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Establishment of a Mouse Asthenospermia Model through Triggering D-Galactose Mediated Oxidative Stress Injury
Nanjun Liu1, Qianxing Wang1, Lin Li1
1Department of Cell Biology, Zunyi Medical University, Zunyi 563000, China.
Background:
Asthenospermia is defined as the forward motility of sperm less than 32%.
Aim/Objective:
This study aimed to establish a mouse model of asthenospermia through triggering D-galactose mediated oxidative stress.
Methods:
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.
Results:
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.
Conclusion:
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.
Insights
This study created a mouse model of asthenospermia using D-galactose to induce oxidative stress, showing reduced sperm quality and testicular damage. This model aids in studying asthenospermia in vivo.
Area of Science:
- Reproductive Biology
- Toxicology
- Animal Models
Background:
- Asthenospermia is characterized by sperm forward motility below 32%.
- Oxidative stress is implicated in male infertility.
- Establishing reliable animal models is crucial for studying infertility conditions.
Purpose of the Study:
- To establish a mouse model of asthenospermia.
- To investigate the effects of D-galactose-induced oxidative stress on sperm parameters and testicular tissue.
- To provide an in vivo model for asthenospermia research.
Main Methods:
- Forty Kunming male mice were divided into control, low-dose D-galactose (60 mg/kg), high-dose D-galactose (120 mg/kg), and high-dose+feed addition groups.
- Sperm viability, concentration, motility, and epididymal sperm survival rates were assessed.
- Oxidative stress markers, including superoxide dismutase (SOD) and malondialdehyde (MDA), were measured in testicular homogenates.
Main Results:
- D-galactose administration significantly decreased sperm motility, concentration, and survival rates in a dose-dependent manner.
- High-dose D-galactose groups met the criteria for asthenospermia.
- Testicular tissues showed decreased SOD activity and increased MDA concentration, indicating oxidative damage.
Conclusions:
- D-galactose effectively induces asthenospermia in mice via oxidative stress.
- This established mouse model provides a valuable tool for in vivo research on asthenospermia.
- The findings highlight the role of oxidative stress in asthenospermia pathogenesis.
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