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DNA damage induced in cultured human alveolar (L-132) cells by exposure to dimethylarsinic acid.
TLDR
The present study suggests that the DNA single-strand breaks and DNA-protein cross-links induced by the treatment of L-132 cells with DMAA occurred via the formation of AP sites in the DNA and that the genome was found to bind not only to core histone proteins but also linker histone (H1) and nonhistone proteins.
Induction of lung-specific DNA damage by metabolically methylated arsenics via the production of free radicals.
TLDR
Oral administration to mice of dimethylarsinic acid induced lung-specific DNA damage, i.e., DNA single-strand breaks and the clumping of heterochromatin, suggesting that the strand breaks were induced via the production of free-radical species including active oxygens.
Oral exposure of dimethylarsinic acid, a main metabolite of inorganic arsenics, in mice leads to an increase in 8-Oxo-2'-deoxyguanosine level, specifically in the target organs for arsenic
TLDR
The oral administration of DMA enhanced significantly the amounts of 8-oxodG specifically in the target organs of arsenic carcinogenesis and also in urine, whereas arsenite did not.
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