Abstract
Male germ cells are unique because they lose a bulk of their cytoplasm as cytoplasmic droplets when they develop, leading to a decrease in endogenous antioxidant and hence a dependence on extracellular antioxidant system to overcome oxidative stress. Spermatozoa are particularly vulnerable to oxidative stress because their plasma membrane is rich in polyunsaturated fatty acids and membrane-bound NADPH oxidase. To protect spermatozoa from oxidative attack, an optimal amount of reactive oxygen species is maintained by balancing the reactive oxygen species generated during sperm maturation in the epididymidis and antioxidants in secretions of the male reproductive tract. The male accessory sex glands secretions have been shown to be the major source of antioxidant enzymes in the ejaculate and have the important function of preserving sperm DNA integrity from oxidative stress experienced in the uterine environment. In our in vivo golden hamster model, ablation of the five major male accessory sex glands, namely the ampullary glands, coagulating glands, dorsolateral prostate, ventral prostate and seminal vesicle, was found to cause higher incidence and greater degree of DNA damage in spermatozoa. These damaged sperm are able to undergo fertilization at the same rate as intact ones; however, the outcome of embryos sired is seriously affected.
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