Etiologies of sperm oxidative stress

Abstract

Sperm is particularly susceptible to reactive oxygen species (ROS) during critical phases of spermiogenesis. However, the level of seminal ROS is restricted by seminal antioxidants which have beneficial effects on sperm parameters and developmental potentials. Mitochondria and sperm plasma membrane are two major sites of ROS generation in sperm cells. Besides, leukocytes including polymer phonuclear (PMN) leukocytes and macrophages produce broad category of molecules including oxygen free radicals, non-radical species and reactive nitrogen species. Physiological role of ROS increase the intracellular cAMP which then activate protein kinase in male reproductive system. This indicates that spermatozoa need small amounts of ROS to acquire the ability of nuclear maturation regulation and condensation to fertilize the oocyte. There is a long list of intrinsic and extrinsic factors which can induce oxidative stress to interact with lipids, proteins and DNA molecules. As a result, we have lipid peroxidation, DNA fragmentation, axonemal damage, denaturation of the enzymes, over generation of superoxide in the mitochondria, lower antioxidant activity and finally abnormal spermatogenesis. If oxidative stress is considered as one of the main cause of DNA damage in the germ cells, then there should be good reason for antioxidant therapy in these conditions.

Warfarin‐induced vitamin K deficiency affects spermatogenesis in Sprague‐Dawley rats

“…The testes are known to be associated with free radicals be- Bahmani, Kheradmand, & Rafieian-Kopaei, 2017). This free radical induces oxidative stress in the testes which will significantly lead to the production of abnormal sperm, reduction in the sperm concentration and increase in sperm DNA fragmentation (Sabeti, Pourmasumi, Rahiminia, Akyash, & Talebi, 2016). Vitamin K has the ability to act as an antioxidant, and according to Sanyaolu et al (2018), the two natural forms of vitamin K exhibit an antioxidant potential in the testis.…”

The protective effect of N-acetyl cysteine against carbon tetrachloride toxicity in rats

“…In normal condition male, reproductive system has a balance between ROS creation and antioxidant activity. But the increase of ROS in semen can affect sperm or seminal plasma antioxidant defense mechanisms and cause oxidative stress (Sabeti, Pourmasumi, Rahiminia, Akyash, & Talebi, 2016). The different CCL4 metabolic pathways result in ROS generation and alteration of antioxidant defense systems in animals (Stal & Olson, 2000).…”

Low-dose radiation-induced risk in spermatogenesis

“…ROS are also important mediators of apoptosis through induction of cytochrome c release and activation of caspases 9 and 3 (Said 2004). High levels of ROS levels in semen resulting in abnormal spermatozoa are a main cause of decreased fertility as observed in teratozoospermia (Rato et al 2012;Sabeti et al 2016), further supporting ROS as a mechanism of DNA damage at low doses.…”