Dose-related proximal tubular dysfunction in male rats chronically exposed to lead
| Autor: | Adolf Vyskočil, Lucie Kašparová, Jan Pancl, Alfred Bernard, Eva Ettlerova, Vladimir Semecky, Miloslav Tušl, Robert Lauwerys |
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| Rok vydání: | 1989 |
| Předmět: |
Male
medicine.medical_specialty Urinary system Urine Toxicology Kidney Nephrotoxicity Excretion Kidney Tubules Proximal chemistry.chemical_compound Glycosuria Internal medicine Lactate dehydrogenase medicine Animals Dose-Response Relationship Drug L-Lactate Dehydrogenase Chemistry Rats Inbred Strains Organ Size Rats Lead Poisoning Proteinuria Endocrinology medicine.anatomical_structure Lead acetate beta 2-Microglobulin Sodium acetate |
| Zdroj: | Journal of applied toxicology : JAT. 9(6) |
| ISSN: | 0260-437X |
| Popis: | 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 beta 2-microglobulin (beta 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 beta 2-m only. At the 2% lead acetate dose the elevation of beta 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. |
| Databáze: | OpenAIRE |
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