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维生素B缺乏期间亚精胺参与寿命缩短过程。

Involvement of Spermidine in the Reduced Lifespan of During Vitamin B Deficiency.

作者信息

Bito Tomohiro, Okamoto Naho, Otsuka Kenji, Yabuta Yukinori, Arima Jiro, Kawano Tsuyoshi, Watanabe Fumio

机构信息

Department of Agricultural, Life and Environmental Sciences, Faculty of Agriculture, Tottori University, Tottori 680-8553, Japan.

The United Graduate School of Agricultural Sciences, Tottori University, Tottori 680-8553, Japan.

出版信息

Metabolites. 2019 Sep 19;9(9):192. doi: 10.3390/metabo9090192.

DOI:10.3390/metabo9090192
PMID:31546940
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC6780408/
Abstract

Vitamin B deficiency leads to various symptoms such as neuropathy, growth retardation, and infertility. Vitamin B functions as a coenzyme for two enzymes involved in amino acid metabolisms. However, there is limited information available on whether amino acid disorders caused by vitamin B deficiency induce such symptoms. First, free amino acid levels were determined in vitamin B-deficient to clarify the mechanisms underlying the symptoms caused by vitamin B deficiency. Various amino acids (valine, leucine, isoleucine, methionine, and cystathionine, among others) metabolized by vitamin B-dependent enzymes were found to be significantly changed during conditions of B deficiency, which indirectly affected certain amino acids metabolized by vitamin B-independent enzymes. For example, ornithine was significantly increased during vitamin B deficiency, which also significantly increased arginase activity. The accumulation of ornithine during vitamin B deficiency constitutes the first report. In addition, the biosynthesis of spermidine from ornithine was significantly decreased during vitamin B deficiency, likely due to the reduction of -adenosylmethionine as a substrate for -adenosylmethionine decarboxylase, which catalyzes the formation of spermidine. Moreover, vitamin B deficiency also demonstrated a significant reduction in worm lifespan, which was partially recovered by the addition of spermidine. Collectively, our findings suggest that decreased spermidine is one factor responsible for reduced lifespan in vitamin B-deficient worms.

摘要

维生素B缺乏会导致多种症状,如神经病变、生长发育迟缓及不育。维生素B作为参与氨基酸代谢的两种酶的辅酶发挥作用。然而,关于维生素B缺乏引起的氨基酸紊乱是否会引发此类症状,目前可用信息有限。首先,测定了维生素B缺乏情况下的游离氨基酸水平,以阐明维生素B缺乏所致症状的潜在机制。发现在维生素B缺乏期间,多种由维生素B依赖酶代谢的氨基酸(如缬氨酸、亮氨酸、异亮氨酸、蛋氨酸和胱硫醚等)发生了显著变化,这间接影响了某些由维生素B非依赖酶代谢的氨基酸。例如,在维生素B缺乏期间鸟氨酸显著增加,这也显著提高了精氨酸酶活性。维生素B缺乏期间鸟氨酸的积累尚属首次报道。此外,在维生素B缺乏期间,由鸟氨酸合成亚精胺的过程显著减少,这可能是由于作为腺苷甲硫氨酸脱羧酶底物的S-腺苷甲硫氨酸减少,该酶催化亚精胺的形成。此外,维生素B缺乏还导致蠕虫寿命显著缩短,添加亚精胺后可部分恢复。总体而言,我们的研究结果表明,亚精胺减少是维生素B缺乏蠕虫寿命缩短的一个原因。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/64b6/6780408/d3701b3824ae/metabolites-09-00192-g008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/64b6/6780408/1fa03fe0eb48/metabolites-09-00192-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/64b6/6780408/9b83b60650c6/metabolites-09-00192-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/64b6/6780408/b99d1584ead8/metabolites-09-00192-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/64b6/6780408/fdfdef5c089b/metabolites-09-00192-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/64b6/6780408/26b650c31673/metabolites-09-00192-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/64b6/6780408/272521027c62/metabolites-09-00192-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/64b6/6780408/8710332cf08e/metabolites-09-00192-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/64b6/6780408/d3701b3824ae/metabolites-09-00192-g008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/64b6/6780408/1fa03fe0eb48/metabolites-09-00192-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/64b6/6780408/9b83b60650c6/metabolites-09-00192-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/64b6/6780408/b99d1584ead8/metabolites-09-00192-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/64b6/6780408/fdfdef5c089b/metabolites-09-00192-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/64b6/6780408/26b650c31673/metabolites-09-00192-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/64b6/6780408/272521027c62/metabolites-09-00192-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/64b6/6780408/8710332cf08e/metabolites-09-00192-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/64b6/6780408/d3701b3824ae/metabolites-09-00192-g008.jpg

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