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At least 127 records · Page 7Linked to original sources
PubMed1995

Cancer induction by an organic arsenic compound, dimethylarsinic acid (cacodylic acid), in F344/DuCrj rats after pretreatment with five carcinogens.

Arsenic (As) is environmentally ubiquitous and an epidemiologically significant chemical related to certain human cancers. Dimethylarsinic acid (cacodylic acid; DMA) is one of the major methylated metabolites of ingested arsenicals in most mammals. To evaluate the effects of DMA on chemical carcinogenesis, we conducted a multiorgan bioassay in rats given various doses of DMA. One-hundred twenty-four male F344/DuCrj rats were divided randomly into 7 groups (20 rats each for groups 1-5; 12 rats each for groups 6 and 7). To initiate multiple organs and tissues, animals in groups 1-5 were treated sequentially with diethylnitrosamine (100 mg/kg body weight, i.p., single dose at the commencement) and N-methyl-N-nitrosourea (20 mg/kg body weight, i.p., 4 times, on days 5, 8, 11, and 14). Thereafter, rats received 1,2-dimethylhydrazine (40 mg/kg body weight, s.c., 4 times, on days 18, 22, 26, and 30). During the same period, the animals were sequentially administered N-butyl-N-(4-hydroxybutyl)nitrosamine (0.05% in the drinking water, during weeks 1 and 2) and N-bis(2-hydroxypropyl)nitrosamine (0.1% in the drinking water, during weeks 3 and 4; DMBDD treatment). After a 2-week interval, groups 2-5 were given 50, 100, 200, or 400 ppm DMA, respectively, in the drinking water. Groups 6 and 7, which were not given DMBDD treatment, received 100 and 400 ppm DMA during weeks 6-30. All rats were killed at the end of week 30. In the initiated groups (groups 1-5), DMA significantly enhanced the tumor induction in the urinary bladder, kidney, liver, and thyroid gland, with respective incidences in group 5 (400 ppm DMA) being 80, 65, 65, and 45%. Induction of preneoplastic lesions (glutathione S-transferase placental form-positive foci in the liver and atypical tubules in the kidney) was also significantly increased in DMA-treated groups. Ornithine decarboxylase activity in the kidneys of rats treated with 100 ppm DMA was significantly increased compared with control values (P < 0.001). In conclusion, DMA is acting as a promoter of urinary bladder, kidney, liver, and thyroid gland carcinogenesis in rats, and we speculate that this may be related to cancer induction by As in humans.

Acetyltransferases↗
PubMed2004

Simultaneous determination of twelve inorganic and organic arsenic compounds by liquid chromatography-ultraviolet irradiation-hydride generation atomic fluorescence spectrometry.

A coupling between column liquid chromatography (LC) and atomic fluorescence spectrometry was developed for arsenic speciation. After separation, the compounds are oxidised on-line by UV irradiation, volatilised by hydride-generation and carried to the detector by a stream of argon. A combination of anion-exchange and hydrophobic interactions in a single column (Dionex AS7) was found suitable for the simultaneous separation of organic and inorganic species. Twelve compounds (arsenite, arsenate, monomethylarsonic acid, dimethylarsinic acid, arsenobetaine, arsenocholine, trimethylarsine oxide, tetramethylarsonium ion and four arsenosugars) were separated using an acetate buffer and a nitric acid solution as mobile phases. Limits of detection are 4-22 pg. The technique was applied to three marine samples. Arsenobetaine was detected as the main species in all samples, with concentrations varying from 59 to 1947 ng(As) g(-1) of fresh mass.

Animals↗
PubMed1998

Enzymatic methylation of arsenic compounds. VI. Characterization of hamster liver arsenite and methylarsonic acid methyltransferase activities in vitro.

