Establishment of a Mouse Asthenospermia Model through Triggering D-Galactose Mediated Oxidative Stress Injury.

Abstract

Asthenospermia is defined as the forward motility of sperm less than 32%. This study aimed to establish a mouse model of asthenospermia through triggering D-galactose mediated oxidative stress. A total of 40 Kunming male mice were randomly divided into control group, low-dose group (administrating D-galactose at 60 mg/kg), high-dose group (administrating D-galactose at 120 mg/kg), and high-dose+feed addition group (administrating D-galactose at 120 mg/kg together with oral D-galactose). The testicular weight, testicular organ coefficient, sperm viability, sperm concentration, and survival rate of the tail of epididymis were measured. Oxidative damage of D-- galactose to the reproductive system of mice was evaluated by measuring superoxide dismutase (SOD) and malondialdehyde (MDA) in the testicular homogenate of mice. The sperm motility, motility rate, concentration, and survival rate of low-dose, high-dose and high-dose+feed addition group were decreased, compared to that in the control group. However, there background:was a significant difference between high-dose group/high dose+feed group and the control group (p<0.05): the forward motile sperm motility rate and total motility rate are accorded with critical criteria of asthenospermia. As compared with the control group, the activity of SOD of model group mice significantly decreased, and MDA concentration significantly increased (p<0.05), except for low-dose versus control group for SOD activity. This suggests that testicular tissues suffered from oxidative damage. This study successfully established a mouse asthenospermia model through D-galactose mediated oxidative stress injury. The establishment of asthenospermia model in this study would provide new promising insight and act as a potential approach for studying asthenospermia in vivo levels.