Dose‐related proximal tubular dysfunction in male rats chronically exposed to lead

Abstract

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.

Renal Effects of Environmental and Occupational Lead Exposure

“…1). Histologic changes include eosinophilic intranuclear indusions in proximal tubular cells consisting of lead-protein complexes, and mitochondrial swelling (29)(30)(31)(32)(33). Renal manifestations of acute lead poisoning have been well described both in animal models and in humans; these include glycosuria, aminoaciduria (34,35), and phosphaturia, collectively representing the Fanconi syndrome (36)(37)(38).…”

Lipoic acid in combination with a chelator ameliorates lead-induced peroxidative damages in rat kidney

“…Several researchers have reported nephrotoxic effects in animals fed various doses of lead (Vyskocil et al 1989), and studies conducted in humans (Bennet 1985) and children (Hu 1991) have indicated that high levels of lead exposure may impair renal function. The renal toxicity of lead is closely related to its selective accumulation in the kidneys (Choie and Richter 1980).…”

Experimental Studies of Achyranthes aspera (L) Preventing Nephrotoxicity Induced by Lead in Albino Rats

“…Maruhn et al (1983) 39) and Vyskocil (1995) 40) have proposed that increased excretion of LDH in urine occurs after exposure to lead acetate along with a profound increase in kidney weight. Urinary β-Glucuronidase derives from the lysosomes of tubular cells and from the epithelial cells of urinary tract.…”