Hepatic polyamine metabolism in children with Reye's syndrome.

Enzyme Pub Date : 1991-01-01 DOI:10.1159/000468891
A Mukhopadhyay, D R Deshmukh, A P Sarnaik
{"title":"Hepatic polyamine metabolism in children with Reye's syndrome.","authors":"A Mukhopadhyay,&nbsp;D R Deshmukh,&nbsp;A P Sarnaik","doi":"10.1159/000468891","DOIUrl":null,"url":null,"abstract":"<p><p>Acute mitochondrial insult has been suggested as a primary reason for the clinical, histopathological and biochemical abnormalities seen in Reye's syndrome. However, the etiology of mitochondrial dysfunction has not been identified. Polyamines have been known to alter the mitochondrial structure and function. Influenza infection may cause an increase in ornithine decarboxylase activity and thereby channel ornithine for polyamine biosynthesis, leading to mitochondrial dysfunction in Reye's syndrome. To test this hypothesis, the hepatic concentrations of polyamines, polyamine-metabolizing enzymes and urea cycle enzyme activities in Reye's syndrome patients were determined and compared with patients who died from illnesses other than Reye's syndrome. The hepatic concentration of putrescine, spermidine and spermine were increased in Reye's syndrome patients. The activity of ornithine decarboxylase was elevated but, due to the small number of samples, these values did not reach statistical significance. Ornithine carbamoyltransferase activity was decreased in the liver of Reye's syndrome patients. Our results suggest that increased synthesis of polyamines from ornithine may initiate mitochondrial injury in Reye's syndrome.</p>","PeriodicalId":11933,"journal":{"name":"Enzyme","volume":null,"pages":null},"PeriodicalIF":0.0000,"publicationDate":"1991-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1159/000468891","citationCount":"2","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Enzyme","FirstCategoryId":"1085","ListUrlMain":"https://doi.org/10.1159/000468891","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"","JCRName":"","Score":null,"Total":0}
引用次数: 2

Abstract

Acute mitochondrial insult has been suggested as a primary reason for the clinical, histopathological and biochemical abnormalities seen in Reye's syndrome. However, the etiology of mitochondrial dysfunction has not been identified. Polyamines have been known to alter the mitochondrial structure and function. Influenza infection may cause an increase in ornithine decarboxylase activity and thereby channel ornithine for polyamine biosynthesis, leading to mitochondrial dysfunction in Reye's syndrome. To test this hypothesis, the hepatic concentrations of polyamines, polyamine-metabolizing enzymes and urea cycle enzyme activities in Reye's syndrome patients were determined and compared with patients who died from illnesses other than Reye's syndrome. The hepatic concentration of putrescine, spermidine and spermine were increased in Reye's syndrome patients. The activity of ornithine decarboxylase was elevated but, due to the small number of samples, these values did not reach statistical significance. Ornithine carbamoyltransferase activity was decreased in the liver of Reye's syndrome patients. Our results suggest that increased synthesis of polyamines from ornithine may initiate mitochondrial injury in Reye's syndrome.

雷氏综合征患儿肝脏多胺代谢的研究。
急性线粒体损伤被认为是Reye综合征临床、组织病理学和生化异常的主要原因。然而,线粒体功能障碍的病因尚未确定。已知多胺可以改变线粒体的结构和功能。流感感染可引起鸟氨酸脱羧酶活性增加,从而引导鸟氨酸用于多胺生物合成,导致Reye综合征的线粒体功能障碍。为了验证这一假设,我们测定了雷氏综合征患者的肝脏多胺浓度、多胺代谢酶和尿素循环酶活性,并将其与死于非雷氏综合征的患者进行了比较。Reye综合征患者肝脏腐胺、亚精胺、精胺浓度升高。鸟氨酸脱羧酶活性升高,但由于样本数量少,这些值没有达到统计学意义。雷氏综合征患者肝脏鸟氨酸氨基甲酰转移酶活性降低。我们的研究结果表明,鸟氨酸合成多胺的增加可能引发Reye综合征的线粒体损伤。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
求助全文
约1分钟内获得全文 求助全文
来源期刊
自引率
0.00%
发文量
0
×
引用
GB/T 7714-2015
复制
MLA
复制
APA
复制
导出至
BibTeX EndNote RefMan NoteFirst NoteExpress
×
提示
您的信息不完整,为了账户安全,请先补充。
现在去补充
×
提示
您因"违规操作"
具体请查看互助需知
我知道了
×
提示
确定
请完成安全验证×
copy
已复制链接
快去分享给好友吧!
我知道了
右上角分享
点击右上角分享
0
联系我们:info@booksci.cn Book学术提供免费学术资源搜索服务,方便国内外学者检索中英文文献。致力于提供最便捷和优质的服务体验。 Copyright © 2023 布克学术 All rights reserved.
京ICP备2023020795号-1
ghs 京公网安备 11010802042870号
Book学术文献互助
Book学术文献互助群
群 号:481959085
Book学术官方微信