Lead acetate

About: Lead acetate is a research topic. Over the lifetime, 2636 publications have been published within this topic receiving 69739 citations.

Lead Toxicity as Related to Glutathione Metabolism

Abstract: The effect of lead poisoning on glutathione metabolism was studied in rat pups born of dams receiving a commercial laboratory diet supplemented with 0.5% lead acetate. Results showed that the body weight gain of the first 3 weeks of life and at the age of 6 weeks was significantly less in both male and female pups nourished by lead-fed dams than those raised by dams receiving the lab diet. Lead ingestion decreased hematocrit levels and hemoglobin values and increased the weights of liver, kidney, spleen and brain. Concentrations of plasma free histidine, glutamic acid and serine were decreased in lead-poisoned rats but glycine levels were markedly increased. After 4 weeks of lead feeding, both sexes had an increased glutathione concentration in erythrocytes, liver and kidney. Isotope studies further indicated that the incorporation of cystine-35S was significantly increased in glutathione but decreased in protein of liver and kidney of lead-fed rats. Similarly, lead ingestion significantly increased glycine-1-14C incorporation into renal glutathione. However, the activities of glutathione reductase and glutathione peroxidase were unaffected by lead poisoning. The data suggest a compensatory mechanism operates to overcome the toxicity of ingested lead by maintaining a high concentration of glutathione in the liver and kidney.

In vitro genotoxicity of lead acetate: induction of single and double DNA strand breaks and DNA-protein cross-links.

Abstract: Lead is present in the natural and occupational environment and is reported to interact with DNA, but the mechanism of this interaction is not fully understood. Using the alkaline comet assay we showed that lead acetate at 1–100 μM induced DNA damage in isolated human lymphocytes measured the change in the comet tail length. At 1 and 10 μM we observed an increase in the tail length, whereas at 100 μM a decrease was seen. The former effect could follow from the induction of DNA strand breaks and/or alkali-labile sites (ALS), the latter from the formation of DNA–DNA and/or DNA–protein cross-links. No difference was observed between tail length for the alkaline and pH 12.1 versions of the assay, which indicates that strand breaks and not ALS are responsible for the tail length increase induced by lead. The neutral version of the test revealed that lead acetate induced DNA double-strand breaks at all concentrations tested. The presence of spin traps, 5,5-dimethyl-pyrroline N-oxide (DMPO) and N-tert-butyl-α-phenylnitrone (PBN) did not influence the level of DNA damage induced by lead. Post-treatment of the lead-damaged DNA (at 100 μM treatment concentration) by endonuclease III (Endo III) and formamidopyrimidine-DNA glycosylase (Fpg), enzymes recognizing oxidized DNA bases, as well as 3-methyladenine-DNA glycosylase II, an enzyme recognizing alkylated bases, gave rise to a significant increase in the extent of DNA damage. Proteinase K caused an increase in comet tail length, suggesting that lead acetate might cross-link DNA with nuclear proteins. Vitamin A, E, C, calcium chloride and zinc chloride acted synergistically on DNA damage evoked by lead. The results obtained suggest that lead acetate may induce single-strand breaks (SSB) and double-strand breaks (DSB) in DNA as well as DNA–protein cross-links. The participation of free radicals in DNA-damaging potential of lead is not important and it concerns other reactive species than could be trapped by DMPO or PBN.