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462094 
Journal Article 
Effect of lead acetate on cytosolic thioredoxin reductase activity and oxidative stress parameters in rat kidneys 
Conterato, GMM; Augusti, PR; Somacal, S; Einsfeld, L; Sobieski, R; Torres, JRV; Emanuelli, T 
2007 
1 
Basic & Clinical Pharmacology & Toxicology
ISSN: 1742-7835
EISSN: 1742-7843 
101 
2 
96-100 
English 
17651309 
WOS:000248689000005 
Oxidative stress has been suggested to be an important molecular mechanism of toxic effects of lead in the kidney. Thioredoxin reductase-1 is a selenoprotein involved in many cellular redox processes. This study evaluated the effect of acute and chronic exposure intraperitoneally to lead acetate on thioredoxin reductase-1 activity and on other oxidative stress parameters in the rat kidney, as well as on indicators of renal function commonly used to assess lead poisoning. Acute exposure to 25 mg/kg lead acetate increased superoxide dismutase and thioredoxin reductase-1 activity (after 6, 24 and 48 hr), while exposure to 50 mg/kg lead acetate increased catalase activity (after 48 hr) and inhibited delta-aminolevulinate dehydratase activity (after 6, 24 and 48 hr) in the kidney (P < 0.05). Chronic exposure (30 days) to 5 mg/kg lead acetate inhibited delta-aminolevulinate dehydratase and increased glutathione S-transferase, non-protein thiol groups, catalase, thioredoxin reductase-1 and uric acid plasma levels, while exposure to 25 mg/kg lead acetate reduced body weight and delta-aminolevulinate dehydratase, but increased glutathione S-transferase, non-protein thiol groups and uric acid plasma levels (P < 0.05). No changes were observed in thiobarbituric acid reactive substances, glutathione peroxidase, creatinine or inorganic phosphate levels after either acute or chronic exposure. Our results suggest that thioredoxin reductase-1 may be an early indicator of acute exposure to low lead doses. 
vein endothelial-cells; glutathione-peroxidase; acid; liver; expression; induction; catalase; selenium; cadmium; damage 
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