Home General Physiology and Biophysics 2017 General Physiology and Biophysics Vol.36, No.2, p.219–227, 2017

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Quarterly, 80 pp. per issue
Founded: 1982
ISSN  1338-4325 (online)

Published in English

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General Physiology and Biophysics Vol.36, No.2, p.219–227, 2017

Title: Inhibition of Kupffer cell functions modulates arsenic intoxication in Wistar rats
Author: Oluyomi S. Adeyemi, Ekong Meyakno, Musbau A. Akanji
Abstract: Study determined the influence of the inhibition of Kupffer cell functions by GdCl3 in arsenic intoxication. Twenty-four Wistar rats weighing between 150 and 160 g were randomly assigned into four groups. Group 1 received sodium arsenite (1.5 mg/kg b.w.) once a day, Group 2 received GdCl3 (2 mg/kg b.w.) once, 24 hours before commencing the arsenite (1.5 mg/kg b.w.) treatment. Group 3 received GdCl3 (2 mg/kg b.w.) once and subsequently given distilled water. Group 4 received distilled water only. The treatments were daily by oral gavage and lasted for 28 days. Animals were euthanized 24 hours after the last treatment. Arsenic exposure elevated the activities of rat plasma AST, ALT, ALP and γ-GT, indicative of liver injury. Arsenic exposure in rat lowered GSH concentration but potentiated inflammation and oxidative stress evidenced in the raised levels of MPO, NO and MDA. Rats with arsenic exposure were predisposed to atherosclerosis, lowering the HDL-C but elevated the LDL-C concentration. The histopathological assessment showed degenerating cellular lesion caused by arsenic. However, the inhibition of Kupffer cell functions by GdCl3 suppressed arsenic intoxication improving the liver function indices, oxidative stress status, lipid profile, neutrophilic inflammation and ultimately restored the cellular architecture. Data suggest that specific inhibition of Kupffer cells by GdCl3 protected against arsenic intoxication.
Keywords: Arsenic — Atherosclerosis — Hepatotoxicity — Kupffer cells — Metals
Published online: 07-Mar-2017
Year: 2017, Volume: 36, Issue: 2 Page From: 219, Page To: 227
doi:10.4149/gpb_2016041


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