Effect of age‐dependent exposure to lead on hepatotoxicity and nephrotoxicity in male rats

Abstract

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.

The effect of occupational lead exposure on lipid peroxidation, protein carbonylation, and plasma viscosity

“…Our results are in accordance with data reported by Berrahal et al (2011), who reported a decrease in thiol levels in liver homogenates from rats that were administered lead acetate. Similar observations were reported by Tandon et al (2002) and El-Missiry (2000).…”

Chronic exposure to low doses of Pb induces hepatotoxicity at the physiological, biochemical, and transcriptomic levels of mice

“…Heavy metals including Pb have been reported to impact organs involved in mammalian toxicity . According to previous reports, acute exposure of animals to high doses of Pb had limited effects on growth factors such as body weights; however, decreases in liver weight and hepatic damage have been observed in different experimental models . In the present study, we observed that the liver weights decreased significantly (Figure ), no significant difference of body weights was observed between the Pb‐treated groups and control group, suggesting that chronic exposure to very low doses of Pb for 15 weeks had limited effects on growth.…”

Association of blood lead levels with urinary F2-8α isoprostane and 8-hydroxy-2-deoxy-guanosine concentrations in first-grade Uruguayan children

“…Evidence from experiments in animals and observational studies in occupationally-exposed adults suggest that exposure to high levels of Pb can induce the generation of lipid peroxidation products, alter the activities of antioxidant enzymes and cause changes to nucleic acid bases or structural damage to DNA molecules (Berrahal et al, 2011; Haleagrahara et al, 2011; Sandhir et al, 1995; Bizon et al, 2013; Garcon et al, 2007; Grover et al, 2010; Kasperczyk et al, 2012; Khan et al, 2008; Malekirad et al, 2010; Olewińska et al, 2010; Permpongpaiboon et al, 2011; Bizon et al, 2013; Garcon et al, 2004; Garcia-Leston et al, 2012; Khan et al, 2008; Moro et al, 2010; Permpongpaiboon et al, 2011). Further, among non-occupationally exposed non-pregnant US adults with low blood lead level (BLL), a positive association was reported between BLL and serum γ-glutamyltranferase (GGT), a liver enzyme and an early marker of OS, after adjusting for age, sex, race and socio-economic status (Lee et al, 2006).…”