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降低结肠中的硫化合物会损害结肠细胞营养:对溃疡性结肠炎的影响。

Reducing sulfur compounds of the colon impair colonocyte nutrition: implications for ulcerative colitis.

作者信息

Roediger W E, Duncan A, Kapaniris O, Millard S

机构信息

Cell Physiology Laboratory, University of Adelaide, South Australia.

出版信息

Gastroenterology. 1993 Mar;104(3):802-9. doi: 10.1016/0016-5085(93)91016-b.

DOI:10.1016/0016-5085(93)91016-b
PMID:8440437
Abstract

BACKGROUND

Mercaptides (sodium hydrogen sulfide and sodium methanethiol) and mercapto-fatty acid (sodium mercaptoacetate) are reducing agents that help to maintain anaerobic conditions in the colonic lumen. The metabolic effect of these agents on n-butyrate and glucose oxidation in human colonocytes is unknown.

METHODS

Isolated human colonocytes were prepared from 31 colectomy specimens, and generation of oxidative metabolites from [1-14C]n-butyrate and [6-14C]glucose was measured in the presence and absence of reducing agents. Injury to cells was judged by diminished production of metabolites.

RESULTS

The injurious action of mercaptides at all sites of the colon was of the order of sodium hydrogen sulfide > methanethiol > mercaptoacetate. Significant inhibition of n-butyrate (< 0.005) but not glucose oxidation was observed with sodium hydrogen sulfide in the ascending colon, splenic flexure, and rectosigmoid region. Hydrogen sulfide more significantly inhibited fatty acid oxidation in the rectosigmoid than in the ascending colon (P < 0.02).

CONCLUSIONS

Metabolic effects of sodium hydrogen sulfide on butyrate oxidation along the length of the colon closely mirror metabolic abnormalities observed in active ulcerative colitis, and the increased production of sulfide in ulcerative colitis suggests that the action of mercaptides may be involved in the genesis of ulcerative colitis.

摘要

背景

硫醇(硫化氢钠和甲硫醇钠)以及巯基脂肪酸(巯基乙酸钠)是有助于维持结肠腔内厌氧环境的还原剂。这些物质对人结肠细胞中丁酸和葡萄糖氧化的代谢作用尚不清楚。

方法

从31份结肠切除术标本中制备分离的人结肠细胞,并在有和没有还原剂存在的情况下测量[1-14C]丁酸和[6-14C]葡萄糖氧化代谢产物的生成。通过代谢产物生成减少来判断细胞损伤情况。

结果

硫醇在结肠所有部位的损伤作用顺序为硫化氢钠>甲硫醇>巯基乙酸钠。在升结肠、脾曲和直肠乙状结肠区域,硫化氢可显著抑制丁酸氧化(<0.005),但对葡萄糖氧化无显著抑制作用。硫化氢对直肠乙状结肠中脂肪酸氧化的抑制作用比对升结肠更显著(P<0.02)。

结论

硫化氢对结肠全长丁酸氧化的代谢作用与活动期溃疡性结肠炎中观察到的代谢异常密切相关,溃疡性结肠炎中硫化物生成增加表明硫醇的作用可能参与了溃疡性结肠炎的发病机制。

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Reducing sulfur compounds of the colon impair colonocyte nutrition: implications for ulcerative colitis.降低结肠中的硫化合物会损害结肠细胞营养:对溃疡性结肠炎的影响。
Gastroenterology. 1993 Mar;104(3):802-9. doi: 10.1016/0016-5085(93)91016-b.
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