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Renal vascular and cardiac fibrosis in rats exposed to passive smoking and industrial dust fibre amosite

机译:暴露于被动吸烟和工业粉尘金属烟尘中的大鼠的肾血管和心脏纤维化

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摘要

Passive smoking is an independent risk factor for cardiovascular diseases. Industrial fibrous dust, e.g. the asbestos group member, amosite, causes lung cancer and fibrosis. No data are available on renal involvement after inhalational exposure to these environmental pollutants or of their combination, or on cardiovascular and renal toxicity after exposure to amosite. Male Wistar rats were randomized into four groups (n= 6): control and amosite group received initially two intratracheal instillations of saline and amosite solution, respectively. Smoking group was subjected to standardized daily exposure to tobacco smoke for 2 hrs in a concentration resembling human passive smoking. Combined group was exposed to both amosite and cigarette smoke. All rats were killed after 6 months. Rats exposed to either amosite or passive smoking developed significant glomerulosclerosis and tubulointerstitial fibrosis. Combination of both exposures had additive effects. Histomorphological changes preceded the clinical manifestation of kidney damage. In both groups with single exposures, marked perivascular and interstitial cardiac fibrosis was detected. The additive effect in the heart was less pronounced than in the kidney, apparent particularly in changes of vascular structure. Advanced oxidation protein products, the plasma marker of the myeloperoxidase reaction in activated monocytes/macrophages, were increased in all exposed groups, whereas the inflammatory cytokines did not differ between the groups. In rats, passive smoking or amosite instillation leads to renal, vascular and cardiac fibrosis potentially mediated via increased myeloperoxidase reaction. Combination of both pollutants shows additive effects. Our data should be confirmed in subjects exposed to these environmental pollutants, in particular if combined.
机译:被动吸烟是心血管疾病的独立危险因素。工业纤维粉尘石棉小组成员铁石棉导致肺癌和纤维化。尚无关于吸入这些环境污染物或它们的组合后肾脏受累的数据,或暴露于铁石棉后的心血管和肾脏毒性的数据。将雄性Wistar大鼠随机分为四组(n = 6):对照组和铁石棉组分别分别接受两次气管内滴注盐水和铁石棉溶液。吸烟组以与人类被动吸烟相似的浓度每天标准暴露于烟草烟雾中2小时。合并组同时接触铁石棉烟和香烟烟雾。 6个月后杀死所有大鼠。暴露于非吸烟或被动吸烟的大鼠均出现明显的肾小球硬化和肾小管间质纤维化。两次接触的组合具有累加作用。组织形态学改变先于肾脏损害的临床表现。在单次接触的两组中,均检测到明显的血管周围和间质性心脏纤维化。与肾脏相比,心脏的累加作用不明显,尤其是在血管结构改变中。在所有暴露的组中,高级氧化蛋白产物,即活化的单核细胞/巨噬细胞中髓过氧化物酶反应的血浆标志物,均增加,而各组的炎性细胞因子无差异。在大鼠中,被动吸烟或铁石棉滴注可能通过增加的髓过氧化物酶反应介导肾,血管和心脏纤维化。两种污染物的组合显示出累加效应。我们的数据应在暴露于这些环境污染物的受试者中得到确认,尤其是如果将其合并使用。

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