{"title":"[牛磺酸治疗线粒体疾病]。","authors":"Yoshihide Sunada","doi":"10.11477/mf.1416202748","DOIUrl":null,"url":null,"abstract":"<p><p>Mitochondrial myopathy, encephalopathy, lactic acidosis, and stroke-like episodes (MELAS) syndrome is characterized by a mitochondrial DNA mutation that leads to defective taurine modification of the leucine tRNA anticodon, with consequent impaired translation of the UUG codon. This defect reduces synthesis of respiratory chain complexes, which causes energy failure. Taurine supplementation improved mitochondrial function in MELAS model cells. A physician-initiated clinical trial reported that high-dose taurine supplementation therapy suppressed stroke-like episodes and improved taurine modification rates in leukocytes.</p>","PeriodicalId":52507,"journal":{"name":"Brain and Nerve","volume":"76 10","pages":"1127-1135"},"PeriodicalIF":0.0000,"publicationDate":"2024-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":"{\"title\":\"[Taurine for Mitochondrial Diseases].\",\"authors\":\"Yoshihide Sunada\",\"doi\":\"10.11477/mf.1416202748\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<p><p>Mitochondrial myopathy, encephalopathy, lactic acidosis, and stroke-like episodes (MELAS) syndrome is characterized by a mitochondrial DNA mutation that leads to defective taurine modification of the leucine tRNA anticodon, with consequent impaired translation of the UUG codon. This defect reduces synthesis of respiratory chain complexes, which causes energy failure. Taurine supplementation improved mitochondrial function in MELAS model cells. A physician-initiated clinical trial reported that high-dose taurine supplementation therapy suppressed stroke-like episodes and improved taurine modification rates in leukocytes.</p>\",\"PeriodicalId\":52507,\"journal\":{\"name\":\"Brain and Nerve\",\"volume\":\"76 10\",\"pages\":\"1127-1135\"},\"PeriodicalIF\":0.0000,\"publicationDate\":\"2024-10-01\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"\",\"citationCount\":\"0\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Brain and Nerve\",\"FirstCategoryId\":\"1085\",\"ListUrlMain\":\"https://doi.org/10.11477/mf.1416202748\",\"RegionNum\":0,\"RegionCategory\":null,\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"\",\"PubModel\":\"\",\"JCR\":\"Q3\",\"JCRName\":\"Medicine\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"Brain and Nerve","FirstCategoryId":"1085","ListUrlMain":"https://doi.org/10.11477/mf.1416202748","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q3","JCRName":"Medicine","Score":null,"Total":0}
引用次数: 0
摘要
线粒体肌病、脑病、乳酸酸中毒和中风样发作(MELAS)综合征的特征是线粒体 DNA 变异导致亮氨酸 tRNA 反密码子的牛磺酸修饰缺陷,从而影响 UUG 密码子的翻译。这种缺陷减少了呼吸链复合物的合成,导致能量衰竭。补充牛磺酸可改善 MELAS 模型细胞的线粒体功能。一项由医生发起的临床试验报告称,大剂量牛磺酸补充疗法可抑制中风样发作,并改善白细胞中的牛磺酸修饰率。
Mitochondrial myopathy, encephalopathy, lactic acidosis, and stroke-like episodes (MELAS) syndrome is characterized by a mitochondrial DNA mutation that leads to defective taurine modification of the leucine tRNA anticodon, with consequent impaired translation of the UUG codon. This defect reduces synthesis of respiratory chain complexes, which causes energy failure. Taurine supplementation improved mitochondrial function in MELAS model cells. A physician-initiated clinical trial reported that high-dose taurine supplementation therapy suppressed stroke-like episodes and improved taurine modification rates in leukocytes.