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Journal of Environmental Pathology, Toxicology and Oncology
Главный редактор: Qian Peng (open in a new tab)

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ISSN Печать: 0731-8898

ISSN Онлайн: 2162-6537

The Impact Factor measures the average number of citations received in a particular year by papers published in the journal during the two preceding years. 2017 Journal Citation Reports (Clarivate Analytics, 2018) IF: 2.4 To calculate the five year Impact Factor, citations are counted in 2017 to the previous five years and divided by the source items published in the previous five years. 2017 Journal Citation Reports (Clarivate Analytics, 2018) 5-Year IF: 2.8 The Immediacy Index is the average number of times an article is cited in the year it is published. The journal Immediacy Index indicates how quickly articles in a journal are cited. Immediacy Index: 0.5 The Eigenfactor score, developed by Jevin West and Carl Bergstrom at the University of Washington, is a rating of the total importance of a scientific journal. Journals are rated according to the number of incoming citations, with citations from highly ranked journals weighted to make a larger contribution to the eigenfactor than those from poorly ranked journals. Eigenfactor: 0.00049 The Journal Citation Indicator (JCI) is a single measurement of the field-normalized citation impact of journals in the Web of Science Core Collection across disciplines. The key words here are that the metric is normalized and cross-disciplinary. JCI: 0.59 SJR: 0.429 SNIP: 0.507 CiteScore™:: 3.9 H-Index: 49

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Protective Role of Zinc in Ameliorating Arsenic-Induced Oxidative Stress and Histological Changes in Rat Liver

Том 29, Выпуск 2, 2010, pp. 91-100
DOI: 10.1615/JEnvironPatholToxicolOncol.v29.i2.30
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Краткое описание

The aim of present work was to gain insight into the role of dietary zinc in ameliorating the adverse effects caused by arsenic on rat liver. Male Wistar rats received arsenic alone in the form of sodium arsenite in drinking water at a dose level of 100 ppm, zinc alone in the form of zinc sulfate in drinking water at a dose level of 227 mg/L, or arsenic + zinc treatments in the combined group for a total duration of 3 months. Arsenic treatment resulted in a significant increase in lipid peroxidase (LPO); however, glutathione (GSH) levels and the activities of superoxide dismutase (SOD), glutathione peroxidase (GPx), glutathione reductase (GR), and catalase (CAT) were found to be significantly decreased following arsenic treatment. Furthermore, arsenic treatment resulted in a significant decrease in hepatic zinc levels. Histological studies showed well-differentiated signs of focal hepatitis, lobular inflammation, prominent hepatocyte degeneration, and severe periportal necrosis. Administration of zinc to arsenic-treated rats significantly decreased the level of LPO but increased the level of GSH compared with arsenic-treated rats. Further, the zinc level and activities of SOD, GPx, GR, and CAT were found to be significantly increased following zinc treatment. The administration of zinc to arsenic-treated rats caused signs of improvement in liver histoarchitecture, but a few focal areas of degeneration and necrosis were still occasionally seen. In conclusion, the results of this study suggest that zinc can be beneficial against arsenic-induced hepatotoxicity in rats.

Ключевые слова: arsenic, liver, antioxidants
ЦИТИРОВАНО В
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