Non-enzymatic oxidative damage of DNA in the male germ cell line is believed to be one of the key mechanisms of premature apoptosis of spermatozoa and in pathogenesis of male subfertility. High motility of sperm cells requires high activity of energetic metabolism and mitochondrial functioning that makes them subject to excessive influence of reactive oxygen species (ROS). Low volume of cytoplasm, where antioxidative enzymes, such as glutathione peroxidase (GPx), catalase and superoxide dismutase work, complicates the delivery of antioxidants into different compartments of a spermatozoon. Hence, the protection of sperm against oxidative stress is provided mostly by antioxidants produced by male reproductive tract and antioxidative machinery of the oocyte. The lifespan of sperm cells is to a significant degree regulated by Ras dependent cell signaling pathways, such as phosphatidylinositol 3-kinase (PI3K)/Akt. Factors, inducing oxidative stress in human spermatozoa and their regulation mechanisms are discussed.

Peripheral-nerve injury is a frequent cause of disability. Presently, no clinically effective neuroprotectors have been found. We have studied the NO-dependent expression of p53 in the neurons and glial cells of the dorsal root ganglia (DRG) of a rat’s spinal cord, as well as the role of NO in the death of these cells under the conditions of axonal stress, using sciatic-nerve axotomy as a model. It was found out that axotomy led to the nuclear–cytoplasmic redistribution of p53 in neurons, 24 h after trauma. The NO donor led to a considerable increase in the level of p53 in nuclei and, to a smaller degree, in the cytoplasm of neurons and karyoplasm of glial cells 4 and 24 h after axotomy. Application of a selective inhibitor of inducible NO-synthase (iNOS) provided the opposite effect. Introduction of the NO donor resulted in a significant increase in cell death in the injured ipsilateral DRG, 24 h and 7 days after trauma. The selective inhibitor of iNOS demonstrated a neuroprotective effect. Axotomy was shown to upregulate the iNOS in nuclei and cytoplasm of DRG cells. The NO-dependent expression of p53, which is particularly achieved through iNOS activation, is believed to be a putative signaling mechanism of neural and glial-cell death after axotomy.