Genotoxic effects of lead: an updated review.

Antioxidant effect of vitamin E and selenium on lipid peroxidation, enzyme activities and biochemical parameters in rats exposed to aluminium.

The carcinogenicity of lead compounds has received renewed attention because of continuing environmental and occupational sources of exposure in many countries. The epidemiological evidence for an association between lead exposures and human cancer risk has been strengthened by recent studies, and new data on mechanisms of action provide biological plausibility for assessing lead as a human carcinogen. Both epidemiological and mechanistic data are consistent with a facilitative role for lead in carcinogenesis, that is, lead by itself may not be both necessary and sufficient for the induction of cancer, but at a cellular and molecular level lead may permit or enhance carcinogenic events involved in DNA damage, DNA repair, and regulation of tumor suppressor and promoter genes. Some of these events may also be relevant to understanding mechanisms of lead-induced reproductive toxicity.

Facilitative mechanisms of lead as a carcinogen.

Lead (Pb) is an element present in the environment that negatively affects all living organisms. To diminish its high toxicity, micro-organisms have developed several mechanisms that allow them to survive exposure to Pb(II). The main mechanisms of lead resistance involve adsorption by extracellular polysaccharides, cell exclusion, sequestration as insoluble phosphates, and ion efflux to the cell exterior. This review describes the various lead resistance mechanisms, and the regulation of their expression by lead binding regulatory proteins. Special attention is given to the Pbr system from Cupriavidus metallidurans CH34, which involves a unique mechanism combining efflux and lead precipitation.

Lead resistance in micro-organisms.

Molecular mechanism of heavy metals (Lead, Chromium, Arsenic, Mercury, Nickel and Cadmium) - induced hepatotoxicity - A review.

Lead effect on DNA and albumin in chicken blood and the protection of selenium nutrition have been investigated to gain insight into initial molecular events following exposure to lead. The concentration of lead used in this paper is 11.6 μg/dL. Single cell electrophoresis technique was utilized to measure DNA strand breaks in chicken blood cells treated with lead, the DNA strand breakage was observed and the percentage of damaged cells increased significantly, organic selenium (Kappa‐selenocarrageenan) had a strong non‐special protection ability to decrease the percentage of damaged cells exposed to lead. Further study with FT‐IR spectroscopy combined with other techniques indicated that with the addition of Pb2+ ion, the chicken serum albumin (CSA) molecule underwent conformational transitions from α‐helix to β‐sheet and turn structures, the binding site of Pb2+ ion in the chicken serum albumin molecule were C=O and C‐N groups of CSA.

Lead effect on DNA and albumin in chicken blood and the protection of selenium nutrition

The accumulation effect of lead on DNA damage and the protection of selenium against lead were studied in mice blood cells of three generations. The test animals were divided into four groups: controls, Pb group, Se group, Pb + Se group. Lead and Selenium were administered to mice in the drinking water. The concentrations of lead (in form of lead acetate) and selenium (in form of Kappa-selenocarrageenan) used in this paper were 1 microgram/ml and 0.25 microgram/ml respectively. The percentage of damaged cells (DNA comets) was examined and detected conveniently by the single-cell gel electrophoresis (comet) assay. Results showed that 1 microgram/ml lead did not damage the female mice blood cells of the first generation seriously. However, there was a significant damage effect in both sexes of the second and third generations, suggesting the accumulation effect of lead was very significant starting from the second generation. In addition, under normal physiological conditions, Kappa-Se did not appear to enhance the protective ability on DNA damage significantly, whereas under lead exposure conditions, administration of Kappa-Se displayed the occurrence of a good protection against lead intoxication which was started from the female mice of the second generation.

The accumulation effect of lead on DNA damage in mice blood cells of three generations and the protection of selenium.

The DNA damage and repair effects of yeast (Saccharomyces cerevisiae) cells induced by lead (Pb) were tested in this study. Yeast cells were cultured for 72 h at the following Pb concentrations: 0 (controls), 1ppm (11.6 μg/dl) and 8 ppm (92.6 μg/dl), and 0.1 g kappa‐selenocarrageenan (10000 μg Se/g) used as repair reagent was added directly to the yeast culture medium (100 ml) for the repair assays. The percentage of damaged cells was observed from fluorescence microscope. Statistical analysis showed that the two lead doses damaged DNA structure of yeast cells significantly, and the higher concentration made more serious damage than that of the lower concentration. With the addition of kappa‐selenocarrageenan, DNA damage was repaired to some degree. Furthermore, the accumulation effects of DNA damage from the parent generation to the filial generation yeast cells was also investigated. At the lower lead concentration, the accumulation effects were more significant than that at the higher concentr...

Xiaofan Yuan

Papers

Lead effect on DNA and albumin in chicken blood and the protection of selenium nutrition

The accumulation effect of lead on DNA damage in mice blood cells of three generations and the protection of selenium.

DNA damage and repair in yeast (saccharomyces cerevisiae) cells exposed to lead