Department of Histology-Embryology, Medical School, Athens University, Greece.
Reprod Toxicol. 2012 Nov;34(3):298-307. doi: 10.1016/j.reprotox.2012.06.007. Epub 2012 Jun 28.
Reactive oxygen species (ROS) are active byproducts of aerobic metabolism. Although they are constantly produced during normal cellular activities in the mitochondria, their action is counteracted by inherent antioxidant systems. This equilibrium is distorted in the case of acute or chronic inflammation, which results in increased ROS production and, ultimately, oxidative stress. In sperm, ROS are produced by both spermatozoa and circulating leucocytes and may be part of normal adaptive reactions, such as the capacitation process. However, a number of external toxicants may also contribute to ROS production in the testis and epididymis, leading to a decrease in sperm viability and motility and, therefore, an increased onset of the male factor of infertility. Such pro-oxidative conditions include, among others, exposure to radiation, extreme temperature, certain drugs, toxins, heavy metals, smoking and biological hazards. The current review paper summarizes the available evidence incriminating ROS and oxidative stress as the underlying pathophysiological mechanism leading to the onset of reproductive toxicity in each of these settings.
活性氧（ROS）是需氧代谢的活性副产物。虽然它们在细胞线粒体的正常活动中不断产生，但它们的作用会被内在的抗氧化系统抵消。在急性或慢性炎症的情况下，这种平衡会被打破，导致 ROS 产生增加，最终导致氧化应激。在精子中，ROS 由精子和循环白细胞产生，可能是正常适应反应的一部分，如获能过程。然而，一些外部毒物也可能导致睾丸和附睾中 ROS 的产生，导致精子活力和运动能力下降，从而增加男性不育因素的发生。这种促氧化条件包括暴露于辐射、极端温度、某些药物、毒素、重金属、吸烟和生物危害等。本文综述了现有的证据，表明 ROS 和氧化应激是导致这些情况下生殖毒性发生的潜在病理生理机制。
