Gallic acid attenuates chromium-induced thyroid dysfunction by modulating antioxidant status and inflammatory cytokines

•We investigate the thyroprotective effect of gallic acid (GA) against potassium dichromate.•SOD, GST activities and their mRNA expression were significantly decreased.•GA attenuated the expression of iNOS, TNF-α, IL-6 and COX-2.•GA up-regulated SOD and GST gene expression levels.

Hexavalent chromium-mediated oxidative stress causes severe organ damage. The present study was designed to investigate the possible thyroprotective effect and underlying mechanisms of gallic acid using rat model of potassium dichromate-induced thyroid dysfunction. Forty adult male albino rats were divided into 4 groups: control, gallic acid (20 mg GA/kg b. wt), potassium dichromate (2 mg PD/kg b. wt) and the fourth group was co-treated with PD and GA. PD-injection resulted in decreased serum free triiodothyonine (FT3), free thyroxine (FT4) with concomitant significant increase in thyroid stimulating hormone (TSH) levels. Superoxide dismutase (SOD), glutathione-S-transferase (GST) activities and their respective mRNA expression and reduced glutathione (GSH) content were significantly decreased. Thyroid nitrosative stress marker (NO level and iNOS mRNA and protein expression) and pro-inflammatory cytokines (serum TNF-α, IL-6 and thyroid TNF-α, IL-6 and COX-2 gene and protein expression levels) were disturbed. Histopathological changes revealed distended, collapsed and degenerated follicles with vacuolated cytoplasm. GA co-treatment attenuated pro-inflammatory cytokines, the thyroid expression of iNOS, TNF-α, IL-6 and COX-2, decreased the elevated lipid peroxidation biomarkers and NO level and up- regulated SOD and GST mRNA expression levels. In conclusion, GA has shown strong modulatory potential against PD-induced inflammation and oxidative stress in albino rats.