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Effect of Lead Acetate on Cytosolic Thioredoxin Reductase Activity and Oxidative Stress Parameters in Rat Kidneys
Author(s) -
Conterato Greicy M. M.,
Augusti Paula R.,
Somacal Sabrina,
Einsfeld Lídia,
Sobieski Rocheli,
Torres Juliana R.V.,
Emanuelli Tatiana
Publication year - 2007
Publication title -
basic and clinical pharmacology and toxicology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.805
H-Index - 90
eISSN - 1742-7843
pISSN - 1742-7835
DOI - 10.1111/j.1742-7843.2007.00084.x
Subject(s) - thioredoxin reductase , lead acetate , chemistry , oxidative stress , glutathione reductase , glutathione peroxidase , uric acid , glutathione , catalase , superoxide dismutase , thioredoxin , endocrinology , medicine , biochemistry , dehydratase , enzyme , biology , toxicity , organic chemistry
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 δ‐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 δ‐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 δ‐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.