Disease relevance of CCRIS 7636

• To determine if dibromoacetic acid (DBA) affects ovarian folliculogenesis, four groups of female Dutch-belted rabbits were exposed daily to 0, 1, 5, or 50 mg DBA/kg body weight in drinking water beginning in utero from gestation day 15 throughout life [1].
• These studies demonstrate that the testicular toxicity induced by DCA are similar to those produced by the analogue, dibromoacetic acid [2].

High impact information on CCRIS 7636

• Our findings suggest a critical window of exposure with respect to fetal development during weeks 33-40 for the effects of dibromoacetic acid and during weeks 37-40 for the effects of dichloroacetic acid [3].
• Sub-chronic exposure to dibromoacetic acid, a water disinfection by-product, does not affect gametogenic potential in mice [4].
• It is proposed that a reaction subset yielding low molecular weight carboxylic acids is predominant in samples with NaBr, whereas a pathway leading to dibromoacetic acid or tribromoacetic acid production is the major process in samples without NaBr [5].
• The ED(50)s for decreases in fertility assessed by intrauterine insemination were 3.5 mg/kg and 2.7 mg/kg for DBA and BCA [6].
• Effect of dibromoacetic acid on DNA methylation, glycogen accumulation, and peroxisome proliferation in mouse and rat liver [7].

Chemical compound and disease context of CCRIS 7636

• In this report we present the results of acute toxicity and acute spermatotoxicity studies of monobromoacetic acid (MBAA) and dibromoacetic acid (DBAA) [8].

Biological context of CCRIS 7636

• Dibromoacetic acid (DBA) is a by-product of drinking water disinfection that alters spermatogenesis in adult male rats [9].
• Xenopus embryos (150-400/concentration group) were exposed to 0, 8000, 10,000, 12,000, or 14,000 ppm BCA or 0, 10,000, 12,000, 14,000, or 16,000 ppm DBA for 96 h beginning from stage 8 (mid-blastula) to stage 46 (when primary organogenesis is complete) [10].
• The current studies demonstrate that BCA is more potent than DBA or DCA at disrupting embryogenesis since shorter exposures alter morphogenesis [11].
• Elevated gavage exposures to the drinking water disinfection by-product dibromoacetic acid (DBA) have been found to disrupt estrous cyclicity in the rat and induce increases in estradiol concentrations in both cycling (day of estrus) and ovariectomized/estradiol-implanted females [12].

Anatomical context of CCRIS 7636

• Dibromoacetic acid, a prevalent by-product of drinking water disinfection, compromises the synthesis of specific seminiferous tubule proteins following both in vivo and in vitro exposures [9].
• The present report details histopathologic changes in the testis and epididymis of rats gavaged daily for 2 to 79 d with a by-product of water disinfection, dibromoacetic acid (DBAA) [13].
• To investigate whether the mechanism of dibromoacetic acid (DBA) toxicity involves disruption of primordial germ cell migration and/or follicular formation, pregnant and lactating female Sprague-Dawley rats were gavaged daily with 0, 1, 5, or 50 mg DBA/kg body weight beginning on gestation day 17 and continuing through postnatal day 7 [14].
• Gestation day 8 (3-6 somite pairs) CD-1 mouse conceptuses were exposed to 11,000muM dichloroacetic acid (DCA), 300muM dibromoacetic acid (DBA) or 300muM bromochloroacetic acid (BCA) for culture periods of 1, 3, 6 or 26h [11].

Associations of CCRIS 7636 with other chemical compounds

• An evaluation of potential adverse human health effects of disinfection byproducts requires study of both cancer and noncancer endpoints; however, no studies have evaluated the neurotoxic potential of a common haloacetic acid, dibromoacetic acid (DBA) [15].
• Dibromoacetic acid (DBA) is a water disinfection byproduct formed by the reaction of chlorine oxidizing compounds with natural organic matter in water containing bromide [16].
• Twenty-week exposures to the drinking water disinfection by-product dibromoacetic acid: reproductive cyclicity and steroid concentrations in the female Sprague-Dawley rat [12].
• Previous data from our laboratory indicated that the drinking water disinfection by-product, dibromoacetic acid (DBA), when applied in vitro to rat preovulatory follicles at a concentration consistent with blood levels found to disrupt estrous cyclicity, was able to block the stimulated secretion of progesterone [17].
• 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) [18].

Gene context of CCRIS 7636

• Dibromoacetate was the only brominated haloacetate that consistently increased acyl-CoA oxidase activity and rates of cell replication in the liver [19].
• Histopathologic changes in the testes of rats exposed to dibromoacetic acid [13].

References