Impact of silymarin on cadmium-induced apoptosis in human spermatozoa.

Abstract

Oxidative stress-induced apoptosis in spermatozoa may lead to male infertility. Environmental pollutants and heavy metals such as cadmium cause harmful effects on the reproductive system and sperm parameters through the induction of oxidative stress. Silymarin, as a potent antioxidant, is able to inhibit oxidative stress. This study was performed to investigate the protective effects of silymarin on cadmium-induced toxicity in human spermatozoa. Sperm samples were divided into the following five groups: (a) spermatozoa at 0min, (b) spermatozoa in the control group, (c) spermatozoa treated with cadmium chloride (20μM), (d) spermatozoa treated with silymarin (2μM)+ cadmium chloride (20μM) and (e) spermatozoa treated with silymarin (2μM). Sperm parameters related to apoptosis, such as DNA fragmentation, nucleus diameter, mitochondrial membrane potential (MMP) and expression of caspase-3, were evaluated in all groups. After 180min, spermatozoa treated with cadmium chloride showed a significant decrease in nucleus diameter and MMP but a significant increase in DNA fragmentation; however, caspase-3 expression remained unchanged. At this time point, silymarin in the silymarin + cadmium chloride group could significantly reverse the adverse effects of cadmium chloride on these parameters.Silymarn could partly compensate for the caspase-independent apoptosis in the spermatozoa. Therefore, oxidative stress could be a consequence for cadmium toxicity.