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首页> 外文期刊>Mutation Research: International Journal on Mutagenesis, Chromosome Breakage and Related Subjects >DNA damage induced by the drinking water mutagen 3-chloro-4-(dichloromethyl)-5-hydroxy-2(5H)-furanone (MX) in mammalian cells in vitro and in mice.
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DNA damage induced by the drinking water mutagen 3-chloro-4-(dichloromethyl)-5-hydroxy-2(5H)-furanone (MX) in mammalian cells in vitro and in mice.

机译：饮用水致突变剂3-chloro-4-（dichloromethyl）-5-hydroxy-2（5H）-呋喃酮（MX）在哺乳动物细胞中和小鼠体外诱发的DNA损伤。

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摘要

3-chloro-4-(dichloromethyl)-5-hydroxy-2[5H]-furanone (MX) formed during chlorination of water containing natural organic substances, is a very potent bacterial mutagen. Recently, tumours at multiple sites were reported in rats given MX-containing drinking water. We have investigated the genotoxicity of MX in mammalian cells exposed in vitro and in vivo using alkaline filter elution to detect DNA single-strand breaks and/or alkali-labile sites (SSBs). Concentrations as high as 100 and 300 microM MX were required to induce detectable levels of SSBs in the HL-60 cells. If MX treatment was carried out in the presence of DNA repair inhibitors (AraC plus hydroxyurea), the sensitivity of the assay to detect MX-induced SSBs was increased by a factor of 100. The presence of serum proteins during exposure resulted in a minor reduction of the MX-induced DNA damage in HL-60 cells at the lowest MX concentrations. In primary cultures of testicular cells as well as in resting human peripheral blood mononuclear cells (PBMC), a slightly increased level of SSBs was observed at MX-concentrations above 30 microM, this effect was not further increased by repair inhibitors. In LLC-PK1 renal proximal tubular epithelial cells and in growth stimulated human peripheral PBMC, increased SSBs were detected at MX concentrations as low as low as 3-10 microM and higher using repair inhibitors, and at 10 times higher concentrations without repair inhibitors. No dose dependent DNA damage was detected in the liver, kidney, spleen and colon of male B6C3F1 mice administrated high doses of MX (40 and 80 mg kg-1). Moderately increased and dose dependent SSBs were detected in the liver and kidney in the presence of DNA repair inhibitors during MX treatment, but no such increase was observed in the spleen and colon. Copyright 1999 Elsevier Science B.V.
机译：在对含天然有机物质的水进行氯化过程中形成的3-氯-4-（二氯甲基）-5-羟基-2 [5H]-呋喃酮（MX）是一种非常有效的细菌诱变剂。最近，有老鼠在饮用含MX的饮用水后发现了多个部位的肿瘤。我们已经使用碱性滤膜洗脱法检测了MX在体外和体内暴露的哺乳动物细胞中的遗传毒性，以检测DNA单链断裂和/或碱不稳定位点（SSB）。诱导HL-60细胞中可检测到的SSB含量需要高达100和300 microM MX的浓度。如果在存在DNA修复抑制剂（AraC加羟基脲）的情况下进行MX处理，则检测MX诱导的SSB的检测灵敏度将增加100倍。暴露过程中血清蛋白的存在导致轻微降低在最低的MX浓度下HL-60细胞中MX诱导的DNA损伤的比例。在睾丸细胞的原代培养以及静息的人外周血单核细胞（PBMC）中，当MX浓度高于30 microM时，观察到的SSB含量略有增加，修复抑制剂并未进一步增强这种作用。在LLC-PK1肾近端肾小管上皮细胞和生长刺激的人外周血PBMC中，使用修复抑制剂在低至3-10 microM或更高的MX浓度下检测到SSB升高，而在没有修复抑制剂的情况下以更高的10倍浓度检测到。在高剂量MX（40和80 mg kg-1）的雄性B6C3F1小鼠的肝，肾，脾和结肠中未发现剂量依赖性DNA损伤。在MX治疗期间，在存在DNA修复抑制剂的情况下，在肝脏和肾脏中检测到适度增加且剂量依赖性的SSB，但在脾脏和结肠中未观察到这种增加。版权所有1999 Elsevier Science B.V.

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