Oxidative Stress: Role in Acetamiprid-Induced Impairment of the Male Mice Reproductive System

Abstract

Acetamiprid has a wide range of influence on physiological functions in mammals. The objective of this study was to examine the effect of acetamiprid on the reproductive function of male mice, and to study the role of oxidative stress in acetamiprid-induced damage to the testes. Fifty adult Kunmin male mice (25–30 g) were divided into five groups (n=10 per group), i.e., control, blank, acetamiprid alone, acetamiprid and vitamin E, and vitamin E alone. All groups were treated for 35 d. The results showed that acetamiprid significantly decreased the body weight and the weight of testosteroneresponsive organs, such as the testis, epididymis, seminal vesicle, and prostate. Furthermore, acetamiprid also significantly reduced the serum testosterone concentration, and decreased sperm count, viability, motility, and the intactness of the acrosome ( P<0.05 for each parameter). The mice treated with acetamiprid had damaged seminiferous tubules and Leydig cells based on the histological structure of testes; there was degeneration of the mitochondria and endoplasmic reticulum of Leydig cells. These deleterious effects of acetamiprid may be mediated by increasing oxidative stress, as acetamiprid increased malondialdehyde and nitric oxide in the testes, reduced the activity of catalase, glutathione peroxidase, superoxide dismutase, and activated p38. The concentration of acetamiprid in the testes was lower than that in liver, so did the concentrations of liver function tests, including aspartate transaminase (AST), alanine transaminase (ALT) and alkaline phosphatase (ALP), which suggest that male reproductive function may be affected through the indirect action of its metabolites. Vitamin E significantly ameliorated the effects of acetamiprid. We conclude that acetamiprid damages male reproductive function through inducing oxidative stress in the testes.