AbstractFemale Wistar rats were given 1 or 0.1 lead acetate in drinking water for 2 or 4 months, respectively. Urinary β2‐microglobulin,N‐acetyl‐β‐D‐glucosaminidase, lactate dehydrogenase and lysozyme were used as markers of tubular dysfunction. Excretion of albumin and glomerular filtration rate were used as indicators of glomerular impairment. Kidney and body weights and morphological changes in the kidney were also studied. Exposure to 1 lead acetate induced a mean blood lead level of 1730 μg−1and caused only an increase of β2‐microglobulin excretion and relative kidney weight. Light microscopy of kidney revealed morphological changes mainly in the epithelial cells of the proximal tubules. The role of acetate or reduced water intake on kidney function was excluded because 1 sodium acetate or the restriction of water intake to the volume consumed by the rats of the lead‐exposed group was ineffective. Exposure to 0.1 lead acetate induced a blood lead level of 376 μg I−1, corresponding to the current level in industry workers, without any sign of nephrotoxicity. Comparison of this study with the results of a previous study on male rats indicates no sex difference in the
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