ArticleEnvironmental health perspectives2001
Formamidopyrimidine-DNA glycosylase enhances arsenic-induced DNA strand breaks in PHA-stimulated and unstimulated human lymphocytes.
Article in Environmental health perspectives, 2001. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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4 citing papers in PubMed, 32 citations in OpenAlex.
- Efficacy of crude extract of Emblica officinalis (amla) in arsenic-induced oxidative damage and apoptosis in splenocytes of mice.Toxicology international · 2014Article
- Immunomodulatory role of Emblica officinalis in arsenic induced oxidative damage and apoptosis in thymocytes of mice.BMC complementary and alternative medicine · 2013Article
- BRCA2-dependent homologous recombination is required for repair of Arsenite-induced replication lesions in mammalian cells.Nucleic acids research · 2009Article
- A Mechanistic Approach for Modulation of Arsenic Toxicity in Human Lymphocytes by Curcumin, an Active Constituent of Medicinal Herb Curcuma longa Linn.Journal of clinical biochemistry and nutrition · 2007Article
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Authors and funding
4 authors at 1 institution in 1 country.
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No grant is acknowledged in the PubMed record.
Abstract
To confirm that arsenic (As) induces oxidative DNA damage in phytohemagglutinin (PHA)-stimulated and unstimulated human lymphocytes, we used the alkaline comet assay combined with specific enzyme [formamidopyrimidine-DNA glycosylase (FPG)] digestion to measure As-induced base damage. The results showed that the enzyme-sensitive sites were readily detected with the alkaline comet assay after the cells were treated with 10 microM As for 2 hr. The repair patterns observed for FPG-created DNA single strand breaks (SSBs) in As-treated cells were comparable to those in hydrogen peroxide (H(2)O(2))-treated cells. The enzyme-created SSBs, As-induced base damage, were more significant in PHA-stimulated lymphocytes. About 63% and 68% of SSBs induced by As and H(2)O(2), respectively, were repaired in PHA-stimulated lymphocytes by 2-hr repair incubation, but about 34% and 43%, respectively, were repaired in unstimulated cells. About 40% and 49% of base damage induced by As and H(2)O(2), respectively, were repaired in PHA-stimulated lymphocytes, but about 19% and 21%, respectively, were repaired in unstimulated cells. These results indicated that As induced oxidative DNA damage in human lymphocytes at micromolar concentrations. The damaged bases could be chiefly purines or formamidopyrimidines. Like the damage induced by H(2)O(2), As-induced DNA damage was repaired more slowly in unstimulated lymphocytes.
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