Studies On Cadmium,Lead-induced Damage Of SD Rats' Kidney And The Antagonism Of Antioxidants To The Damage

Lead (Pb) and Cadmium (Cd) are both widely spread environmental and industrial pollutants that affect various organs in humans and animals through occupational and environmental exposure. A body of evidence accumulated implicating the free radical generation with subsequent oxidative stress is the biochemical and molecular mechanisms of Pb and Cd toxicity. We carried out this study to investigate the mechanisms of Cd and Pb poisoning, and the protective effects of antioxidants.In experimental rats, orally administration of Cd and Pb to rats for four weeks. Meanwhile co-administrated of NAC and Pb,Cd as protective group . The activity of SOD,GSH-Px and MDA content were measured, and histological structure of kidney was analysed. The results showed that the activity of SOD,GSH-Px and MDA content both increased significantly (P<0.05) in Pb or Cd -treated group compared with control group; the activity of SOD,GSH-Px decreased notably (P<0.05), and the MDA content increased considerably (P<0.05) in Cd and Pb co-treated group, as compared to control group; co-administrated of NAC with Pb,Cd leads to pronounced increase in GSH-Px activity (P<0.05) and remarkably decrease in MDA content, compared to Pb and Cd treated group. (P<0.05); the histopathological studies showed that Pb and Cd exposure respectively or combined both caused severe damage to the architecture of renal and renal cells, NAC didn't preserved this lesion.To elucidate the effcts of Pb and Cd on apoptotic rates and intracellular ROS level of RTECs. We primary cultured RTECs, then different concentrations of Pb2+ and Cd2+ incubated with RTECs for 12h, Se-Met co-incubation with Pb and Cd as protective groups. After incubation, FCM assessed the level of intracellular ROS level and apoptotic rates of RTECs , using fluorescent probe DHR123 and Annexinâ…¤-PI Assay Kit respectively. The results showed that: low concentrations of Cd2+ and Pb2+ decreased intracellular ROS level, and mideum and high concentrations significantly increased it. In Pb and Cd combined poisoned groups, ROS level all increased obviously, compared to control group. Pb and Cd both pronounced increased RTECs apoptotic rates compared to control group, with increasing Pb2+ or Cd2+ concentration, apoptotic rates first arised then declined.. In antioxidant treated group, ROS level and apoptotic rates both abated compared to no antioxidant poisoned groups, and the reduced magnitude was shoftened accompany riasing Pb2+ and Cd2+ concentrations.This study confirmed the increased ROS level and subsequent oxidative stress are important mechanisms of Pb and Cd poisoning. Antioxidants have shown to exert significant protection against Pb and Cd toxicity by ameliorate oxidative stress both in vivo and in vitro, but have little benefit in restoring the compromised tissue.