二溴乙酸 - CAS号 631-64-1

物化性质

熔点：

32-38 °C (lit.)
沸点：

128-130 °C/16 mmHg (lit.)
密度：

2.382 g/mL at 25 °C (lit.)
闪点：

>230 °F
溶解度：

DMSO：100 mg/mL（459.05 mM；需要超声波）
颜色/状态：

Hygroscopic crystals
蒸汽压力：

2.3X10-2 mm Hg at 25 °C (est)
亨利常数：

4.42e-09 atm-m3/mole
分解：

When heated to decomposition it emits toxic vapors of /bromide./
解离常数：

pKa = 1.48 at 25 °C
稳定性/保质期：

在常温常压下，该物质保持稳定。

计算性质

辛醇/水分配系数(LogP)：

1.5
重原子数：

6
可旋转键数：

1
环数：

0.0
sp3杂化的碳原子比例：

0.5
拓扑面积：

37.3
氢给体数：

1
氢受体数：

2

ADMET

毒理性

致癌物分类

国际癌症研究机构致癌物：二溴乙酸

IARC Carcinogenic Agent:Dibromoacetic acid

来源:International Agency for Research on Cancer (IARC)

毒理性

致癌物分类

国际癌症研究机构（IARC）致癌物分类：2B组：可能对人类致癌

IARC Carcinogenic Classes:Group 2B: Possibly carcinogenic to humans

来源:International Agency for Research on Cancer (IARC)

毒理性

致癌物分类

国际癌症研究机构专论：第101卷：（2012年）工业和消费品、食品和饮用水中存在的一些化学品

IARC Monographs:Volume 101: (2012) Some Chemicals Present in Industrial and Consumer Products, Food and Drinking-water

来源:International Agency for Research on Cancer (IARC)

毒理性

副作用

Dermatotoxin - 皮肤烧伤。 IARC致癌物 - 第3类：根据国际癌症研究机构的分类，这些化学品无法归类。 NTP致癌物 - 有理由预期为人类致癌物。

Dermatotoxin - Skin burns. IARC Carcinogen - Class 3: Chemicals are not classifiable by the International Agency for Research on Cancer. NTP Carcinogen - Reasonably anticipated to be a human carcinogen.

来源:Haz-Map, Information on Hazardous Chemicals and Occupational Diseases

毒理性

相互作用

二溴乙酸(DBA)是一种消毒副产物，已在雌性大鼠中发现能增加循环中的雌二醇(E2)和雌酮(E1)的浓度。这种效应似乎至少部分是由于肝脏分解代谢的抑制。目前的研究调查了DBA是否通过增加性激素水平，能够增强触发促黄体生成激素(LH)激增的的下丘脑上调作用，或者影响神经毒素亚硝基二甲基硫脲(DMDC)阻断激增的能力。斯普拉格-道利大鼠在14天内通过胃管给予DBA(0-150 mg/kg)，并在给药第11天进行卵巢切除，同时植入雌二醇胶囊以产生每日的LH激增。在14天下午13:00给予0.1 mM/kg DMDC注射，并在下午采集血液样本。DBA诱导了与总雌激素剂量相关的增加。对于确定的激增，LH曲线下的区域分为两组，包括两个较低剂量(0和37.5 mg/kg DBA)和两个较高剂量(75和150 mg/kg)的处理组。因此，低DBA组和高DBA组进行比较，发现它们有显著差异。在150 mg DBA/0.1 mM DMDC的情况下，可识别的LH峰值的时机与非DMDC雌性相似，而37.5 mg DBA/0.1 mM DMDC组中峰值浓度的出现被延迟。单独DBA处理没有显著效果。结果表明，这种DBA暴露导致了与总雌激素浓度剂量相关的增加，这与DMDC阻断LH激增的减弱相平行。这种效应似乎归因于增强与雌激素相关的下丘脑上调作用，刺激激增的大脑机制。

The disinfection by-product dibromoacetic acid (DBA) has been found in female rats to increase circulating concentrations of both estradiol (E2) and estrone (E1). This effect is apparently due, at least in part, to a suppression in hepatic catabolism. The present study investigated whether DBA, by increasing sex steroid levels, is able either to augment the hypothalamic up-regulation involved in triggering a luteinizing hormone (LH) surge, or to affect the ability of the neurotoxicant sodium dimethyldithiocarbamate (DMDC) to block the surge. Sprague-Dawley rats were gavaged for 14 days with DBA (0-150 mg/kg) and ovariectomized on dosing day 11, and at the same time implanted with an estradiol capsule to generate daily LH surges. An injection of 0.1 mM/kg DMDC was administered at 13:00 hr on day 14 and blood was sampled over the afternoon. DBA induced a dose-related increase in total estrogens. For identified surges, areas under the LH curve partitioned into two groups, comprising the two lower (0 and 37.5 mg/kg DBA) and the two higher (75 and 150 mg/kg) treatment groups. Consequently, low and high DBA groups were compared and found to be significantly different. At 150 mg DBA/0.1 mM DMDC, the timing of an identifiable LH peak was comparable to non-DMDC females, unlike the 37.5mg DBA/0.1 mM DMDC group in which the appearance of peak concentrations was delayed. A significant effect with DBA treatment alone was not present. Results indicated that this exposure to DBA induced a dose-related increase in total estrogen concentrations that paralleled a diminished DMDC blockade of the LH surge. The effect appeared to be attributable to an augmentation in the estrogen-associated up-regulation in brain mechanisms stimulating the surge.