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正常大鼠和亚硫酸盐氧化酶缺乏大鼠呼吸道中吸入二氧化硫及内源性生成亚硫酸盐的分布、代谢与毒性

Distribution, metabolism and toxicity of inhaled sulfur dioxide and endogenously generated sulfite in the respiratory tract of normal and sulfite oxidase-deficient rats.

作者信息

Gunnison A F, Sellakumar A, Currie D, Snyder E A

出版信息

J Toxicol Environ Health. 1987;21(1-2):141-62. doi: 10.1080/15287398709531008.

Abstract

We report on the distribution, metabolism, and toxicity of sulfite in the respiratory tract and other tissues of rats exposed to endogenously generated sulfite or to inhaled sulfur dioxide (SO2). Graded sulfite oxidase deficiency was induced in several groups of rats by manipulating their tungsten to molybdenum intake ratio. Endogenously generated sulfite and S-sulfonate compounds (a class of sulfite metabolite) accumulated in the respiratory tract tissues and in the plasma of these rats in inverse proportion to hepatic sulfite oxidase activity. In contrast to this systemic mode of exposure, sulfite exposure of normal, sulfite oxidase-competent rats via inhaled SO2 (10 and 30 ppm) was restricted to the airways. Minor pathological changes consisting of epithelial hyperplasia, mucoid degeneration, and desquamation of epithelium were observed only in the tracheas and bronchi of the rats inhaling SO2, even though the concentration of sulfite plus S-sulfonates in the tracheas and bronchi of these rats was considerably lower than that in the endogenously exposed rats. We attribute this histological damage to hydrogen ions stemming from inhaled SO2, not to the sulfite/bisulfite ions that are also a product of inhaled SO2. In addition to the lungs and trachea, all other tissues examined, except the testes, appeared to be refractory to high concentrations of endogenously generated sulfite. The testes of grossly sulfite oxidase-deficient rats were severely atrophied and devoid of spermatogenic cells.

摘要

我们报告了亚硫酸盐在暴露于内源性生成的亚硫酸盐或吸入二氧化硫(SO₂)的大鼠呼吸道及其他组织中的分布、代谢和毒性。通过控制大鼠钨与钼的摄入比例,在几组大鼠中诱导出不同程度的亚硫酸盐氧化酶缺乏。内源性生成的亚硫酸盐和S - 磺酸盐化合物(一类亚硫酸盐代谢物)在这些大鼠的呼吸道组织和血浆中积累,且与肝脏亚硫酸盐氧化酶活性成反比。与这种全身性暴露方式不同,正常的、具有亚硫酸盐氧化酶活性的大鼠通过吸入SO₂(10 ppm和30 ppm)接触亚硫酸盐时,暴露局限于气道。尽管吸入SO₂的大鼠气管和支气管中亚硫酸盐加S - 磺酸盐的浓度明显低于内源性暴露大鼠,但仅在吸入SO₂的大鼠气管和支气管中观察到了由上皮增生、黏液样变性和上皮脱落组成的轻微病理变化。我们将这种组织学损伤归因于吸入SO₂产生的氢离子,而非同样由吸入SO₂产生的亚硫酸盐/亚硫酸氢根离子。除肺和气管外,所有其他检查的组织(除睾丸外)似乎对高浓度的内源性生成的亚硫酸盐具有耐受性。严重缺乏亚硫酸盐氧化酶的大鼠的睾丸严重萎缩,且没有生精细胞。

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