Abstract
Taurine is a naturally occurring sulfur-containing amino acid that is found abundantly in excitatory tissues, such as the heart, brain, retina and skeletal muscles. Taurine was first isolated in the 1800s, but not much was known about this molecule until the 1990s. In 1985, taurine was first approved as the treatment among heart failure patients in Japan. Accumulating studies have shown that taurine supplementation also protects against pathologies associated with mitochondrial defects, such as aging, mitochondrial diseases, metabolic syndrome, cancer, cardiovascular diseases and neurological disorders. In this review, we will provide a general overview on the mitochondria biology and the consequence of mitochondrial defects in pathologies. Then, we will discuss the antioxidant action of taurine, particularly in relation to the maintenance of mitochondria function. We will also describe several reported studies on the current use of taurine supplementation in several mitochondria-associated pathologies in humans.
Highlights
Mitochondrial dysfunction, along with oxidative stress, is a key hallmark of various pathologies, such as aging [1,2], cardiovascular diseases [3,4], mitochondrial diseases [5,6], metabolic syndrome [7,8], cancer [9,10] and neurological disorders, such as neurodegenerative diseases [11,12] and neurodevelopmental disorders [13,14]
Impairment of mitochondrial function has been commonly reported in pathologies such as aging, cardiovascular diseases, mitochondrial diseases, metabolic syndrome, cancer and neurological disorders [1,2,3,4,5,6,7,9,10,11,13,14,75]
While many other studies [28,78,81,82,83,84,88,89,93,99,117,145] have shown that taurine supplementation protects against mitochondrial dysfunction without definite underlying mechanisms, it is likely that the antioxidant function of taurine is associated with its role in the conjugation reaction with the uridine of the mitochondrial tRNALeu(UUR)
Summary
Mitochondrial dysfunction, along with oxidative stress, is a key hallmark of various pathologies, such as aging [1,2], cardiovascular diseases [3,4], mitochondrial diseases [5,6], metabolic syndrome [7,8], cancer [9,10] and neurological disorders, such as neurodegenerative diseases [11,12] and neurodevelopmental disorders [13,14]. Known as the powerhouse of the cell, mitochondria provide cellular energy by generating ATP via oxidative phosphorylation Reducing equivalents, such as NADH and FADH2, produced via the tricarboxylic acid (TCA) cycle, deliver electrons along the electron transport chain to reduce molecular oxygen to water. Oxidation of cardiolipin induces mitochondrial dysfunction, as has been shown in several in vitro studies These studies have shown impaired cellular metabolism and a sluggish activity of the electron transport chain [64,66,67], as well as enhanced cell death, as evidenced by mitochondrial permeability transport pore opening and cytochrome c release [68,69]. To counteract excessive ROS production, the cell contains an antioxidant defense system, which encompasses enzymatic antioxidants such as mitochondria-localized manganese superoxide dismutase (MnSOD), cytosolic-localized zinc SOD (ZnSOD) and copper SOD (CuSOD), catalase and glutathione peroxidase. Often, increased oxidative stress further exacerbates cellular damage [73,74]
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