Methylation of inorganic arsenic to methylarsonic acid (MMA) and dimethylarsinic acid (DMA) has been considered to be the major pathway of inorganic arsenic biotransformation and detoxification. Comparative studies, in vivo, have demonstrated variation in the abilities of animals to methylate inorganic arsenic. We propose that the rate of inorganic arsenite methylation may be one of the factors responsible for observed species variation. Arsenite and MMA methyltransferases of Golden Syrian hamster liver have been partially purified 40- and 67-fold, respectively. The monothiol L-cysteine promotes greater activities, in vitro, of these enzymes than similar concentrations of either glutathione or dithiothreitol. The pH optima of the partially purified arsenite and MMA methyltransferase activities are 7.6 and 8.0, respectively. Both activities display classic Michaelis-Menten enzyme kinetics. The K(m) and Vmax of hamster liver arsenite methyltransferase are 1.79 x 10(-6) M and 0.022 pmol/mg protein/60 min, respectively. Hamster liver MMA methyltransferase has K(m) and Vmax values of 7.98 x 10(-4) M and 0.007 pmol/mg protein/60 min, respectively. A similar kinetic relationship of these activities is also observed in the liver of the rabbit, which, like the hamster, excretes higher amounts of MMA than most other species studied. The higher K(m) and lower Vmax of MMA methyltransferase, compared to arsenite methyltransferase, measured in these two species suggests that MMA may be produced at a rate higher than it can be subsequently methylated to DMA, thereby allowing MMA to accumulate and be excreted.

Animals↗
PubMed2005

Treatment of groundwater polluted by arsenic compounds by zero valent iron.

Batch experiments were carried out to study the kinetics and efficiency of inorganic arsenic removal by zero valent iron (ZVI) powder, and as well as the effects of pH, anions, and humic material (HM) on this process. Moreover, column experiment was conducted for 31 days to treat arsenate solution of 500 microg As/L using waste iron chippings as filling. Batch experiments showed that both arsenate and arsenite compounds could be removed efficiently from simulated groundwater by ZVI under aerobic and relative anaerobic conditions. Aerobic condition was favorable to arsenic removal especially for arsenate, while arsenite could be removed more rapidly than arsenate in relative anaerobic condition. Oxidation of arsenite to arsenate by iron species in aerobic environment was observed, which is thought to be an important pathway of arsenite removal. In an unsealed system, the removal efficiency of both arsenate and arsenite decreased at higher pH value. In a sealed system, acidic and alkaline condition seemed to be favorable for arsenate and arsenite removal, respectively. Phosphate and low concentration sulfate caused a decrease in arsenate removal, while high concentration sulfate as well as nitrate caused slight increase in arsenate removal. Presence of HM in solution slightly inhibited arsenic removal. Arsenic removal efficiency in column study was influenced by flow rate and work period of the column. More than 98% of arsenate could be removed stably with a hydraulic resident time of 2 h at last, and the effluent meet the drinking water standard.

Arsenic↗
PubMed2005

Inorganic arsenic compounds cause oxidative damage to DNA and protein by inducing ROS and RNS generation in human keratinocytes.

Arsenic is a naturally occurring element that is present in food, soil, and water. Inorganic arsenic can accumulate in human skin and is associated with increased risk of skin cancer. Oxidative stress due to arsenic exposure is proposed as one potential mode of carcinogenic action. The purpose of this study is to investigate the specific reactive oxygen and nitrogen species that are responsible for the arsenic-induced oxidative damage to DNA and protein. Our results demonstrated that exposure of human keratinocytes to trivalent arsenite caused the generation of 8-hydroxyl-2'-deoxyguanine (8-OHdG) and 3-nitrotyrosine (3-NT) in a concentration- and time-dependent manner. Pentavalent arsenate had similar effects, but to a significantly less extent. The observed oxidative damage can be suppressed by pre-treating cells with specific antioxidants. Furthermore, we found that pre-treating cells with Nomega-nitro-L-arginine methyl ester (L-NAME), an inhibitor of nitric oxide synthase (NOS), or with 5,10,15,20-tetrakis (N-methyl-4'-pyridyl) porphinato iron (III) chloride (FeTMPyP), a decomposition catalyst of peroxynitrite, suppressed the generation of both 8-OHdG and 3-NT, which indicated that peroxynitrite, a product of the reaction of nitric oxide and superoxide, played an important role in arsenic-induced oxidative damage to both DNA and protein. These findings highlight the involvement of peroxynitrite in the molecular mechanism underlying arsenic-induced human skin carcinogenesis.

8-Hydroxy-2'-Deoxyguanosine↗