ArticleJournal of nephropathology2017
Ameliorative effect of vitamin E on trichloroethylene-induced nephrotoxicity in rats.
Article in Journal of nephropathology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
2 citing papers in PubMed, 8 citations in OpenAlex.
- HMGB 1 acetylation mediates trichloroethylene-induced immune kidney injury by facilitating endothelial cell-podocyte communication.Ecotoxicology and environmental safety · 2023Article
- Article
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
background1,1,2-Trichloroethylene (TCE) is an important organic solvent which is widespread in the environment. Work place exposure to TCE has been associated adverse effects in many organs including kidney. Vitamin E is an antioxidant that can overcome oxidative stress.
objectivesThe aim of the present study is to examine the role of vitamin E against destructive effects of TCE on rat kidney. MATERIALS AND
methodsA total of 35 male Wistar rats were randomly divided into seven groups of equal number in each. The rats in group I were the controls received vehicle only. Animals in groups III, V and VII received intraperitoneal injection (i.p) of corn oil. Rats in groups of II, IV, and VI were received vitamin E at a dose of 200 mg/kg; 30 minutes later, animals were received TCE (i.p) at doses of 1000 mg/kg (groups II and III), 1500 mg/kg (groups of IV and V), and 2000 mg/kg (groups of VI and VII) respectively. The experiment repeated for 7 consecutive days. Twenty-four hours after last administration, animals were killed with overdose of sodium pentobarbital. Blood samples were analyzed for blood urea nitrogen (BUN) and creatinine (Cr). One part of the kidney tissues were excised for measuring malondialdehyde (MDA) and glutathione (GSH) concentrations. Another part were excised for histopathological estimation.
resultsTCE induced a dose-dependent elevation in BUN, Cr, MDA and markedly decreased GSH level when compared to those in control rats. TCE-induced dose-dependent injury in rat kidney tissue. Vitamin E significantly decreased BUN, Cr, MDA and increased GSH levels and protected kidney damage in TCE treated animals.
conclusionsThe observations suggest that vitamin E may have a protective effect against TCE-induced oxidative stress in the rat kidney.
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