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在缺乏抗坏血酸的大鼠中,脂多糖刺激引起明显的亚硝化作用。

Marked nitrosation by stimulation with lipopolysaccharide in ascorbic acid-deficient rats.

作者信息

Kosaka H, Tsuda M, Kurashima Y, Esumi H, Terada N, Ito Y, Uozumi M

机构信息

Division of Environmental Health Research, Osaka Prefectural Institute of Public Health, Japan.

出版信息

Carcinogenesis. 1990 Oct;11(10):1887-9. doi: 10.1093/carcin/11.10.1887.

DOI:10.1093/carcin/11.10.1887
PMID:2208602
Abstract

Marked formation of N-nitrosothioproline (N-nitrosothiazolidine-4-carboxylic acid) by stimulation with Escherichia coli lipopolysaccharide (LPS) was demonstrated in ascorbic acid-deficient mutant rats (osteogenic disorder syndrome rats; ODS rats) unable to synthesize ascorbic acid. The amounts of urinary nitrate and N-nitrosothioproline excretion after thioproline administration was measured in ODS rats with and without ascorbic acid supplement before and after the injection of LPS. LPS caused marked increase of urinary nitrate excretion in both groups. Urinary N-nitrosothioproline excretion increased 6-fold after LPS injection in ODS rats not supplied with ascorbic acid, but supplement with ascorbic acid markedly decreased the excretion of N-nitrosothioproline.

摘要

在无法合成抗坏血酸的抗坏血酸缺乏突变大鼠(成骨障碍综合征大鼠;ODS大鼠)中,证明了用大肠杆菌脂多糖(LPS)刺激会显著形成N-亚硝基硫代脯氨酸(N-亚硝基噻唑烷-4-羧酸)。在注射LPS之前和之后,对补充和未补充抗坏血酸的ODS大鼠给予硫代脯氨酸后,测量其尿硝酸盐和N-亚硝基硫代脯氨酸的排泄量。LPS使两组大鼠的尿硝酸盐排泄量显著增加。在未补充抗坏血酸的ODS大鼠中,注射LPS后尿N-亚硝基硫代脯氨酸排泄量增加了6倍,但补充抗坏血酸显著降低了N-亚硝基硫代脯氨酸的排泄量。

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