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Dose‐related proximal tubular dysfunction in male rats chronically exposed to lead
Author(s) -
Vyskocil Adolf,
Pancl Jan,
Tusl Miloslav,
Ettlerova Eva,
Semecky Vladimir,
Kašparová Lucie,
Lauwerys Robert,
Bernard Alfred
Publication year - 1989
Publication title -
journal of applied toxicology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.784
H-Index - 87
eISSN - 1099-1263
pISSN - 0260-437X
DOI - 10.1002/jat.2550090605
Subject(s) - lead acetate , nephrotoxicity , endocrinology , medicine , chemistry , lactate dehydrogenase , kidney , sodium acetate , lysozyme , excretion , urinary system , toxicity , urine , biochemistry , enzyme , chromatography
Male Wistar rats were given 0.5 and 2% lead acetate in drinking water for 2 months, 1% lead acetate for 3 months and sodium acetate equimolar to 2% lead acetate for 3 months. Glucose, total proteins, lactate dehydrogenase (LDH), lysozyme and β 2 ‐microglobulin (β 2 ‐m) were measured in 24‐h urine every month. Kidney weight and histology were also examined. At the three doses, lead exposure produced a significant elevation of the kidney weight. No significant change in urinary parameters was observed in rats given 0.5% lead acetate. Exposure to 1% lead acetate increased the urinary excretion of β 2 ‐m only. At the 2% lead acetate dose the elevation of β 2 ‐m excretion was accompanied by an increased urinary output of glucose, total proteins, lysozyme and LDH. Observations of the kidneys by light microscopy were in agreement with these biochemical findings. The nephrotoxic effect of acetate was excluded by the lack of biochemical or histological effects of sodium acetate on the kidney. It is concluded that a proximal tubular dysfunction is induced in rats chronically exposed to high doses of lead.