| Summary: | Taurine is the most abundant non-proteinogenic sulphur amino acid in humans, and its level decreases dramatically with aging. In humans, the highest levels of taurine are present in retina, leukocytes, heart, skeletal muscles and brain. Taurine is necessary to ensure proper homeostasis and recent research in animals (for example mice and monkeys) have shown that it significantly increases life expectancy and improves health. At the cellular level, taurine is involved in a number of processes such as osmoregulation, modulation of calcium levels and stabilization of cell membranes. Moreover, it has an inhibitory effect on the central nervous system and has antioxidant, anti-apoptotic and anti-inflammatory activity. The development of neurodegenerative diseases is associated with improper functioning of mitochondria, oxidative stress, development of inflammation, excessive activation of ionotropic and metabotropic glutamate receptors and neuronal apoptosis. In vitro and in vivo studies have shown that taurine inhibits the above-mentioned pathological processes and has neuroprotective properties. The antioxidant effect of taurine results from neutralizing hypochlorous acid, a strong oxidant that is produced by neutrophils at the site of the inflammation. Taurine chloramine (Tau-Cl) produced in this reaction reduces oxidative stress and inhibits the production of pro-inflammatory cytokines (e.g. TNF-α, IL-1β, IL-6), nitric oxide (NO) and prostaglandin E2. Moreover, this compound stimulates the expression of antioxidant enzymes (e.g. peroxiredoxin 1, thioredoxin-1, hemooxygenase-1, glutathione peroxidase, catalase). Within the nervous tissue, the anti-inflammatory and antioxidant effect of taurine is related to reduced expression of IL-1α, IL-1β, TNF-α, IFN-γ, IL-6 and GM-CSF, and increase in the activity of antioxidant enzymes (peroxidase-, reductase- and S- glutathione transferase, superoxide dismutase) and glutathione concentration. Taurine is necessary for the proper functioning of mitochondria. Its deficiency blocks the synthesis of taurine-modified leucine tRNA (τm5U-tRNALeu), which results in inhibition of the synthesis of NADH-ubiquinone oxidoreductase, improper functioning of complex I of the respiratory chain and increase in oxidative stress. Endoplasmic reticulum (ER) stress is a hallmark of neurodegenerative diseases and can lead to neuronal apoptosis. Taurine deficiency increases the accumulation of misfolded cellular proteins and induces ER stress. Taurine supplementation reduces neuronal ER stress by inhibiting ATF6- and IRE-1-dependent signalling pathways. Moreover, taurine inhibits apoptosis of neuronal cells by increasing the expression of Bcl-2, decreasing the expression of p53, CHOP and Bax and reducing the activity of caspase-3. In the central nervous system, taurine also serves as an inhibitory neurotransmitter due to binding with γ-aminobutyric acid and glycine receptors (GABAA and GlyR, respectively). Such interactions causes an increased influx of chloride ions into neurons, hyperpolarization of the cell membrane and, consequently, inhibition of glutamatergic neurotransmission and excitotoxicity induced by glutamic acid. The neuroprotective activity of taurine is due to its pleiotropic effects related to the inhibition of apoptosis, oxidative stress, ER stress, and also to its anti-inflammatory activity and inhibition of neuronal excitability.
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