Gallic acid ameliorates sodium arsenite-induced renal and hepatic toxicity in rats.

Authors:
Babak Gholamine
Babak Gholamine
Iran University of Medical Sciences
Iran
Dr. Gholamreza Houshmand, PhD
Dr. Gholamreza Houshmand, PhD
Department of Pharmacology and Toxicology, School of Pharmacy
Assistance Professor
Ahvaz | Iran (Islamic Republic of)
dr Azam Hosseinzadeh, PhD
dr Azam Hosseinzadeh, PhD
iran university of medical science
tehran | iran
Mojtaba Kalantar
Mojtaba Kalantar
Toxicology Research Center
Pomezia | Italy
Dr. Saeed Mehrzadi, PhD
Dr. Saeed Mehrzadi, PhD
Iran/Tehran University of Medical Sciences
Tehran | Iran
Mehdi Goudarzi
Mehdi Goudarzi
Institute of Cell Biology
Germany

Drug Chem Toxicol 2019 Mar 25:1-12. Epub 2019 Mar 25.

e Medicinal Plant Research Center , Ahvaz Jundishapur University of Medical Sciences , Ahvaz , Iran.

Chronic exposure to toxic inorganic arsenic results in the adverse health effects including skin lesions, cardiovascular diseases, diabetes, neurological disorders, and liver and kidney diseases. Gallic acid (GA) is an important phenolic compound, which could protect different tissues from oxidative stress induced damage. The present study investigated effects of GA against sodium arsenite (SA)-induced renal and hepatic toxicity. Thirty-five rats were randomly divided in to five groups; group 1 was treated with normal saline (2 ml/kg/day, p.o.; for 21 days); group 2 was exposed to SA (10 mg/kg/day, p.o.; for 14 days); groups 3 and 4 were treated with GA (10 and 30 mg/kg/day, respectively; for 7 days) prior to exposure to SA, and treatment was continued up to 21 days in parallel with SA administration; group 5 was treated with GA (30 mg/kg/day, p.o.; for 21 days). The level of MDA, IL-1β, NO and glutathione (GSH) and the activity of glutathione peroxidase (GPx), superoxide dismutase (SOD) and catalase (CAT) were evaluated in kidney and liver tissues. Histopathological parameters and serum levels of ALT, AST, ALP, Cr and BUN were also assessed. Treatment with GA remarkably improved SA-induced alteration of hematological and histopathological parameters; these protective effects were associated with the reduction of SA-induced elevation of MDA, IL-1β and NO levels as well as reduction of GSH level and GPx, SOD and CAT activity. Our results suggest that GA may inhibit SA-induced kidney and liver toxicity through scavenging reactive free radicals and increasing intracellular antioxidant capacity.

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https://www.tandfonline.com/doi/full/10.1080/01480545.2019.1
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http://dx.doi.org/10.1080/01480545.2019.1591434DOI Listing
March 2019
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References

(Supplied by CrossRef)
Article in Toxicology
Bonetto J.G. et al.
Toxicology 2014

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