Effect of Chronic Lead Exposure on Kidney Function in Male and Female Rats: Determination of a Lead Exposure Biomarker

Abstract

Several cytotoxic chemical pollutants inducing peroxidative damages are liable to induce kidney failure. Among these pollutants we find heavy metals such as: lead, nickel, cadmium, vanadium and mercury. Lead is one of the most dangerous metals because it is widely spread in the environment, and because it may be a source of several nervous diseases. The aim of this study is to provide evidence concerning the effect of this metal on the renal function and to try to determine a storage corner in the organism which serves as an indicator of a lead intoxication. Lead acetate was administered by oral route in the drinking water to adult rats aged three months at the rate of 0.3% (P1) and 0.6% (P2). Reference rats received distilled water to drink under the same conditions. The treatment continued for 15, 30, 45, 60 and 90 days. The creatinemia, uremia, glycemia and creatinuria are determined by colorimetric techniques. Lead concentration in blood as well as the lead content of the tail are determined by atomic absorption after nitroperchloric mineralization at the liquid stage. The results showed an increase of creatinemia on the 30th day of the experiment for both sexes in (P1 and P2). The same happened for ureamia. The increase of these two parameters would indicate a renal deficiency which is confirmed by a decrease of creatinuria and urinary pH observed mainly on and after the 45th day of the experiment. An increase of the renal relative weight was noticed in P1 and P2 on the 30th day of the treatment. The determination of the concentration of lead in the blood shows that this factor increases among treated subjects in a constant way, independently of the dose and the duration of the treatment. Nevertheless, the rate increase of lead in the tail seems to be dose-dependent. In conclusion, lead administered by oral route causes a renal deficiency to the rat without distinction between males and females. In addition, the tail seems to be a reliable exposure biomarker that demonstrates lead intoxication. The tail seems to be a dosimeter of lead bio-accumulation. It constitutes an endogenous source of lead impregnation. The concentration of lead in the blood is only an indicator of recent exposure.

Haemato-Biochemical Alterations as Biomarkers of Lead Induced Toxicity in Male Wistar Rats

“…Rats treated with lead had significantly decreased urine urea and slight increase in serum urea has been reported to increase in acute and chronic intrinsic renal disease and also when there is decreased renal perfusion (Cameron and Greger, 1998). Ghorbe et al (2001) illustrated that oral administration of lead acetate caused significant increase in blood urea and serum creatinine.…”

Ameliorative Effect of Different Concentration of Mushroom (<i>Pleurotus Tuberregium</i>) on Pathomorphological Changes Induced By Lead Toxicity in Liver and Kidney of Wistar Albino Rats

“…The necrosis of the proximal tubule could be attributed to the inflammatory effects of lead on the walls of the kidney tubules (Tawari-fufeyin et al, 2008). It has been reported that oral dosing of experimental animals with lead induced necrosis, hemorrhage and degenerative changes (Abdel-kalek et al, 2000;Ghorbe et al. 2001;Elnattat et al 2003).…”

Protective Effect of Morocco Carob Honey Against Lead-Induced Anemia and Hepato-Renal Toxicity

“…Lead exposure causes kidney toxicity. It was found that lead acetate administered by oral route to adult rats at the rate of 0.3% and 0.6% increased SCr on the 30th day of the experiment [23]. Lead can cause increase in intracellular calcium and reactive oxygen species, and it can trigger apoptosis through the cytochrome C release and a fall in the mitochondrial potential [24,25].…”