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首页> 外文期刊>Journal of applied toxicology >Differential effects of dihalogenated and trihalogenated acetates in the liver of B6C3F1 mice.
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Differential effects of dihalogenated and trihalogenated acetates in the liver of B6C3F1 mice.

机译：B6C3F1小鼠肝脏中二卤代和三卤代乙酸酯的差异作用。

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摘要

Haloacetates are produced in the chlorination of drinking water in the range 10--100 microg l(-1). As bromide concentrations increase, brominated haloacetates such as bromodichloroacetate (BDCA), bromochloroacetate (BCA) and dibromoacetate (DBA) appear at higher concentrations than the chlorinated haloacetates: dichloroacetate (DCA) or trichloroacetate (TCA). Both DCA and TCA differ in their hepatic effects; TCA produces peroxisome proliferation as measured by increases in cyanide-insensitive acyl CoA oxidase activity, whereas DCA increases glycogen concentrations. In order to determine whether the brominated haloacetates DBA, BCA and BDCA resemble DCA or TCA more closely, mice were administered DBA, BCA and BDCA in the drinking water at concentrations of 0.2--3 g l(-1). Both BCA and DBA caused liver glycogen accumulation to a similar degree as DCA (12 weeks). The accumulation of glycogen occurred in cells scattered throughout the acinus in a pattern very similar to that observed in control mice. In contrast, TCA and low concentrations of BDCA (0.3 g l(-1)) reduced liver glycogen content, especially in the central lobular region. The high concentration of BDCA (3 g l(-1)) produced a pattern of glycogen distribution similar to that in DCA-treated and control mice. This effect with a high concentration of BDCA may be attributable to the metabolism of BDCA to DCA. All dihaloacetates reduced serum insulin levels. Conversely, trihaloacetates had no significant effects on serum insulin levels. Dibromoacetate was the only brominated haloacetate that consistently increased acyl-CoA oxidase activity and rates of cell replication in the liver. These results further distinguish the effects of the dihaloacetates from those of peroxisome proliferators like TCA. Copyright 2001 John Wiley & Sons, Ltd.
机译：饮用水氯化过程中产生的卤乙酸盐范围为10--100 microg l（-1）。随着溴化物浓度的增加，溴化卤代乙酸盐（如溴代二氯乙酸酯（BDCA），溴代氯乙酸酯（BCA）和二溴乙酸酯（DBA））的浓度高于氯化卤代乙酸盐：二氯乙酸酯（DCA）或三氯乙酸酯（TCA）。 DCA和TCA的肝效应不同。通过对氰化物不敏感的酰基辅酶A氧化酶活性的增加来衡量，TCA会产生过氧化物酶体增殖，而DCA则增加了糖原浓度。为了确定溴化卤代乙酸盐DBA，BCA和BDCA是否更类似于DCA或TCA，在饮用水中以0.2--3 g l（-1）的浓度给小鼠施用DBA，BCA和BDCA。 BCA和DBA引起的肝糖原积聚与DCA相似（12周）。糖原的积累发生在散布在整个腺泡中的细胞中，其模式与对照小鼠中观察到的模式非常相似。相反，TCA和低浓度的BDCA（0.3 g l（-1））会降低肝糖原含量，尤其是在小叶中央区。高浓度的BDCA（3 g l（-1））产生的糖原分布模式与DCA治疗和对照小鼠相似。高浓度BDCA的这种作用可能归因于BDCA代谢为DCA。所有二卤代乙酸盐均降低血清胰岛素水平。相反，三卤代乙酸盐对血清胰岛素水平无明显影响。二溴乙酸盐是唯一能持续增加酰基辅酶A氧化酶活性和肝细胞复制速度的溴代卤代乙酸盐。这些结果进一步区分了二卤代乙酸盐的影响与过氧化物酶体增殖剂（如TCA）的影响。版权所有2001 John Wiley＆Sons，Ltd.

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