Styrene-induced alterations in the respiratory tract of rats treated by inhalation or intraperitoneally.

T Coccini, C Fenoglio, R Nano, P De Piceis Polver, G Moscato, L Manzo
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引用次数: 32

Abstract

Although exposure to styrene occurs primarily via inhalation, the action of this agent on the respiratory tract has scarcely been investigated. This article describes morphological and biochemical changes occurring in the respiratory tract of rats after either inhalation of styrene vapors (300 ppm, 6 h/d, 5 d/wk, for 2 wk) or systemic (ip) treatment with 40 or 400 mg/kg styrene for 3 consecutive days. Electron microscopy analysis showed diffuse cell damage involving the tracheal, bronchiolar, and alveolar epithelium. In the tracheal epithelium, several cell types were affected. Ciliated cells presented vacuolation, detachment of cilia, blebbing of the apical cytoplasm, and compound cilia. Most secretory cells showed scant secretory granules and blebbings. Dense bodies and fibrillary inclusions were seen in intermediate and basal cells. Styrene also caused alterations of cytoplasmic components in type II pneumocytes and bronchiolar cells as well as thickness of the alveolar wall. These abnormalities were accompanied by depletion of glutathione (GSH) in the lung tissue. Pneumotoxic effects of systemic administration of styrene were dose dependent and tended to be more severe than those seen in the animals exposed for longer periods to styrene by inhalation. Metabolic activation of styrene and subsequent cell damage induced by the reactive metabolite styrene oxide may be involved in the sequence of events culminating in the toxic insult to the respiratory tract.

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吸入或腹腔注射苯乙烯对大鼠呼吸道的影响。
虽然对苯乙烯的暴露主要是通过吸入发生的,但这种物质对呼吸道的作用几乎没有研究。本文描述了大鼠吸入苯乙烯蒸气(300 ppm, 6小时/天,5天/周,连续2周)或连续3天系统(40或400 mg/kg苯乙烯)后呼吸道发生的形态学和生化变化。电镜分析显示弥漫性细胞损伤累及气管、细支气管和肺泡上皮。在气管上皮中,几种细胞类型受到影响。纤毛细胞表现为空泡化、纤毛脱落、顶端细胞质起泡和复合纤毛。多数分泌细胞表现为分泌颗粒少、小泡。中间细胞和基底细胞可见致密体和原纤维包涵体。苯乙烯还引起II型肺细胞和细支气管细胞的细胞质成分以及肺泡壁厚度的改变。这些异常伴有肺组织中谷胱甘肽(GSH)的耗竭。全身吸入苯乙烯的肺毒性作用是剂量依赖性的,往往比长期吸入苯乙烯的动物更严重。苯乙烯的代谢激活和随后由反应性代谢物苯乙烯氧化物引起的细胞损伤可能参与了最终导致呼吸道毒性损伤的一系列事件。
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