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Toxicity of dimethylmonothioarsinic acid toward human epidermoid carcinoma A431 cells.
TLDR
The results suggest that although DMMTA (V) is a pentavalent arsenical, it is taken up efficiently by cells and causes various levels of toxicity, in a manner different from that of nonthiolated pentavalents arsenicals. Expand
Trivalent arsenicals are bound to proteins during reductive methylation.
TLDR
It was proposed that inorganic arsenic was successively methylated reductively in the presence of glutathione, rather than a stepwise oxidative methylation, and pentavalent arsenicals were present as end products of metabolism,rather than intermediates. Expand
Arsenic metabolism and thioarsenicals in hamsters and rats.
TLDR
It is indicated that in hamsters, arsenic does not accumulate in RBCs, and therefore, hamsters exhibit a more uniform tissue distribution and faster urinary excretion of arsenic than rats. Expand
Metabolism, toxicity and anticancer activities of arsenic compounds
TLDR
The arsenic metabolic pathway, the roles of the methylated arsenic metabolites in toxicity and in the therapeutic efficacy for the treatments of solid tumors, APL and/or non-APL malignancies are focused on. Expand
Disruption of the arsenic (+3 oxidation state) methyltransferase gene in the mouse alters the phenotype for methylation of arsenic and affects distribution and retention of orally administered
TLDR
A central role for As3mt in the metabolism of inorganic arsenic is confirmed and phenotypes for arsenic retention and distribution are markedly affected by the null genotype for arsenic methylation, indicating a close linkage between the metabolism and retention of arsenicals. Expand
Comparative toxicity of arsenic metabolites in human bladder cancer EJ-1 cells.
TLDR
DMMTA(V) may be one of the most toxicologically potent arsenic species, relevant to arsenic-induced carcinogenicity in the urinary bladder, and causes cell death through oxidative stress. Expand
Arsenic metabolism and thioarsenicals.
TLDR
It is concluded that the methylation reaction takes place with simultaneous reductive rather than stepwise oxidative methylation, and production of pentavalent methylated arsenic metabolites are suggested to be as the end product of metabolism, rather than intermediates. Expand
A Novel Pathway for Arsenic Elimination: Human Multidrug Resistance Protein 4 (MRP4/ABCC4) Mediates Cellular Export of Dimethylarsinic Acid (DMAV) and the Diglutathione Conjugate of
TLDR
Human MRP4 expressed in HEK293 cells reduced the cytotoxicity and cellular accumulation of arsenate, MMAIII, MMAV, DMAIII, and DMAV while two other hepatic basolateral MRPs (MRP3 and MRP5) did not, suggesting that human MRP 4 could be a major player in the elimination of arsenic. Expand
Mitochondria are the main target organelle for trivalent monomethylarsonous acid (MMA(III))-induced cytotoxicity.
TLDR
The mechanism underlying cell death is different among As(III), MMA( III), and DMA(III, with mitochondria being one of the primary target organelles for MMA(III)-induced cytotoxicity. Expand
Formation of dimethylthioarsenicals in red blood cells.
TLDR
It was proposed that arsenic is excreted from hepatocytes into the bloodstream in the form of DMAIII and then taken up by RBCs in humans, where it is transformed into DMMTA(V) and then excreting again into the waters of the bloodstream. Expand
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