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Aluminium phosphide-induced testicular toxicity through oxidative stress in Wistar rats: Ameliorative role of hesperidin

机译:磷铝对Wistar大鼠的氧化应激诱导的睾丸毒性:橙皮苷的改善作用

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摘要

The present study was designed to investigate aluminium phosphide (ALP)-induced testicular toxicity, including its effects on sperm parameters and histological alterations in Wistar rats, and the possible protective role of hesperidin (HSD). Oral administration of ALP at 1.15 mg/kg body weight (1/10 LD50) for 30 days resulted in a significant increase in testicular malondialdehyde, lipid hydroperoxides, and oxidized protein levels. These indicators of oxidative stress were accompanied by decreased activity of the antioxidant enzymes superoxide dismutase, catalase and glutathione peroxidase, followed by a drastic reduction in the non-enzymatic antioxidant indices of glutathione and total antioxidant capacity when compared to control. Furthermore, ALP treatment produced a marked reduction in sperm count, motility and viability while increasing abnormal sperm morphology and adverse histopathological changes in testis. Co-administration with HSD significantly ameliorated ALP-induced testicular damage by suppressing oxidative stress indices and enhancing antioxidant status while also improving the sperm parameters and histological alterations in ALP-treated rats. The results of the present study indicated that testicular toxic effects of ALP are due to oxidative imbalance and that HSD could be a potential therapeutic agent against ALP-induced testicular damage.
机译:本研究旨在研究磷化铝(ALP)诱导的睾丸毒性,包括其对Wistar大鼠精子参数和组织学改变的影响,以及橙皮苷(HSD)的可能的保护作用。口服ALP剂量为1.15 mg / kg体重(1/10 LD50)30天导致睾丸丙二醛,脂质氢过氧化物和氧化蛋白质水平显着增加。这些氧化应激指标伴随着抗氧化酶超氧化物歧化酶,过氧化氢酶和谷胱甘肽过氧化物酶的活性降低,与对照相比,谷胱甘肽的非酶促抗氧化指数和总抗氧化能力急剧下降。此外,ALP治疗可显着减少精子数量,运动性和活力,同时增加异常精子形态和睾丸组织病理学不良变化。与HSD共同给药可通过抑制氧化应激指数和增强抗氧化剂状态来显着改善ALP诱导的睾丸损伤,同时还可改善ALP治疗大鼠的精子参数和组织学改变。本研究的结果表明,ALP的睾丸毒性作用是由于氧化失衡引起的,HSD可能是对抗ALP引起的睾丸损伤的潜在治疗剂。

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