Stereochemistry | ACHIRAL |
Molecular Formula | C2H7AsO2 |
Molecular Weight | 137.9974 |
Optical Activity | NONE |
Defined Stereocenters | 0 / 0 |
E/Z Centers | 0 |
Charge | 0 |
SHOW SMILES / InChI
SMILES
C[As](C)(O)=O
InChI
InChIKey=OGGXGZAMXPVRFZ-UHFFFAOYSA-N
InChI=1S/C2H7AsO2/c1-3(2,4)5/h1-2H3,(H,4,5)
Cacodylic acid also known as dimethylarsinic acid (DMA) has been used as a herbicide. As a part of agent blue it used to destroy broadleaf plants and trees, especially rice paddies during the Vietnam War. DMA is the major metabolite formed after exposure to tri- (arsenite) or pentavalent (arsenate) inorganic arsenic (iAs) via ingestion or inhalation in both humans and rodents. DMA induces an organ-specific lesion--single strand breaks in DNA. Mechanistic studies have suggested that this damage is due mainly to the peroxyl radical of DMA and production of active oxygen species by pulmonary tissues. Multi-organ initiation-promotion studies have demonstrated that DMA acts as a promotor of urinary bladder, kidney, liver and thyroid gland cancers in rats and as a promotor of lung tumors in mice. Thus it was shown, that DMA played a role in the carcinogenesis of inorganic arsenic.
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PubMed
Patents
Sample Use Guides
mutagenicity in rats: The purpose of present study is to evaluate the in vivo mutagenicities of dimethylarsinic acid (DMAV), (Cacodylic acid) and sodium arsenite (iAs) in rat urinary bladder epithelium and liver using gpt delta F344 rats. Ten-week old male gpt delta F344 rats were randomized into 3 groups and administered 0, 92 mg/L dimethylarsinic acid (DMAV), or 87mg/L sodium arsenite (iAs) (each 50mg/L As) for 13 weeks in the drinking water.
Route of Administration:
Oral
Gene damage in cultured human alveolar (L-132) cells induced by exposure to dimethylarsinic acid (DMAA) was stidued. DNA single-strand breaks and DNA-protein cross-links were induced by the treatment of L-132 cells with 10 mM DMAA. These kinds of damage appeared at 8 hr after start of exposure to DMAA. As regards DNA-protein cross-links, the DNA was found to bind not only to core histone proteins but also linker histone (H1) and nonhistone proteins. Furthermore, the cross-links were formed by the binding to serine or threonine residues of H1 or nonhistone proteins through phosphate moieties of the DNA. The induction of the alkali-labile sites in DNA in DMAA-treated L-132 cells was observed prior to that of DNA single-strand breaks and DNA-protein cross-links. As one of the alkali-labile sites in DNA, we estimated apurinic/apyrimidinic (AP) sites in DNA.