首页> 美国卫生研究院文献>Infection and Immunity >Effects of gastrointestinal candidiasis antibiotics dietary arabinitol and cortisone acetate on levels of the Candida metabolite D-arabinitol in rat serum and urine.
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Effects of gastrointestinal candidiasis antibiotics dietary arabinitol and cortisone acetate on levels of the Candida metabolite D-arabinitol in rat serum and urine.

机译:胃肠道念珠菌病抗生素饮食阿拉伯糖醇和醋酸可的松对大鼠血清和尿液中念珠菌代谢产物D-阿拉伯糖醇水平的影响。

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摘要

We studied the effects of gastrointestinal (GI) colonization by Candida albicans, dietary arabinitol, intragastric antibiotics, and cortisone on levels of the Candida metabolite D-arabinitol in rat serum and urine. Rats given conventional laboratory chow, intragastric gentamicin and chloramphenicol, and 6.0 x 10(8) live C. albicans B311 blastoconidia by gavage had minimal invasive GI disease and no more DL-arabinitol in the urine than controls given killed C. albicans. However, colonized and uncolonized rats given intragastric antibiotics had transiently higher urine arabinitol levels than the corresponding controls given saline. Rats given conventional laboratory chow (which contained 50 micrograms of arabinitol per g) had higher serum and urine arabinitol levels than rats given no dietary arabinitol, but the differences were less than expected. Moreover, intragastric antibiotics did not cause increased arabinitol excretion in rats given no dietary arabinitol. Rats given intragastric antibiotics and live C. albicans but no dietary arabinitol had no more arabinitol in their serum or urine than controls given antibiotics and killed C. albicans or saline and live or killed C. albicans. Lastly, cortisone acetate (10 mg/kg of body weight per day intramuscularly for 10 days) did not cause increased serum or urine arabinitol levels. We conclude that neither GI colonization by C. albicans nor cortisone should interfere with the usefulness of arabinitol as a marker for invasive candidiasis; antibiotics appear to increase arabinitol excretion by suppressing GI bacteria capable of consuming dietary arabinitol.
机译:我们研究了白色念珠菌,饮食阿拉伯糖醇,胃内抗生素和可的松对胃肠道(GI)的定殖对大鼠血清和尿液中念珠菌代谢产物D-阿拉伯糖醇水平的影响。给予常规实验室食物,胃内庆大霉素和氯霉素,以及通过管饲法给予6.0 x 10(8)的活白色念珠菌B311狂犬病的大鼠,其侵袭性GI病微乎其微,与对照组相比,尿中的DL-阿拉伯糖醇含量更高。然而,接受胃内抗生素治疗的定殖和未定殖的大鼠的尿中阿拉伯糖醇水平暂时高于给予生理盐水的相应对照组。接受常规实验室食物(每克含50微克阿拉伯糖醇)的大鼠的血清和尿液中的阿拉伯糖醇水平高于未饮食的阿拉伯糖醇的大鼠,但差异小于预期。而且,在不给予饮食阿拉伯糖醇的大鼠中,胃内抗生素不会引起阿拉伯糖醇排泄的增加。给予胃内抗生素和活白念珠菌但饮食中的阿拉伯糖醇的大鼠,其血清或尿液中的阿糖醇含量不高于接受抗生素并杀死白念珠菌或生理盐水以及活或杀白念珠菌的对照组。最后,醋酸可的松(肌肉每天10毫克/千克,连续10天)不会引起血清或尿液阿拉伯糖醇水平的升高。我们得出的结论是,白色念珠菌和可的松的胃肠道定植均不应干扰阿拉伯糖醇作为侵袭性念珠菌病标记的作用。抗生素似乎通过抑制能够食用膳食阿拉伯糖醇的胃肠道细菌来增加阿拉伯糖醇的排泄。

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