bromochloroacetic-acid and bromoacetate

A capillary zone electrophoresis (CZE) system for determining haloacetic acids in water was optimized with indirect photometric detection. Two different carrier electrolytes, potassium hydrogenphthalate and sodium 2,6-naphthalenedicarboxylate, were evaluated in terms of sensitivity and two different electroosmotic flow modifiers, tetradecyltrimethylammonium bromide and hexadecyltrimethylammonium bromide, were tested. Parameters such as electrolyte concentration and pH, and the concentration of the electroosmotic flow modifiers, which affect the CZE separations, were investigated. The method was used to determine haloacetic acids in chlorine tap water using the liquid-liquid extraction process.

Topics: Acetates; Cetrimonium; Cetrimonium Compounds; Chlorine; Dichloroacetic Acid; Disinfection; Electrophoresis, Capillary; Hydrogen-Ion Concentration; Quaternary Ammonium Compounds; Surface-Active Agents; Trichloroacetic Acid; Trimethyl Ammonium Compounds; Water

Brominated and chlorinated haloacetates (HAs) are by-products of drinking water disinfection. Dichloroacetate (DCA) and trichloroacetate (TCA) are hepatocarcinogenic in rodents, but the brominated analogs have received little study. Prior work has indicated that acute doses of the brominated derivatives are more potent inducers of oxidative stress and increase the 8-hydroxydeoxyguanosine (8-OH-dG) content of the nuclear DNA in the liver. Since, DCA and TCA are also known as weak peroxisome proliferators, the present study was intended to determine whether this activity might be exacerbated by peroxisomal proliferation. Classical responses to peroxisome proliferators, cyanide-insensitive acyl-CoA oxidase activity and increased 12-hydroxylation of lauric acid, were elevated in a dose-related manner in mice maintained on TCA and clofibric acid (positive control), but not with DCA, dibromoacetate (DBA) or bromochloroacetate (BCA). Administration of the HAs in drinking water to male B6C3F1 mice for periods from 3 to 10 weeks resulted in dose-related increases in 8-OH-dG in nuclear DNA of the liver with DBA and BCA, but not with TCA or DCA. These findings indicate that oxidative damage induced by the haloacetates is, at least in part, independent of peroxisome proliferation. In addition, these data suggest that oxidative damage to DNA may play a more important role in the chronic toxicology of brominated compared to the chlorinated haloacetates.

Topics: 8-Hydroxy-2'-Deoxyguanosine; Acetates; Acyl-CoA Oxidase; Animals; Cell Division; Chromatography, High Pressure Liquid; Clofibric Acid; Cytochrome P-450 CYP4A; Cytochrome P-450 Enzyme System; Deoxyguanosine; Dichloroacetic Acid; DNA Damage; Drinking; Fresh Water; Hydroxylation; Lauric Acids; Liver; Male; Mice; Microbodies; Mixed Function Oxygenases; Oxidative Stress; Oxidoreductases; Reference Standards; Water Pollutants, Chemical