The kidney is more severely affected by lead toxicity than are other tissues because it is the fundamental route for elimination, and thus the main organ providing protection against lead poisoning (Landrigan et al. 1984; Nolan & Shaikh, 1992). The process of glomerular filtration followed by reabsorption from the tubules results in the accumulation of large quantities of lead in the tubular epithelium. Direct absorption of lead from the blood (Vostal & Séller, 1968; Victery et al. 1979; Ladrón de Guevara & Moya, 1995) causes as much damage to the glomeruli as to the proximal tubules, hence chronic exposure to lead affects glomerular filtration and clearance as well as tubular reabsorption.
To study this effect some physiological parameters were evaluated in two groups of 10 young male rats. One group was treated with lead acetate (300 p.p.m.) in the drinking water during a period of 30 days; the other group received distilled water during the same time and served as controls. After the treatment, rats were humanely killed and the kidneys removed and separated into medulla and cortex. The organosomatic index (kidney wt/body wt ratio), the total quantity of proteins (Bradford, 1976), the concentration of malondialdehyde (Uchiyama y Mihara, 1978), total lipids (Folch, 1957), and the alkaline phosphatase (ALP; Kuftiniec y Miller, 1972) and catalase enzymes were measured.
Statistical analysis showed that in lead-treated rats the weight of the kidney, and its organosomatic index, increased by 21% compared with the control group. Since the weight of the animals did not differ significantly between the groups, this increase could be due to a lead-induced retention of liquid in the kidney. The lead caused a decrease in the values for lipid peroxidation by as much as 51 % and 27 % in the medulla and cortex, respectively. The susceptibility of lead-treated kidneys to lipid peroxidation in vitro was 30 % lower than in controls. This suggested the activation of some type of antioxidant defence mechanism in the treated animals and a decrease of 30% in the susceptibility to lipid peroxidation in the medulla. Lead also caused a decrease of 12% in the alkaline phosphatase activity in the medulla.