FORMATION OF UREA IN LIVER HOMOGENATES FROM CITRULLINE AND VARIOUS N-ALKYL DERIVATIVES OF ASPARTIC ACID.

R. Charbonneau, L. Berlinguet
{"title":"FORMATION OF UREA IN LIVER HOMOGENATES FROM CITRULLINE AND VARIOUS N-ALKYL DERIVATIVES OF ASPARTIC ACID.","authors":"R. Charbonneau, L. Berlinguet","doi":"10.1139/Y63-259","DOIUrl":null,"url":null,"abstract":"The effects of various N-alkylated derivatives of aspartic acid on the synthesis of urea by rat liver homogenates have been studied. At 5 × 10−3 M concentration, N-methyl, N-ethyl, N-isopropyl, and N-cyclohexyl aspartic acids are not utilized and have no effect on the formation of urea. At this concentration, N-allyl-DL-aspartic acid inhibits the formation of endogenous urea by 77%. At concentrations of 2.5 to 7.5 × 10−2 M, N-methyl, N-ethyl, and N-isopropyl aspartic acids slightly increase the formation of endogenous urea; this is about 15% of the value obtained when aspartic acid alone is added at the same concentration. In the case of simple N-alkylated aspartic acids, liver homogenates are able to cleave the alkylated chain with the result that a small amount of urea synthesis is possible. N-allylaspartic acid totally inhibits the formation of urea from aspartic acid at a relatively low concentration of 6.2 × 10−3 M. N-cyclohexylaspartic acid has also an inhibitory effect which is ten times less prono...","PeriodicalId":9531,"journal":{"name":"Canadian journal of biochemistry and physiology","volume":"67 1","pages":"2297-305"},"PeriodicalIF":0.0000,"publicationDate":"1963-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"2","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Canadian journal of biochemistry and physiology","FirstCategoryId":"1085","ListUrlMain":"https://doi.org/10.1139/Y63-259","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

The effects of various N-alkylated derivatives of aspartic acid on the synthesis of urea by rat liver homogenates have been studied. At 5 × 10−3 M concentration, N-methyl, N-ethyl, N-isopropyl, and N-cyclohexyl aspartic acids are not utilized and have no effect on the formation of urea. At this concentration, N-allyl-DL-aspartic acid inhibits the formation of endogenous urea by 77%. At concentrations of 2.5 to 7.5 × 10−2 M, N-methyl, N-ethyl, and N-isopropyl aspartic acids slightly increase the formation of endogenous urea; this is about 15% of the value obtained when aspartic acid alone is added at the same concentration. In the case of simple N-alkylated aspartic acids, liver homogenates are able to cleave the alkylated chain with the result that a small amount of urea synthesis is possible. N-allylaspartic acid totally inhibits the formation of urea from aspartic acid at a relatively low concentration of 6.2 × 10−3 M. N-cyclohexylaspartic acid has also an inhibitory effect which is ten times less prono...
查看原文
分享 分享
微信好友 朋友圈 QQ好友 复制链接
本刊更多论文
肝脏中的尿素是由瓜氨酸和各种天冬氨酸的正烷基衍生物形成的。
研究了天门冬氨酸n -烷基化衍生物对大鼠肝脏匀浆合成尿素的影响。在5 × 10−3 M浓度下,n -甲基、n -乙基、n -异丙基和n -环己基天冬氨酸不被利用,对尿素的形成没有影响。在此浓度下,n -烯丙基- dl -天冬氨酸抑制内源性尿素的形成达77%。在2.5 ~ 7.5 × 10−2 M浓度下,n -甲基、n -乙基和n -异丙基天冬氨酸略微增加内源性尿素的生成;这大约是以相同浓度单独添加天冬氨酸时所获得的值的15%。在简单n -烷基化天冬氨酸的情况下,肝脏匀浆能够切割烷基化链,结果是少量的尿素合成是可能的。在相对较低的6.2 × 10−3 M浓度下,n -烯丙天冬氨酸完全抑制天冬氨酸生成尿素。n -环己基天冬氨酸也有抑制作用,其抑制作用是前…
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 去求助
来源期刊
自引率
0.00%
发文量
0
期刊最新文献
A method for the detection of atypical forms of human serum cholinesterase; determination of dibucaine numbers. THE RELEASE OF ACETYLCHOLINE FROM A SYMPATHETIC GANGLION BY CARBACHOL. RELATIONSHIP TO THE FUNCTIONAL SIGNIFICANCE OF THE LOCALIZATION OF ACETYLCHOLINESTERASE. ACETYLCHOLINE IN INVERTEBRATE NERVOUS SYSTEMS. THE ACTION OF CATECHOLAMINES IN SYMPATHETIC GANGLIA. CHOLINERGIC TRANSMISSION AND ACETYLCHOLINE OUTPUT.
×
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
现在去查看 取消
×
提示
确定
0
微信
客服QQ
Book学术公众号 扫码关注我们
反馈
×
意见反馈
请填写您的意见或建议
请填写您的手机或邮箱
已复制链接
已复制链接
快去分享给好友吧!
我知道了
×
扫码分享
扫码分享
Book学术官方微信
Book学术文献互助
Book学术文献互助群
群 号:481959085
Book学术
文献互助 智能选刊 最新文献 互助须知 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 Book学术 All rights reserved.
ghs 京公网安备 11010802042870号 京ICP备2023020795号-1