段无关。由于缺乏精子DNA修复系统，并且，如果鸡蛋无法纠正精子的氧化碱基，则存在从头突变传播至胚胎的风险。这些将被延续到未来个体及其后代的每个细胞中。从而，除了影响妊娠本身的生存能力外，精子中DNA碱基的氧化还可能与年轻人和未来成年人的状况发展有关。尽管存在这些重要问题，但由于缺乏评估父系基因组此类损伤的简单，可靠，快速和协商一致的方法，因此精子DNA碱基的氧化并未引起临床医生的广泛兴趣。除了这些技术问题之外，解释为什么不将精子DNA氧化测量值包括在男性生育能力中的另一个原因可能是由于缺乏强有力的证据证明其在妊娠结局中的作用。但是，越来越明显的是，对DNA碱基氧化的评估可以提高辅助生殖技术的效率，并提供有关后代中胚胎发育失败和病理的重要信息。这项工作的目的是回顾在精子DNA碱基氧化及其相关的遗传和表观遗传学后果领域进行的相关研究。