Effect of aluminum and lead salts on lipid peroxidation and cell survival in human skin fibroblasts

Abstract

The aim of this study was to see whether aluminum (Al) and lead (Pb) salts are toxic for cultured human fibroblasts under different experimental conditions, in the controllable situation offered by cell cultures. Cell survival and membrane lipid peroxidation served as markers of Al and Pb toxicity. Evaluation of the living cells was carried out using a colorimetric method, the mitochondrial reduction of 1-(4,5-dimethylthiazol-2-yl)-2,5-diphenyl tetrazolium bromide (MTT). Lipoperoxidation assay was performed on whole cell homogenates by measuring thiobarbituric acid-reactive substances (TBARS) produced after incubation with ascorbic acid-ferrous sulfate. Al(III) and Pb(II) salts (300 microM) produce a considerable decrease in cell survival after an exposure period of 4d, evident with the three fetal calf serum concentrations in the culture media: 2, 5, and 10%. Taking into account in vitro cell aging, the cytotoxic effects of Al(III) and Pb(II) are greater in senescent fibroblasts than in young cells. Lead-induced cytotoxicity is higher than Al-induced cytotoxicity. A mechanism that contributes to cellular toxicity is membrane lipid peroxidation; our results demonstrate that Al(III) and Pb(II) ions, 400 microM, exert an antioxidant-like effect or a pro-oxidant action on cell membranes depending on exposure time. We describe significant increases in TBARS formation associated with the presence of 400 microM Al(III) or Pb(II) salts in the culture media. Our study also revealed that these heavy metals induce a cell age-dependent action on membrane lipoperoxidation that is greater in senescent fibroblasts and this could have severe consequences for maintenance of cellular integrity.

Effects of Humic Substances and Phenolic Compounds on the In Vitro Toxicity of Aluminium

“…Aluminium can form lipid soluble chelates with these phenolic compounds, which can easily penetrate into the cells and exert their toxic e!ects or impair the membrane (the "rst step of many toxicological process). Such phenomena have recently been observed by Dominguez et al (1995), who demonstrated that Al(III) was able to ALUMINIUM, HUMIC SUBSTANCES, AND PHENOLIC COMPOUNDS enhance lipid peroxidation of the membranes of human "broblasts.…”

Lipids, lipid peroxidation and 7-ketocholesterol in workers exposed to lead

“…38 Research on cell cultures (human fibroblasts, aorta endothelial cells, rat hepatocytes and ovarian cells) has confirmed that addition of lead ions to cell cultures induced increased free-radical processes of fatty acid oxidation. 16,34,39 24-hour incubation of erythrocyte suspension and whole blood with lead ions in a concentration of 100 pg/dL did not induce an increase in lipid peroxides. 40 These concentrations of LP products were also noted in people exposed to lead compounds.…”

Cytotoxicity of dental glass ionomers evaluated using dimethylthiazol diphenyltetrazolium and neutral red tests

“…Analysis of the water extracts in this study showed no detectable levels of arsenic, but two materials released lead. Lead is considered more toxic than aluminum (30), and the extract of freshly cured Ketac Silver contained a lead concentration far above what is considered to be the toxic level for aluminum. Studies have reported that glass ionomers also release small amounts non-polymerized monomers (32,33).…”