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不同氯乙烯暴露水平下大鼠硫代二乙醇酸的尿排泄及游离巯基的肝脏含量

Urinary excretion of thiodiglycollic acid and hepatic content of free thiols in rats at different levels of exposure to vinyl chloride.

作者信息

Tarkowski S, Wisniewska-Knypl J M, Klimczak J, Dramiński W, Wróblewska K

出版信息

J Hyg Epidemiol Microbiol Immunol. 1980;24(3):253-61.

PMID:7003010
Abstract

In order to assess the process of oxidation and conjugation involved in biotransformation of vinyl chloride (VC), rats were exposed to 50, 200, 500, 1000 and 20,000 ppm inhaled VC. The rate of urinary excretion of thiodiglycollic acid (TDGA) after exposure to each investigated concentration of VC depends on the activity of microsomal monooxygenase. In general, higher levels of TDGA in urine were reflected by a more significant depression of non-protein sulfhydryl content in the liver of rats, whereas no changes were observed in those with inhibited activity of microsomal monooxygenase and depressed urinary levels of TDGA. The significance of alcohol dehydrogenase in the metabolism of low concentrations of VC has not been confirmed. Metabolism of VC in the range of 50--2 000 ppm is mediated by microsomal monooxygenase followed by conjugation with thiols.

摘要

为了评估氯乙烯(VC)生物转化过程中的氧化和结合过程,将大鼠暴露于50、200、500、1000和20000 ppm的吸入VC中。暴露于每种研究浓度的VC后,硫代二乙醇酸(TDGA)的尿排泄率取决于微粒体单加氧酶的活性。一般来说,大鼠肝脏中非蛋白巯基含量的更显著降低反映在尿中TDGA水平较高,而微粒体单加氧酶活性受到抑制且尿中TDGA水平降低的大鼠未观察到变化。尚未证实乙醇脱氢酶在低浓度VC代谢中的重要性。50-2000 ppm范围内的VC代谢由微粒体单加氧酶介导,随后与硫醇结合。

相似文献

1
Urinary excretion of thiodiglycollic acid and hepatic content of free thiols in rats at different levels of exposure to vinyl chloride.不同氯乙烯暴露水平下大鼠硫代二乙醇酸的尿排泄及游离巯基的肝脏含量
J Hyg Epidemiol Microbiol Immunol. 1980;24(3):253-61.
2
Comparison of the impact of continuous and intermittent exposure to vinyl chloride, including phenobarbital effect.连续和间歇性接触氯乙烯的影响比较,包括苯巴比妥的作用。
J Hyg Epidemiol Microbiol Immunol. 1985;29(2):111-20.
3
Influence of exposure mode on vinyl chloride action.暴露模式对氯乙烯作用的影响。
Arch Toxicol. 1984 Sep;55(3):195-8. doi: 10.1007/BF00316128.
4
Roles of 2-haloethylene oxides and 2-haloacetaldehydes derived from vinyl bromide and vinyl chloride in irreversible binding to protein and DNA.由溴乙烯和氯乙烯衍生的2-卤代环氧乙烷和2-卤代乙醛在与蛋白质和DNA不可逆结合中的作用。
Cancer Res. 1981 Nov;41(11 Pt 1):4391-8.
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[Biochemical changes in vinyl chloride poisoning. I. Effect of different conditions of vinyl chloride exposure on lipid metabolism in rats].[氯乙烯中毒的生化变化。I. 不同氯乙烯暴露条件对大鼠脂质代谢的影响]
Med Pr. 1981;32(4):247-53.
6
Metabolic activation of vinyl chloride and vinyl bromide by isolated hepatocytes and hepatic sinusoidal cells.氯乙烯和溴乙烯在分离的肝细胞和肝窦状细胞中的代谢活化作用。
J Environ Pathol Toxicol. 1980 Aug;4(1):411-7.
7
Urinary thiodiglycolic acid levels for vinyl chloride monomer-exposed polyvinyl chloride workers.氯乙烯单体暴露的聚氯乙烯工人的尿硫代二乙醇酸水平。
J Occup Environ Med. 2001 Nov;43(11):934-8. doi: 10.1097/00043764-200111000-00002.
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Metabolism of vinyl chloride: destruction of the heme of highly purified liver Microsomal cytochrome P-450 by a metabolite.氯乙烯的代谢:一种代谢产物对高度纯化的肝微粒体细胞色素P-450血红素的破坏。
Mol Pharmacol. 1977 Nov;13(6):993-1004.
9
Thiodiglycollic acid in neonatal urine: an indication of novel metabolism, not toxic exposure to vinyl chloride.新生儿尿液中的硫代二甘醇酸:一种新代谢的指标,而非氯乙烯的毒性暴露。
Lancet. 1984 Aug 11;2(8398):359. doi: 10.1016/s0140-6736(84)92733-8.
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Biochemical alterations in livers of rats exposed to vinyl chloride.暴露于氯乙烯的大鼠肝脏中的生化改变。
J Toxicol Environ Health. 1979 Nov;5(6):1119-32. doi: 10.1080/15287397909529818.

引用本文的文献

1
Chromatographic determination of thiodiglycolic acid - a metabolite of vinyl chloride.氯乙烯代谢物硫代二甘醇酸的色谱测定
Arch Toxicol. 1981 Nov;48(4):289-92. doi: 10.1007/BF00319657.
2
Hepatic content of free sulfhydryl compounds in animals exposed to vinyl acetate.暴露于醋酸乙烯酯的动物肝脏中游离巯基化合物的含量。
Int Arch Occup Environ Health. 1982;51(2):185-9. doi: 10.1007/BF00378162.
3
Sensitive flame-photometric-detector analysis of thiodiglycolic acid in urine as a biological monitor of vinyl chloride.尿中硫代二甘醇酸的灵敏火焰光度检测器分析作为氯乙烯的生物监测指标
Int Arch Occup Environ Health. 1983;52(3):281-4. doi: 10.1007/BF00526527.
4
Influence of exposure mode on vinyl chloride action.暴露模式对氯乙烯作用的影响。
Arch Toxicol. 1984 Sep;55(3):195-8. doi: 10.1007/BF00316128.