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Nutrients 2017, 9(8), 795; doi:10.3390/nu9080795

Role of Mitochondria and Endoplasmic Reticulum in Taurine-Deficiency-Mediated Apoptosis

1
Department of Pharmacology, College of Medicine, University of South Alabama, Mobile, AL 36688, USA
2
Faculty of Biotechnology, Fukui Prefectural University, Fukui 910-1195, Japan
3
Program in Integrative Biology and Center for Complex Systems and Brain Sciences, College of Medicine, Florida Atlantic University, Boca Raton, FL 33431, USA
*
Author to whom correspondence should be addressed.
Received: 18 May 2017 / Revised: 18 July 2017 / Accepted: 19 July 2017 / Published: 25 July 2017
(This article belongs to the Special Issue Antioxidants in Health and Disease)
View Full-Text   |   Download PDF [3944 KB, uploaded 25 July 2017]   |  

Abstract

Taurine is a ubiquitous sulfur-containing amino acid found in high concentration in most tissues. Because of its involvement in fundamental physiological functions, such as regulating respiratory chain activity, modulating cation transport, controlling inflammation, altering protein phosphorylation and prolonging lifespan, taurine is an important nutrient whose deficiency leads to severe pathology and cell death. However, the mechanism by which taurine deficiency causes cell death is inadequately understood. Therefore, the present study examined the hypothesis that overproduction of reactive oxygen species (ROS) by complex I of the respiratory chain triggers mitochondria-dependent apoptosis in hearts of taurine transporter knockout (TauTKO) mice. In support of the hypothesis, a 60% decrease in mitochondrial taurine content of 3-month-old TauTKO hearts was observed, which was associated with diminished complex I activity and the onset of mitochondrial oxidative stress. Oxidative damage to stressed mitochondria led to activation of a caspase cascade, with stimulation of caspases 9 and 3 prevented by treatment of 3-month-old TauTKO mice with the mitochondria specific antioxidant, MitoTempo. In 12 month-old, but not 3-month-old, TauTKO hearts, caspase 12 activation contributes to cell death, revealing a pathological role for endoplasmic reticulum (ER) stress in taurine deficient, aging mice. Thus, taurine is a cytoprotective nutrient that ensures normal mitochondrial and ER function, which is important for the reduction of risk for apoptosis and premature death. View Full-Text
Keywords: oxidative stress; mitochondria; endoplasmic reticulum stress; apoptosis; caspase cascade; respiratory chain; mitochondria encoded proteins; tRNALeu(UUR) oxidative stress; mitochondria; endoplasmic reticulum stress; apoptosis; caspase cascade; respiratory chain; mitochondria encoded proteins; tRNALeu(UUR)
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This is an open access article distributed under the Creative Commons Attribution License which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. (CC BY 4.0).

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MDPI and ACS Style

Jong, C.J.; Ito, T.; Prentice, H.; Wu, J.-Y.; Schaffer, S.W. Role of Mitochondria and Endoplasmic Reticulum in Taurine-Deficiency-Mediated Apoptosis. Nutrients 2017, 9, 795.

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