Article ID | Journal | Published Year | Pages | File Type |
---|---|---|---|---|
2584404 | Environmental Toxicology and Pharmacology | 2008 | 6 Pages |
The toxicity of polychlorinated biphenyls (PCBs) has been attributed widely to receptor-mediated effects, buttressed by the popularity of the toxic equivalency factor. We propose that a crucial toxic mechanism of lower chlorinated PCBs is their enzymatic biotransformation to electrophiles, including quinoid metabolites, that bind intracellular sulfhydryl groups, such as those found in microtubulin and enzymes like telomerase. To test this hypothesis, we have examined micronuclei induction, cell cycle, and telomere shortening in cells in culture. Our findings show a large increase in micronuclei frequency and cell cycle perturbation in V79 cells, and a marked decrease in telomere length in HaCaT cells exposed to 2-(4′-chlorophenyl)-1,4-benzoquinone (PCB3pQ).