无法合成抗坏血酸的坏血病突变大鼠中硝酸盐生物合成的减少。

Decrease of nitrate biosynthesis in scorbutic mutant rats unable to synthesize ascorbic acid.

作者信息

Kosaka 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

Life Sci. 1990;46(17):1249-54. doi: 10.1016/0024-3205(90)90500-q.

DOI:10.1016/0024-3205(90)90500-q

PMID:2338889

Abstract

The effect of ascorbic acid deficiency on the urinary excretion of nitrate was investigated using a mutant strain of rats (osteogenic disorder syndrome rats; ODS rats) unable to synthesize ascorbic acid. The amount of urinary nitrate excreted by ODS rats with or without ascorbic acid supplementation were measured before and after the intraperitoneal injection of Escherichia coli lipopolysaccharide (LPS). Urinary nitrate excretion increased markedly after LPS injection. Urinary nitrate excretion by ODS rats not supplied with ascorbic acid was significantly less than that of those supplied with ascorbic acid both before and after LPS injection. These results show that ascorbic acid enhances both LPS-stimulated and constitutive nitrate production in vivo.

摘要

利用无法合成抗坏血酸的大鼠突变株（成骨障碍综合征大鼠；ODS大鼠）研究了抗坏血酸缺乏对尿硝酸盐排泄的影响。在腹腔注射大肠杆菌脂多糖（LPS）前后，测量了补充或未补充抗坏血酸的ODS大鼠尿硝酸盐排泄量。注射LPS后尿硝酸盐排泄量显著增加。在注射LPS前后，未补充抗坏血酸的ODS大鼠尿硝酸盐排泄量均显著低于补充抗坏血酸的大鼠。这些结果表明，抗坏血酸在体内可增强LPS刺激的和组成性的硝酸盐生成。