Sequential development of flagellar defects in spermatids and epididymal spermatozoa of selenium-deficient rats

Abstract

In this study cauda epididymal spermatozoa of rats maintained on a selenium-deficient diet for 5 and 7 months exhibited an array of flagellar defects. Spermatids and spermatozoa were analyzed by light and electron microscopy to define the appearance of flagellar abnormalities during spermiogenesis and post-testicular sperm development. Late spermatids of seleniumdeficient rats displayed normal structural organization of the flagellar plasma membrane, axoneme, outer dense fibers, fibrous sheath and annulus, but they exhibited a premature termination of the mitochondrial sheath. A comparison of late spermatids and caput epididymal spermatozoa revealed that a late step in flagellar differentiation was the structural remodeling of the annulus and its accompanying fusion with both the fibrous sheath and the mitochondrial sheath. In selenium-deficient animals, however, the annulus failed to fuse with the mitochondrial sheath, generating an apparent weak point in the flagellum. After epididymal passage, cauda epididymal spermatozoa of selenium-deficient animals also exhibited extensive flagellar disorganization resulting from the apparent sliding and extrusion of specific outer dense fiber-doublet microtubule complexes from the proximal and the distal ends of the mitochondrial sheath and the accompanying loss of the midpiece plasma membrane. Only fiber complex number 4 was extruded proximally, whereas fibers 4, 5, 6 and 7 were extruded from the mitochondrial sheath-deficient posterior midpiece. Axonemal fibers 8, 9, 1, 2 and 3 retained their normal geometric relationships. These data suggest that the known loss of male fertility in selenium deficiency results from the sequential development of sperm defects expressed during both spermiogenesis and maturation in the epididymis.

Delineating the Molecular Mechanism behind Regulation of Spermatogenesis by Selenium: Involvement of Mitogen Activated Protein Kinase; JNK

“…The general idea, that emerges out again points towards the specific role of GSH-Px in mediating the regulation of spermatogenesis by Se. The observation also strengthens the view that Se is a versatile trace element required for maintenance of male fertility [1] and any alterations in its physiologic concentrations lead to abnormal spermatogenesis [35] and hence male infertility. A decrease in the activity of antioxidant enzymes like MnSOD again shows increased accumulation of superoxide radical in animals under both treatment groups (Se deficient and Se excess) which further indicates the prevalent oxidative stress in the testicular environment.…”

“…The present study further observed reduced sperm count and percentage motility in the treated groups (Se deficient and Se excess). Several studies have been reported till date which support the above observation [35] and also address the molecular mechanism behind the changes observed. The general idea, that emerges out again points towards the specific role of GSH-Px in mediating the regulation of spermatogenesis by Se.…”

The Effect of Compound Herbal Remedy Used in Male Infertility on Spermatogenesis and Pregnancy Rate

“…Increased levels of ROS and oxidative levels (oxidative stress) is one of the proposed mechanisms for impaired spermatogenesis. Vacuole formation in testis tissue is a sign of oxidative stress and is associated with aging which can be neutralized by antioxidants (12)(13)(14)(15). Lack of vitamin A, elements such as flavonoids, carnitine, folate, zinc and selenium and overall reduction of antioxidants in the diet can be one of the reasons for infertility especially oligospermia and asthenozoospermia in humans (16-18).…”

Effect of selenium and vitamin E on acrosome reaction in porcine spermatozoa

“…Se may have a role in the motility of bovine spermatozoa by protecting them from oxidative damage [6]. Se, which commonly replaces sulfur in proteins, is normally incorporated through selenoamino acids (L-selenomethionine, L-selenocysteine) [7] and selenoenzymes, such as GPxs, which reduce glutathione in the antioxidant system and protect cells from oxidative damage [8]. Vitamin E (Vit-E) is one of the most important antioxidative molecules, residing mainly in the cell membranes [9].…”