Oxidative stress: a possible mechanism for lead-induced apoptosis and nephrotoxicity

Abstract

Lead-induced nephrotoxicity is a human health hazard problem. In this study, Human mesangial cells (HMCs) were treated with different concentration of lead acetate (5, 10, 20 μmol/l) in order to investigate the oxidative stress and apoptotic changes. It was revealed that lead acetate could induce a progressive loss in HMCs viability together with a significant increase in the number of apoptotic cells using 3-(4,5-dimethyl-2-thiazolyl)-2,5-diphenyl tetrazolium (MTT) assay and flow cytometry, respectively. The apoptotic morphological changes induced by lead exposure in HMCs were demonstrated by PI-Hochest33342 staining. A DNA laddering pattern in lead-treated cells was shown, which could indicate nuclear fragmentation. In addition, lead acetate significantly increased the levels of malondialehyde (MDA) content and lactate dehydrogenase (LDH) activity. Therefore, it might be concluded that lead could promote HMCs' oxidative stress and apoptosis, which may be the chief mechanisms of lead-induced nephrotoxicity.