Redox Report ( IF 3.8 ) Pub Date : 2017-05-05 , DOI: 10.1080/13510002.2017.1322750 Gbadebo E Adeleke 1 , Oluwatosin A Adaramoye 2
Objectives: N-nitrosodimethylamine (NDMA) is known to elicit carcinogenic activity in the liver and kidney of animals. There is a dearth of information of its effect in testis. This study evaluated the protective role of betulinic acid (BA) against NDMA-induced redox imbalance in testes of rats.
Methodology: Twenty-four male rats were assigned into four groups and treated with normal saline, BA, NDMA and [BA+NDMA]. BA (25 mg/kg) was given for 14 days, while NDMA (5 mg/kg) was given on days 7 and 12.
Results: Administration of NDMA significantly increased the weight and relative weight of testes by 51 and 71%, respectively, while treatment with BA attenuated the weight-gain. Furthermore, NDMA decreased the sperm count, motility and live–dead ratio by 57, 36 and 37%, respectively, and increased total sperm abnormality by 56%. However, BA attenuated the changes in the spermiogram of NDMA-treated rats. NDMA significantly decreased the activities of antioxidative enzymes, follicle-stimulating and luteinizing hormones, while testicular levels of thiobarbituric acid reactive substances and total cholesterol were increased. Also, NDMA increased the activities of aniline hydroxylase and aminopyrine-N-demethylase. Supplementation with BA attenuated NDMA-induced alteration in these biochemical indices.
Conclusion: BA protects against NDMA-induced redox imbalance via activation of antioxidative pathway.
中文翻译:
白桦脂酸可防止大鼠睾丸中 N-亚硝基二甲胺诱导的氧化还原失衡。
目的:已知 N-亚硝基二甲胺(NDMA) 在动物的肝脏和肾脏中引起致癌活性。缺乏关于其在睾丸中作用的信息。本研究评估了白桦脂酸 (BA) 对 NDMA 诱导的大鼠睾丸氧化还原失衡的保护作用。
方法:将24只雄性大鼠分为四组,分别给予生理盐水、BA、NDMA和[BA+NDMA]治疗。BA (25 mg/kg) 给予 14 天,而 NDMA (5 mg/kg) 在第 7 天和第 12 天给予。
结果: NDMA 给药显着增加了睾丸的重量和相对重量,分别为 51% 和 71%,而 BA 治疗则减轻了体重增加。此外,NDMA 使精子数量、活力和活死比分别降低了 57%、36% 和 37%,并使总精子异常增加了 56%。然而,BA 减弱了 NDMA 治疗大鼠精子图的变化。NDMA显着降低了抗氧化酶、促卵泡激素和促黄体生成素的活性,而睾丸中硫代巴比妥酸反应物质和总胆固醇的水平升高。此外,NDMA 增加了苯胺羟化酶和氨基比林-N-去甲基化酶的活性。补充 BA 可减弱 NDMA 诱导的这些生化指标的改变。
结论: BA通过激活抗氧化途径来防止NDMA诱导的氧化还原失衡。