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L-2-氧代噻唑烷-4-羧酸盐,一种半胱氨酸前体,可刺激喂食缺乏硫氨基酸饮食的大鼠的生长并使组织谷胱甘肽浓度正常化。

L-2-oxothiazolidine-4-carboxylate, a cysteine precursor, stimulates growth and normalizes tissue glutathione concentrations in rats fed a sulfur amino acid-deficient diet.

作者信息

Jain A, Madsen D C, Auld P A, Frayer W W, Schwartz M K, Meister A, Mårtensson J

机构信息

Perinatology Center/Department of Pediatrics, Cornell University Medical College, New York, NY 10021, USA.

出版信息

J Nutr. 1995 Apr;125(4):851-6. doi: 10.1093/jn/125.4.851.

DOI:10.1093/jn/125.4.851
PMID:7722686
Abstract

The efficiency of L-2-oxothiazolidine-4-carboxylate, a cysteine precursor, in stimulating glutathione synthesis and growth was evaluated in growing rats. Animals were fed a sulfur amino acid-deficient diet (0.25% L-methionine and no cysteine) supplemented with L-2-oxothiazolidine-4-carboxylate (0.35%) for 3 wk and compared with age-matched animals receiving the sulfur amino acid-deficient diet alone. Rats fed the sulfur amino acid-deficient diet had lower glutathione concentrations in bronchoalveolar lining fluid, lung, lymphocytes, and liver than rats fed a sulfur amino acid-deficient diet supplemented with L-2-oxothiazolidine-4-carboxylate. Rats fed the supplemented diet had normal tissue and bronchoalveolar lining fluid glutathione levels. Central venous plasma glutathione concentrations, mostly reflecting liver excretion, were less affected by L-2-oxothiazolidine-4-carboxylate supplementation. Rats fed L-2-oxothiazolidine-4-carboxylate supplementation had normal weight gain compared with a much lower weight gain in animals fed the sulfur amino acid-deficient diet alone. Thus, L-2-oxothiazolidine-4-carboxylate increased tissue glutathione concentrations and stimulated growth in rats. The lung glutathione status of the rats was reflected by glutathione concentrations in lymphocytes and the bronchoalveolar lining fluid, but not by the central venous plasma glutathione concentrations.

摘要

在生长中的大鼠身上评估了半胱氨酸前体L-2-氧代噻唑烷-4-羧酸刺激谷胱甘肽合成及生长的效率。给动物喂食一种缺乏硫氨基酸的饮食(0.25% L-甲硫氨酸且无半胱氨酸),并补充L-2-氧代噻唑烷-4-羧酸(0.35%),持续3周,然后与仅接受缺乏硫氨基酸饮食的年龄匹配动物进行比较。与喂食补充了L-2-氧代噻唑烷-4-羧酸的缺乏硫氨基酸饮食的大鼠相比,喂食缺乏硫氨基酸饮食的大鼠,其支气管肺泡衬液、肺、淋巴细胞和肝脏中的谷胱甘肽浓度较低。喂食补充饮食的大鼠其组织和支气管肺泡衬液中的谷胱甘肽水平正常。主要反映肝脏排泄情况的中心静脉血浆谷胱甘肽浓度受L-2-氧代噻唑烷-4-羧酸补充的影响较小。与仅喂食缺乏硫氨基酸饮食的动物体重增加低得多相比,喂食补充了L-2-氧代噻唑烷-4-羧酸的大鼠体重增加正常。因此,L-2-氧代噻唑烷-4-羧酸提高了大鼠组织中的谷胱甘肽浓度并刺激了其生长。大鼠的肺谷胱甘肽状态可通过淋巴细胞和支气管肺泡衬液中的谷胱甘肽浓度反映,但不能通过中心静脉血浆谷胱甘肽浓度反映。

相似文献

1
L-2-oxothiazolidine-4-carboxylate, a cysteine precursor, stimulates growth and normalizes tissue glutathione concentrations in rats fed a sulfur amino acid-deficient diet.L-2-氧代噻唑烷-4-羧酸盐,一种半胱氨酸前体,可刺激喂食缺乏硫氨基酸饮食的大鼠的生长并使组织谷胱甘肽浓度正常化。
J Nutr. 1995 Apr;125(4):851-6. doi: 10.1093/jn/125.4.851.
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L-2-oxothiazolidine-4-carboxylate as a cysteine precursor: efficacy for growth and hepatic glutathione synthesis in chicks and rats.L-2-氧代噻唑烷-4-羧酸盐作为半胱氨酸前体:对雏鸡和大鼠生长及肝脏谷胱甘肽合成的功效
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Stimulation of hepatic glutathione formation by administration of L-2-oxothiazolidine-4-carboxylate, a 5-oxo-L-prolinase substrate.通过给予L-2-氧代噻唑烷-4-羧酸(一种5-氧代-L-脯氨酸酶底物)刺激肝脏谷胱甘肽的形成。
Proc Natl Acad Sci U S A. 1981 Feb;78(2):936-9. doi: 10.1073/pnas.78.2.936.
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Elevation of lung glutathione by oral supplementation of L-2-oxothiazolidine-4-carboxylate protects against oxygen toxicity in protein-energy malnourished rats.
FASEB J. 1992 Sep;6(12):3101-7. doi: 10.1096/fasebj.6.12.1521740.
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Regulation of hepatocyte glutathione by amino acid precursors and cAMP in protein-energy malnourished rats.
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Inhibition of glutathione efflux in the recirculating rat liver perfusion by cysteine but not by oxothiazolidine carboxylate, an intracellular cysteine precursor.半胱氨酸可抑制大鼠肝脏循环灌注中谷胱甘肽的外排,但细胞内半胱氨酸前体氧代噻唑烷羧酸盐则无此作用。
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Rats fed a low protein diet supplemented with sulfur amino acids have increased cysteine dioxygenase activity and increased taurine production in hepatocytes.喂食补充了含硫氨基酸的低蛋白饮食的大鼠,其肝细胞中的半胱氨酸双加氧酶活性增加,牛磺酸生成量增加。
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Selective elevation of glutathione levels in target tissues with L-2-oxothiazolidine-4-carboxylate (OTC) protects against hyperoxia-induced lung damage in protein-energy malnourished rats: implications for a new treatment strategy.
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