Abstract

Objective Ethanol treatment induces an increase in oxidative stress. As licorice compounds are potent antioxidants, our aim was to examine whether magnesium isoglycyrrhizinate attenuated lipid peroxidation, the major end-point of oxidative damage resulting from ethanol administration. Methods Four groups(18 animals in each group) of male Kunming mice were used. The first group served as control and received 0.4 ml normal saline daily for 18 days orally. The second group of mice was given 56% ethanol at 16 ml/kg body weight per day for 18 days orally. The third group was given the same dose of ethanol and administrated magnesium isoglycyrrhizinate (15 mg/kg.d, i.p.) for 18 days. The fourth group was given the same dose of ethanol and administrated with magnesium isoglycyrrhizinate (45 mg/kg.d, i.p.) for 18 days. Twenty four hours after 9 days or 18 days of treatment the mice were sacrificed using 10% chloral hydrate. Sperm counts and motility in the epididymis were assessed. The lipid peroxidation and antioxidants of testicular mitochondria were also determined. The pathological changes of testicle tissue of the mice were observed by light microscopy. Results Magnesium isoglycyrrhizinate effectively prevented the ethanol-induced seminiferous epithelium disorganization and degeneration of Sertoli cells and germ cells. Sperm counts and motility of the magnesium isoglycyrrhizinate treated groups were higher than those of the alcohol treated group, but were lower than those of the control group. The drug exhibited an ability to counteract ethanol induced oxidative challenge as it effectively reduced testicular malondialdehyde (MDA) and increased the activities of superoxide dismutase and glutathione peroxidase. Conclusion Magnesium isoglycyrrhizinate is able to inhibit the ethanol-induced lipid peroxidation and has a protective effect against testicular oxidative injury.

Highlights

  • Ethanol is one of the most widely abused drugs in the world

  • In our study, increased oxidative stress and germ cell apoptosis were observed after ethanol treatment

  • Chronic ethanol abuse leads to testicular atrophy and male infertility in alcoholic men

Read more

Summary

Introduction

Chronic alcohol abuse leads to both liver injury and impaired sperm production in humans and Testicular atrophy of these patients demonstrated a marked reduction in seminiferous tubular diameter accompanied by a loss of sperm cells[5]. The mechanisms of ethanol induced testicular injury was previously studied. One proposed mechanism is that ethanol metabolism produces an oxidative stress within the testes[7], and another is that defective steroid hormone metabolism is secondary to altered liver metabolism[8]. An imbalance between ROS production and antioxidant defense has been shown to result in cellular damage via lipid peroxidation, protein oxidation and DNA degradation[9]. Mitochondriaenriched extracts obtained from the testes of alcohol treated rats showed a significant increase in malondialdehyde (MDA) formation accompanied by a significant decrease in superoxide dismutase (SOD) and glutathione peroxidase[10]

Methods
Results
Conclusion
Full Text
Published version (Free)

Talk to us

Join us for a 30 min session where you can share your feedback and ask us any queries you have

Schedule a call