Antioxidant Systems in Rat Epididymal Spermatozoa1

Abstract

Mammalian caput and cauda epididymidal spermatozoa exhibit diverse stages of maturation, and their plasma membrane shows diverse composition and stability levels, thus enabling these spermatozoa to undergo the acrosomal reaction after transit through the epididymis. As a result, the study of antiperoxidative mechanisms is quite relevant, since epididymal spermatozoa must be properly protected against agents such as reactive oxygen species, which can impair the complex maturation process. We considered activities of certain enzymes (glutathione peroxidase [GPx], phospholipid hydroperoxide glutathione peroxidase [PHGPx], glutathione reductase [GR], superoxide dismutase [SOD], and catalase [CAT]) and the vitamin E content in isolated rat caput and cauda epididymidal spermatozoa. The results indicate that caput epididymidal sperm have significantly greater PHGPx (3.5x), GPx (2.4x), and SOD (1.7x) activities, as well as a greater amount of vitamin E (3.8x). There were no detectable differences in the GR and CAT activities of caput and cauda epididymidal spermatozoa. The substantial drop in PHGPx activity during epididymal transit is discussed in relation to an additional function of this enzyme: the use of caput sperm protamines as a sulfhydryl substrate. In vitro peroxidation of the two sperm populations by the free radical generator (azo-initiator) 2,2'-azobis(2-amidinopropane) dihydrochloride revealed that only about 13% of the vitamin E content of the caput epididymidal spermatozoa was consumed, which contrasts with the greater consumption (about 70%) of the vitamin in cauda epididymidal spermatozoa. Selective inhibition of PHGPx, SOD, or CAT did not change this picture. The higher susceptibility of cauda epididymidal spermatozoa to radicals is discussed in relation to the diverse enzymatic activities, vitamin E content, and peroxidative response. These factors are correlated with the different stages of sperm cell maturation, which are characterized-from caput to cauda epididymidis-by progressive destabilization of the plasma and acrosomal membranes.

Testicular apoptosis after dietary zinc deficiency: Ultrastructural and TUNEL studies

“…Lipid peroxidation of PUFA molecules of plasma membrane of spermatozoa is largely responsible for defective spermatozoa and male infertility [Aitken et al 1993]. Lipid peroxidation causes leakiness of sperm plasma membrane which in turn losses its fluidity and integrity [Aitken et al 1993], damaging the mid-piece and axonemal complex leading to decreased concentration and loss of motility as observed in the present study, since disruption of the testicular homeostatic mechanism influences considerably the epididymal reserves and decreases capacitation [Tramer et al 1998;Dandekar et al 2002]. Zinc deficiency adversely affects sperm integrity and modulates testes fatty acid composition by interrupting essential fatty acid metabolism thereby affecting overall testicular function [Merrells et al 2009].…”

An aminoglycoside antibiotic gentamycin induces oxidative stress, reduces antioxidant reserve and impairs spermatogenesis in rats

“…Although the damage of germ cells in the testis appears to be a reason for impaired sperm quality, a possibility of oxidative stress in the epididymis might be yet another reason for this. The reactive oxygen species may cause lipid peroxidation of sperm cell membranes hence damaging the midpiece, axonemal structure, or disrupting the capacitation and acrosomal reaction, finally leading to infertility (Tramer et al, 1998). This indicates that the sperm abnormalities−a sensitive marker of germ cell damage−seen on day 1 might be due to free radicals-induced damage in the epididymis, in addition to that in the testis, or independent of the latter.…”

Vitamin C and oxidative stress in the seminiferous epithelium

“…One male infertility mechanism is the excess production of reactive oxygen species (ROS) in sperm (Sharma & Agarwal, 1996;Chen et al, 2001;Kasahara et al, 2002;Agarwal et al, 2008). This induces nuclear DNA fragmentation, lipid peroxidation and protein cross links and results in cell death (Alvarez et al, 1987;Steenken, 1989;Tramer et al, 1998;Liu et al, 2006). In semen, production of free radicals comes from two main sources; leukocytes and sperm (Tremellen et al, 2008).…”