Lead nitrate and gadolinium chloride administration modify hepatocyte cell surfaces

Abstract

Modifications of hepatocyte cell surface were determined after single i.v. injection to rats of Pb(NO 3 ) 2 (known to induce liver hyperplasia followed by apoptosis) or GdCl 3 (known to induce proliferation of parenchymal cells and Kupffer cell depletion) or administration of GdCl 3 24 h before Pb(NO 3 ) 2 injection (known to reduce hyperplasia and apoptosis induced in the parenchymal liver cells by the single Pb(NO 3 ) 2 injection). Rats were sacrificed at fixed times after the treatments (1, 3 and 5 days) and hepatocytes were isolated by enzymatic liver perfusion. In spite of the intracellular target of the heavy metals, signals leading to liver hyperplasia and apoptosis (with rates different for the different experimental conditions) were generated, which in turn were responsible for cell surface alteration. Increment or decrement of phosphatidylserine (PS) expression, asialoglycoprotein receptors (ASGPRs) and sugar residue expression on hepatocyte surfaces was measured in parallel with apoptosis and proliferation. When GdCl 3 was injected 24 h before Pb(NO 3 ) 2 injection, liver modifications were significantly reduced, thus suggesting that GdCl 3 could prevent and/or reduce liver damage.

Antioxidant enzymes activities and bilirubin level in adult rat treated with lead

“…This result is in agreement with the study undertaken by Patra et al [13], who recorded an increase in MDA content in the liver and the brain of rats subjected to subchronic exposure to lead for a period of four weeks. Pagliara et al [43] showed that lead-induced liver hyperplasia was followed by apoptosis mediated by oxidative stress in Kupffer cells. The group treated with 5 mg Pb/kg b.w [Pb 5] recorded no changes in MDA content in liver compared to controls, suggesting that this may be due to the short duration of the treatment.…”