Oxidation of hydrogen sulfide and methanethiol to thiosulfate by rat tissues: a specialized function of the colonic mucosa

被引:182
作者
Furne, J [1 ]
Springfield, J [1 ]
Koenig, T [1 ]
DeMaster, E [1 ]
Levitt, MD [1 ]
机构
[1] Minneapolis VA Med Ctr, Res Serv, Minneapolis, MN 55417 USA
关键词
hydrogen sulfide; colonic; mucosa; oxidation; thiolsulfate; methanethiol;
D O I
10.1016/S0006-2952(01)00657-8
中图分类号
R9 [药学];
学科分类号
1007 ;
摘要
Colonic bacteria release large quantities of the highly toxic thiols hydrogen sulfide (H2S) and methanethiol (CH3SH). These gases rapidly permeate the colonic mucosa, and tissue damage would be expected if the mucosa could not detoxify these compounds rapidly. We previously showed that rat cecal mucosa metabolizes these thiols via conversion to thiosulfate. The purpose of the present study in rats was to determine if this conversion of thiols to thiosulfate is (a) a generalized function of many tissues, or (b) a specialized function of the colonic mucosa. The tissues studied were mucosa from the cecum, right colon, mid-colon, ileum, and stomach; liver; muscle; erythrocytes; and plasma. The metabolic rate was determined by incubating homogenates of the various tissues with (H2S)-S-35 and (CH3SH)-S-35 and measuring the rate of incorporation of S-35 into thiosulfate and sulfate. The detoxification activity of H2S (expressed as nmol/mg per min) that resulted in thiosulfate production was at least eight times greater for cecal and right colonic mucosa than for the non-colonic tissues. Thiosulfate production from CH3SH was at least five times more rapid for cecal and right colonic mucosa than for the non-colonic tissues. We conclude that colonic mucosa possesses a specialized detoxification system that allows this tissue to rapidly metabolize H2S and CH3SH to thiosulfate. Presumably, this highly developed system protects the colon from what otherwise might be injurious concentrations of H2S and CH3SH. Defects in this detoxification pathway possibly could play a role in the pathogenesis of various forms of colitis. (C) 2001 Elsevier Science Inc. All rights reserved.
引用
收藏
页码:255 / 259
页数:5
相关论文
共 21 条
[1]   ENZYMIC METHYLATION OF FOREIGN SULFHYDRYL COMPOUNDS [J].
BREMER, J ;
GREENBERG, DM .
BIOCHIMICA ET BIOPHYSICA ACTA, 1961, 46 (02) :217-&
[2]  
ELLENHORN MJ, 1997, ELLENHORNS MED TOXIC, P1489
[3]   METABOLISM OF DIETARY SULFATE - ABSORPTION AND EXCRETION IN HUMANS [J].
FLORIN, T ;
NEALE, G ;
GIBSON, GR ;
CHRISTL, SU ;
CUMMINGS, JH .
GUT, 1991, 32 (07) :766-773
[4]  
FLORIN T H J, 1990, Gastroenterology, V98, pA170
[5]  
GIBSON GR, 1991, FEMS MICROBIOL ECOL, V86, P103, DOI 10.1111/j.1574-6968.1991.tb04799.x
[6]  
KEITH RA, 1985, DRUG METAB DISPOS, V13, P669
[7]   Fecal hydrogen sulfide production in ulcerative colitis [J].
Levine, J ;
Ellis, CJ ;
Furne, JK ;
Springfield, J ;
Levitt, MD .
AMERICAN JOURNAL OF GASTROENTEROLOGY, 1998, 93 (01) :83-87
[8]   Detoxification of hydrogen sulfide and methanethiol in the cecal mucosa [J].
Levitt, MD ;
Furne, J ;
Springfield, J ;
Suarez, F ;
DeMaster, E .
JOURNAL OF CLINICAL INVESTIGATION, 1999, 104 (08) :1107-1114
[9]  
MAZEL P, 1964, J PHARMACOL EXP THER, V143, P1
[10]   Colonic luminal hydrogen sulfide is not elevated in ulcerative colitis [J].
Moore, J ;
Babidge, W ;
Millard, S ;
Roediger, W .
DIGESTIVE DISEASES AND SCIENCES, 1998, 43 (01) :162-165