School of Bio Sciences and Technology, VIT, Vellore, Tamil Nadu, 632014, India.
Department of Life Sciences, Kristu Jayanti College (Autonomous), Bengaluru, Karnataka, 560077, India.
Appl Biochem Biotechnol. 2020 Feb;190(2):616-633. doi: 10.1007/s12010-019-03111-0. Epub 2019 Aug 13.
Bromobenzene is an environmental toxin which causes hepatotoxicity, and the secondary metabolites on biotransformation cause nephrotoxicity. The objective of this study was to assess the alleviation of the nephrotoxic effect of bromobenzene by beta carotene in female Wistar albino rats. Beta carotene (10 mg/kg b.w.p.o.) was delivered orally to the rats for 9 days before bromobenzene (10 mM/kg b.w.p.o.) was intragastrically intubated. Kidney markers, antioxidant status and lipid peroxidation were evaluated. In addition, the levels of TNF-α, IL-6 and IL-1β were measured in serum and in kidney tissue homogenate using ELISA. Caspase, COX-2 and NF-κB were measured with the help of Western blotting. Histopathological analysis of the kidney was done for the control and experimental rats. Bromobenzene induction caused elevation in levels of creatinine, urea, uric acid, cytokines and lipid per oxidation along with deterioration in histological observations and antioxidant status. Pre-treatment with beta carotene significantly (*p < 0.05) normalised the levels of kidney markers and pro-inflammatory cytokines. It also reduced oxidative stress and lipid peroxidation, as shown by improved antioxidant status. The anti-apoptotic activity was evidenced by inhibition of protein expression of caspase, COX-2 and NF-κB. This significant reversal (*p < 0.05) of the above variations in comparison with the control group as noticed in the bromobenzene-administered rats demonstrates that beta carotene possesses promising nephroprotective effect through its antioxidant, anti-inflammatory and anti-apoptotic activity and therefore suggests its use as a potential therapeutic agent for protection from bromobenzene and hence environmental pollutant toxicity.
溴苯是一种环境毒素，可导致肝毒性，其生物转化的次生代谢物可导致肾毒性。本研究的目的是评估β-胡萝卜素对雌性 Wistar 白化大鼠溴苯肾毒性的缓解作用。β-胡萝卜素（10mg/kg 体重）经口给予大鼠 9 天，然后经胃内插管给予溴苯（10mM/kg 体重）。评估肾脏标志物、抗氧化状态和脂质过氧化。此外，使用 ELISA 测量血清和肾组织匀浆中 TNF-α、IL-6 和 IL-1β的水平。用 Western blot 测量 caspase、COX-2 和 NF-κB 的水平。对对照组和实验组大鼠的肾脏进行组织病理学分析。溴苯诱导导致肌酐、尿素、尿酸、细胞因子和脂质过氧化水平升高，同时组织学观察和抗氧化状态恶化。β-胡萝卜素预处理显著（*p<0.05）使肾脏标志物和促炎细胞因子水平正常化。它还通过改善抗氧化状态来减少氧化应激和脂质过氧化。抗细胞凋亡活性表现为抑制 caspase、COX-2 和 NF-κB 的蛋白表达。与对照组相比，溴苯给药大鼠的上述变化明显逆转（*p<0.05），这表明β-胡萝卜素通过其抗氧化、抗炎和抗凋亡活性具有有希望的肾脏保护作用，因此表明其可用作预防溴苯和环境污染物毒性的潜在治疗剂。
