Rhamnazin ameliorates 2, 3, 7, 8-tetrachlorodibenzo-p-dioxin-evoked testicular toxicity by restoring biochemical, spermatogenic and histological profile in male albino rats.

Muhammad Umar Ijaz, Shama Mustafa, Qurat Ul Ain, Ali Hamza, Shafaqat Ali
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Abstract

2,3,7,8 tetrachlorodibenzo-p-dioxin (TCDD) is a potential environmental toxin that has the ability to affect male reproductive tract. Rhamnazin is a naturally present flavone that displays multiple medicinal properties. Therefore, the current study was designed to determine the mitigative role of rhamnazin against TCDD induced reproductive damage. 48 adult male albino rats were randomly separated into four groups: control, TCDD (10 µgkg-1), TCDD + rhamnazin (10 µgkg-1 + 5 mgkg-1 respectively) and rhamnazin (5 mgkg-1). The trial was conducted for 56 days. TCDD intoxication notably affected superoxide dismutase (SOD), glutathione peroxidase (GPx), glutathione reductase (GSR) and catalase (CAT) activities, besides reactive oxygen species (ROS) and malondialdehyde (MDA) concentrations were augmented. TCDD administration also lowered sperm motility, viability, sperm number, while it augmented the sperm morphological (tail, neck/midpiece and head) anomalies. Moreover, it decreased the levels of follicle-stimulating hormone (FSH), luteinizing hormone (LH) and plasma testosterone. Moreover, TCDD reduced steroidogenic enzymes i.e., 17-beta hydroxysteroid dehydrogenase (17β-HSD), steroidogenic acute regulatory protein (StAR) and 3-beta hydroxysteroid dehydrogenase (3β-HSD) as well as B-cell lymphoma 2 (Bcl-2) expressions, but increased the expressions of Bcl-2-associated X protein (Bax) and cysteine-aspartic acid protease (Caspase-3). Furthermore, TCDD exposure also induced histopathological anomalies in testicular tissues. However, the supplementation of rhamnazin recovered all the mentioned damages in the testicles. The outcomes revealed that rhamnazin can ameliorate TCDD induced reproductive toxicity due to its anti-oxidant, anti-apoptotic and androgenic nature.

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鼠李嗪通过恢复雄性白化大鼠的生化、生精和组织学特征,改善2,3,7,8-四氯二苯并对二恶英引起的睾丸毒性。
2,3,7,8-四氯二苯并对二恶英(TCDD)是一种潜在的环境毒素,具有影响男性生殖道的能力。鼠李嗪是一种天然存在的黄酮,具有多种药用特性。因此,本研究旨在确定鼠李嗪对TCDD诱导的生殖损伤的缓解作用。48只成年雄性白化大鼠被随机分为四组:对照组、TCDD(10µgkg-1)、TCDD+鼠李嗪(分别为10µgkg-1+5mgkg-1)和鼠李嗪组(5mgkg-1)。试验进行了56天。TCDD中毒显著影响超氧化物歧化酶(SOD)、谷胱甘肽过氧化物酶(GPx)、谷胱甘肽还原酶(GSR)和过氧化氢酶(CAT)的活性,活性氧(ROS)和丙二醛(MDA)浓度增加。TCDD给药还降低了精子活力、活力和精子数量,同时增加了精子形态(尾部、颈部/中段和头部)异常。此外,它还降低了卵泡刺激素(FSH)、黄体生成素(LH)和血浆睾酮的水平。此外,TCDD降低了甾体生成酶,即17β-羟基类固醇脱氢酶(17β-HSD)、甾体生成急性调节蛋白(StAR)和3-β-羟基甾体脱氢酶(3β-HSD)以及B细胞淋巴瘤2(Bcl-2)的表达,但增加了Bcl-2相关X蛋白(Bax)和半胱氨酸天冬氨酸蛋白酶(Caspase-3)的表达。此外,TCDD暴露也引起睾丸组织的组织病理学异常。然而,补充鼠李嗪可以恢复睾丸中的所有上述损伤。结果表明,鼠李嗪具有抗氧化、抗细胞凋亡和雄性激素性质,可改善TCDD诱导的生殖毒性。
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