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台湾二硫化碳暴露作业工人血液氧化应激。

Blood oxidative stress in Taiwan workers exposed to carbon disulfide.

机构信息

Chang Gung Medical College, Tao Yuan, Taiwan, Republic of China.

出版信息

Am J Ind Med. 2011 Aug;54(8):637-45. doi: 10.1002/ajim.20971. Epub 2011 May 31.

DOI:10.1002/ajim.20971
PMID:21630299
Abstract

BACKGROUND

Overexposure to carbon disulfide (CS(2) ) has been associated with an increase in coronary heart disease, but the mechanisms mediating this effect remain unclear. We aimed to examine the relationship between CS(2) exposure and oxidative stress markers, in order to clarify the oxidative mechanisms involved in CS(2) -induced atherosclerosis.

METHODS

A total of 89 workers from a viscose rayon plant were recruited for this study, and 111 workers not exposed to CS(2) served as controls. Cholesterol, triglyceride, malondialdehyde (MDA), superoxide dismutase (SOD), catalase, GSH peroxidase, as well as total antioxidants were analyzed.

RESULTS

The workers exposed to CS(2) had significantly higher MDA levels and lower SOD levels than the controls. The average MDA levels were 776 ± 268.2 (240-1,220) in the high exposure (≥10 ppm; n = 38), 751.6 ± 274 (170-1,320) in the low exposure (<10 ppm; n = 51), and 550.4 ± 199 (115-1,050) mM in the control group (n = 111). The average SOD levels were 36.5 ± 38.8 (0-223.5), 39.3 ± 38.8 (0-160), and 58.8 ± 60.8 (5.25, 400) U/ml in the high exposure-, low exposure-, and control group, respectively. MDA level increased significantly at a cumulative CS(2) exposure of over 60 ppm-years. Dyslipoproteinemia was borderline significantly associated with CS(2) exposure and MDA level.

CONCLUSIONS

These results indicate that CS(2) exposure can induce oxidative stress as well as reduce the levels of antioxidative enzymes, and that a cumulative exposure level of 60 ppm-years may be a threshold value for the oxidative and the antioxidant response. Am. J. Ind. Med. 54:637-645, 2011. © 2011 Wiley-Liss, Inc.

摘要

背景

接触二硫化碳(CS(2) )与冠心病风险增加有关,但介导这种效应的机制尚不清楚。我们旨在研究 CS(2) 暴露与氧化应激标志物之间的关系,以阐明 CS(2) 诱导动脉粥样硬化的氧化机制。

方法

共招募了一家粘胶纤维厂的 89 名工人作为研究对象,另外招募了 111 名未接触 CS(2) 的工人作为对照。分析了胆固醇、甘油三酯、丙二醛(MDA)、超氧化物歧化酶(SOD)、过氧化氢酶、谷胱甘肽过氧化物酶以及总抗氧化能力。

结果

与对照组相比,接触 CS(2) 的工人 MDA 水平明显升高,SOD 水平明显降低。高暴露组(≥10ppm;n=38)的平均 MDA 水平为 776±268.2(170-1220),低暴露组(<10ppm;n=51)为 751.6±274(170-1320),对照组(n=111)为 550.4±199(115-1050)mM。高暴露组、低暴露组和对照组的平均 SOD 水平分别为 36.5±38.8(0-223.5)、39.3±38.8(0-160)和 58.8±60.8(5.25,400)U/ml。CS(2) 累积暴露量超过 60ppm-年时,MDA 水平显著升高。血脂异常与 CS(2) 暴露和 MDA 水平呈临界显著相关。

结论

这些结果表明,CS(2) 暴露可诱导氧化应激,降低抗氧化酶水平,累积暴露水平达到 60ppm-年可能是氧化和抗氧化反应的阈值。美国工业医学杂志 54:637-645,2011。©2011 Wiley-Liss,Inc.

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引用本文的文献

1
No evidence of cardiovascular toxicity in workers exposed below 5 ppm carbon disulfide.在二硫化碳暴露水平低于5 ppm的工人中,没有心血管毒性的证据。
Int Arch Occup Environ Health. 2016 Jul;89(5):835-45. doi: 10.1007/s00420-016-1122-x. Epub 2016 Mar 4.