Lead is known to induce a broad range of physiological, biochemical, and behavioral dysfunctions in laboratory animals and humans. This includes age-specific variations in absorption, retention, and tissue distribution of lead. This study was carried out to investigate the effects of chronic exposure to lead (50 mg/L) on liver and kidneys of two different age groups of male rats treated with lead from delivery until puberty period (40 days) and postpuberty period (65 days). For this purpose, the concentrations of thiobarbituric acid reactive substance (TBARS), total thiol groups (SH), and superoxide dismutase (SOD) activity were measured in the liver and kidney of rats. Renal function was analyzed by determining creatinine, acid uric, and urea. Plasma activities of alanine aminotransferase, aspartate aminotransferase, alkaline phosphatase, and albumin were determined spectrophotometrically to evaluate hepatic function. These markers of damage were determined to assess the level of toxicity in these animals. Our results clearly show that the administration of lead produces oxidative damage in liver and kidney, as strongly suggested by the significant increase in TBARS, decrease in total SH, and the alteration of SOD activity. In young lead-exposed animals, lead-induced perturbations on the synthetic function of the liver and the kidney were more pronounced. However, nephropathy is evident for adult lead-exposed animals. It is concluded that lead induces severe hepatic and renal toxicity, which depends on the age of the animals and the target organ.

Lead toxicity is closely related to its accumulation in several tissues and its interference with bioelements, whose role is critical for several biological processes. Recently, oxidative stress has been proposed as a possible mechanism involved in lead toxicity. This study was carried out to investigate the effect of dose-dependent lead exposure on haematological and oxidative stress parameters. Adult male 'Wistar' rats (150-200 g) were divided into three groups: group [Pb 5] and group [Pb 15] received respectively 5 mg Pb 2+ (n = 16) and 15 mg Pb 2+ /kg b.w. (n = 16) as lead acetate solution i.p. for a period of seven days. Group [T] (n = 16) served as control and received 15 mg Na + /kg b.w. as sodium acetate solution i.p. for the same period. All animals were sacrificed 24 h after the last injection. Blood superoxide dismutase (SOD) and blood glutathione peroxidase (GPx) activities and plasma bilirubin level were measured. Liver was quickly excised for the estimation of alteration in lipid peroxidation indices (MDA). Lead exposure induces, in both treated groups, a marked decline in haematocrit and haemoglobin levels (p < 0.01) when compared to control. The results show also a significant decrease (p < 0.01) in SOD activity, but only in group [Pb 15]. SOD activity did not decrease in group [Pb 5] in comparison with control (p > 0.05). However, lead exposure caused a light increase in GPx activity in group [Pb 15], which remains non-significant (p > 0.05) compared to control. Group [Pb 5] did not record significant changes in the activity of GPx. Lead exposure for a period of seven days resulted in a significant (p < 0.05) increase in bilirubin level in group [Pb 15] compared to control. The bilirubin level from rats of group [Pb 5] did not reach a statistical significance. Changes in liver MDA content in lead-exposed rats from [Pb 5] and [Pb 15] groups did not reach a statistical (p < 0.05) significance. It is concluded that lead induces oxidative stress in a dose-dependent manner. No dose-dependent response was observed in blood GPx activity and liver MDA content. These results could be due to the short duration of the treatment.