Abstract
Lead is a highly toxic metal and a very potent poison. Lead poisoning is a serious condition but
can be treated. Quercetin is a flavonoid with many beneficial uses. The aim of the present study was
to investigate the possible modulating action of quercetin as a model of an antioxidant against the toxic
effects of lead acetate on liver and kidneys of rats. Rats were randomly divided into four groups: (i)
saline group (control); (ii) lead group received i.p. lead acetate (20 mg/kg b.w.); (iii) quercetin group
received i.p. quercetin (50 mg/kg b.w.); (iv) lead and quercetin group received i.p. lead acetate (20 mg/kg b.w.)
followed by i.p. quercetin (50 mg/kg b.w.) for 4 weeks. The lead concentrations were determined in the liver
and kidney tissues. Liver marker enzymes, bilirubin, albumin, total protein, creatinine, uric acid and
urea, were assessed in the serum and light microscopic studies were performed. The results showed that
lead acetate administration was associated with an increase in serum alkaline phosphatase (ALP), alanine
aminotransferase (ALT), aspartate aminotransferase (AST) activities, total bilirubin, creatinine, uric
acid, urea levels. Lead accumulation in kidneys and liver tissues was also found, but were associated with
decrease in albumin and total protein in comparison with the respective mean values of the control. Lead
acetate caused numerous histological alterations in the liver, including chronic inflammation, bilary
hyperplasia, edema, congestion, Kupffer cells hyperplasia and hemosiderosis, and in the kidney, including
tubular dilation, atrophy of glomerular tuft, widening of urinary space and mild fibroblast. In
contrary, administration of lead acetate along with quercetin partially restored the studied parameters
to normal values and improved structure of liver and kidney with significant decreases in the severity of
histopathological changes when compared with the lead acetate group. In conclusion, treatment with
quercetin may provide a modulating action against the toxic effects induced by lead acetate in the liver
and kidney of male rats.