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The ameliorative effect of Moringa oleifera oil on tributyltin-induced brain toxicity in albino rats
Environmental Toxicology ( IF 4.4 ) Pub Date : 2021-07-06 , DOI: 10.1002/tox.23320
Samar Sakr 1 , Walaa A Rashad 2 , Marwa T Abaza 1
Affiliation  

Tributyltin (TBT) is an organotin compound widely used as a biocide in antifouling paints. Moringa oleifera oil (MOO) has a promising antioxidant potential, which necessitates further exploration. This study was conducted to investigate the potential protective effect of MOO against TBT-induced brain toxicity. The 30 rats were grouped into five groups (six each), Group I negative control, Group II positive control (vehicle), Group III MOO (5 ml/kg body weight [b.wt.]), Group IV TBT (10 mg/kg b.wt.), and Group V TBT & MOO. All treatments were given orally for 28 days. Thereafter, brains were exposed to oxidative stress and neurological parameters analyses. Histopathological and immunohistochemical (caspase-3, Bax, Bcl-2) examinations were also carried out. In rats administered TBT, increased malondialdehyde level, decreased reduced glutathione, and low total antioxidant capacity levels were in support of oxidative stress mechanism. Neurotoxicity was indicated by high nitric oxide level and increased acetylcholinestrase activity. Along with the histopathological alterations, the dysregulated expression of caspase-3, Bax, and Bcl-2 were indicative of the apoptotic mechanism mediated by TBT. Co-administration of MOO with TBT ameliorated the aforementioned toxic effects. In conclusion, TBT causes brain toxicity via oxidative, nitrosative, and apoptotic mechanisms. MOO demonstrates protective effect against TBT-induced brain toxicity mostly via potent antioxidant and antiapoptotic properties.

中文翻译:

辣木油对三丁基锡诱导的白化大鼠脑毒性的改善作用

三丁基锡 (TBT) 是一种有机锡化合物,广泛用作防污涂料中的杀菌剂。辣木石油 (MOO) 具有有希望的抗氧化潜力,这需要进一步探索。本研究旨在研究 MOO 对 TBT 诱导的脑毒性的潜在保护作用。30只大鼠分为五组(每组六只),第一组阴性对照,第二组阳性对照(载体),第三组MOO(5ml/kg体重[b.wt.]),第四组TBT(10mg /kg b.wt.),以及 V 组 TBT 和 MOO。所有治疗均口服给药 28 天。此后,大脑暴露于氧化应激和神经参数分析。还进行了组织病理学和免疫组织化学(caspase-3、Bax、Bcl-2)检查。在给予 TBT 的大鼠中,丙二醛水平增加,还原型谷胱甘肽减少,总抗氧化能力水平低,支持氧化应激机制。神经毒性表现为一氧化氮水平高和乙酰胆碱酯酶活性增加。随着组织病理学改变,caspase-3、Bax 和 Bcl-2 的失调表达表明 TBT 介导的细胞凋亡机制。MOO 与 TBT 的共同给药改善了上述毒性作用。总之,三丁基锡化合物通过氧化、亚硝化和凋亡机制引起脑毒​​性。MOO 主要通过有效的抗氧化和抗细胞凋亡特性显示出对 TBT 诱导的脑毒性的保护作用。MOO 与 TBT 的共同给药改善了上述毒性作用。总之,三丁基锡化合物通过氧化、亚硝化和凋亡机制引起脑毒​​性。MOO 主要通过有效的抗氧化和抗细胞凋亡特性显示出对 TBT 诱导的脑毒性的保护作用。MOO 与 TBT 的共同给药改善了上述毒性作用。总之,三丁基锡化合物通过氧化、亚硝化和凋亡机制引起脑毒​​性。MOO 主要通过有效的抗氧化和抗细胞凋亡特性显示出对 TBT 诱导的脑毒性的保护作用。
更新日期:2021-09-02
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