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Antioxidant protection of gallic acid against toxicity induced by Pb in blood, liver and kidney of rats. | LitMetric

AI Article Synopsis

  • The study analyzed how gallic acid (GA) mitigates lead (Pb) toxicity in rats, focusing on the effects on blood, liver, and kidney functions following Pb exposure.
  • Rats were treated with Pb nitrate, leading to reduced body weight, lower blood enzyme activity, elevated Pb levels, and increased oxidative stress indicators.
  • While GA improved certain health indicators and antioxidant defenses after Pb exposure, it did not reduce Pb levels in the body as effectively as the chelating agent EDTA, highlighting GA's potential for treating Pb toxicity through antioxidant benefits rather than detoxification.

Article Abstract

The effect of the antioxidant gallic acid (GA) on Pb toxicity in blood, liver and kidney was investigated in the present study. Rats Wistar received Pb nitrate (50 mg/Kg/day, i.p., 5 days) followed by GA (13.5 mg/Kg, p.o., 3 days) or a chelating agent (EDTA, 55 mg/Kg, i.p.). As result, Pb decreased body weight, hematocrit and blood δ-aminolevulinic acid dehydratase (ALA-D) activity. In addition, high Pb levels were observed in blood and tissues, together with increased (1) lipid peroxidation in erythrocytes, plasma and tissues, (2) protein oxidation in tissues and (3) plasma aspartate transaminase (AST) levels. These changes were accompanied by decreasing in antioxidant defenses, like superoxide dismutase (SOD) activity in tissues and catalase (CAT) activity and reduced glutathione (GSH) in liver. GA was able to reverse Pb-induced decrease in body weight and ALA-D activity, as well as Pb-induced oxidative damages and most antioxidant alterations, however it did not decrease Pb bioaccumulation herein as EDTA did. Furthermore, EDTA did not show antioxidant protection in Pb-treated animals as GA did. In conclusion, GA decreased Pb-induced oxidative damages not by decreasing Pb bioaccumulation, but by improving antioxidant defenses, thus GA may be promising in the treatment of Pb intoxications.

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Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5615824PMC
http://dx.doi.org/10.1016/j.toxrep.2016.02.005DOI Listing

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