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dc.contributor.authorJong, Chian Ju
dc.contributor.authorIto, Takashi
dc.contributor.authorMozaffari, Mahmood S.
dc.contributor.authorAzuma, Junichi
dc.contributor.authorSchaffer, Stephen W
dc.date.accessioned2012-10-26T16:26:53Z
dc.date.available2012-10-26T16:26:53Z
dc.date.issued2010-08-24en_US
dc.identifier.citationJ Biomed Sci. 2010 Aug 24; 17(Suppl 1):S25en_US
dc.identifier.issn1423-0127en_US
dc.identifier.pmid20804600en_US
dc.identifier.doi10.1186/1423-0127-17-S1-S25en_US
dc.identifier.urihttp://hdl.handle.net/10675.2/613
dc.description.abstractBackground: The b-amino acid, taurine, is a nutritional requirement in some species. In these species, the depletion of intracellular stores of taurine leads to the development of severe organ dysfunction. The basis underlying these defects is poorly understood, although there is some suggestion that oxidative stress may contribute to the abnormalities. Recent studies indicate that taurine is required for normal mitochondrial protein synthesis and normal electron transport chain activity; it is known that defects in these events can lead to severe mitochondrial oxidative stress. The present study examines the effect of taurine deficiency on the first step of mitochondrial protein synthesis regulation by taurine, namely, the formation of taurinomethyluridine containing tRNA.
dc.description.abstractMethods: Isolated rat cardiomyocytes were rendered taurine deficient by incubation with medium containing the taurine transport inhibitor, b-alanine. The time course of cellular and mitochondrial taurine depletion was measured. The primer extension method was employed to evaluate the effect of b-alanine treatment on taurinomethyluridine content of tRNALeu. The protein levels of ND6 were also determined by Western blot analysis.
dc.description.abstractResults: b-alanine caused a time-dependent decrease in cellular taurine content, which were reduced in half after 48 hrs of incubation. The amount of taurine in the mitochondria was considerably less than that in the cytosol and was unaffected by b-alanine treatment. Approximately 70% of the tRNALeu in the untreated cell lacked taurinomethyluridine and these levels were unchanged following b-alanine treatment. Protein content of ND6, however, was significantly reduced after 48 hours incubation with b-alanine.
dc.description.abstractConclusions: The taurine levels of the cytosol and the mitochondria are not directly coupled. The b-alaninemediated reduction in taurine levels is too small to affect taurinomethyluridine levels. Nonetheless, it interferes with mitochondrial protein synthesis, as exemplified by a decrease in ND6 protein content. Thus, b-alanine does not cause alterations in mitochondrial protein synthesis through the lowering of taurine levels.
dc.rightsCopyright ©2010 Schaffer et al; licensee BioMed Central Ltd.en_US
dc.subjectReviewen_US
dc.subject.meshAnimalsen_US
dc.subject.meshCells, Cultureden_US
dc.subject.meshHumansen_US
dc.subject.meshMitochondriaen_US
dc.subject.meshMyocytes, Cardiacen_US
dc.subject.meshRNA, Transfer, Leuen_US
dc.subject.meshRatsen_US
dc.subject.meshRats, Wistaren_US
dc.subject.meshTaurineen_US
dc.subject.meshUridineen_US
dc.subject.meshbeta-Alanineen_US
dc.titleEffect of b-alanine treatment on mitochondrial taurine level and 5-taurinomethyluridine contenten_US
dc.typeArticleen_US
dc.identifier.pmcidPMC2994391en_US
dc.contributor.corporatenameDepartment of Oral Biology
refterms.dateFOA2019-04-10T07:45:39Z
html.description.abstractBackground: The b-amino acid, taurine, is a nutritional requirement in some species. In these species, the depletion of intracellular stores of taurine leads to the development of severe organ dysfunction. The basis underlying these defects is poorly understood, although there is some suggestion that oxidative stress may contribute to the abnormalities. Recent studies indicate that taurine is required for normal mitochondrial protein synthesis and normal electron transport chain activity; it is known that defects in these events can lead to severe mitochondrial oxidative stress. The present study examines the effect of taurine deficiency on the first step of mitochondrial protein synthesis regulation by taurine, namely, the formation of taurinomethyluridine containing tRNA.
html.description.abstractMethods: Isolated rat cardiomyocytes were rendered taurine deficient by incubation with medium containing the taurine transport inhibitor, b-alanine. The time course of cellular and mitochondrial taurine depletion was measured. The primer extension method was employed to evaluate the effect of b-alanine treatment on taurinomethyluridine content of tRNALeu. The protein levels of ND6 were also determined by Western blot analysis.
html.description.abstractResults: b-alanine caused a time-dependent decrease in cellular taurine content, which were reduced in half after 48 hrs of incubation. The amount of taurine in the mitochondria was considerably less than that in the cytosol and was unaffected by b-alanine treatment. Approximately 70% of the tRNALeu in the untreated cell lacked taurinomethyluridine and these levels were unchanged following b-alanine treatment. Protein content of ND6, however, was significantly reduced after 48 hours incubation with b-alanine.
html.description.abstractConclusions: The taurine levels of the cytosol and the mitochondria are not directly coupled. The b-alaninemediated reduction in taurine levels is too small to affect taurinomethyluridine levels. Nonetheless, it interferes with mitochondrial protein synthesis, as exemplified by a decrease in ND6 protein content. Thus, b-alanine does not cause alterations in mitochondrial protein synthesis through the lowering of taurine levels.


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