Re:Re:타우린(보충제)에 대하여

[문형철]

BEYOND REASON

타우린은 황을 함유한 아미노산. 

단백질합성, 에너지로 사용되지 않고 각종 인체활성에 필수역할!!

나이가 들면 꼭 먹어야 하는 보충제인듯!!

Cats need taurine like a vitamin, these same deficiency conditions may exist with humans but since we synthesize taurine we are not outright dependent on it. Thus its status as 'conditionally essential'

타우린, 혹은 2-아미노에테인술폰산(2-aminoethanesulfonic acid)은 인간을 비롯한 포유동물의 세포와 조직에 존재하는 유황을 함유하는 아민으로서 1827년 오스트리아 화학자인 프리드리히 티드만(Friedrich Tiedemann)과 레오폴트 그멜린(Leopold Gmelin)에 의해 소의 담즙에서 최초로 분리되어, 1838년 Demarcay에 의해 타우린(영어: taurine)으로 명명되었다. 타우린은 아미노기가 분자구조의 β-탄소에 붙어있는 β-아미노산이며, 카르복실기 대신에 pK값이 더 낮은 sulfonic acid기가 α-탄소에 치환되어 있어 다른 아미노산에 비해 더 낮은 pH에서도 쉽게 이온화되는 성질이 있다. 단백질 합성에 사용되지 않고 대부분의 동물조직과 생체액에서 유리아미노산의 형태로 풍부하게 존재하고 있으며, 식품조직에는 거의 존재하지 않거나 매우 미량으로 존재하고 있다. 특히 포유류의 뇌, 심장, 간, 신장 등의 장기와 골격근육, 혈구세포 등에 고농도로 존재하며, 세포외액에 비하여 세포내액에 매우 높은 농도로 존재한다.^[1] 타우린은 주로 어패류 특히 굴, 가리비 등 조개류나 오징어, 문어, 생선의 검붉은 살 등에 많은 성분으로 소, 돼지, 닭 등 육류에는 함유량이 적다.^[2]

타우린의 생합성[편집]

타우린은 포유류 조직에서 함황아미노사인 cysteine으로부터 생합성되며 주로 뇌와 간에서 활발하게 일어난다. 현재까지 알려진 생합성 경로로는 cysteine sulfinate 경로와 cysteamine 경로가 있는 것으로 알려져 있다. 

Cysteine sulfinate 경로는 cysteine이 cysteine dioxygenase의 작용에 의해 cysteine sulfinate로 산화되고 이는 다시 cysteine sulfinate decarboxylase의 작용에 의해 hypotaurine으로 된 다음 taurine으로 전환되는 경로로서 타우린 생합성의 주된 경로로 알려져 있다. Cysteine sulfinate 경로의 또 다른 경로로서 cysteine이 cysteine dioxygenase의 작용에 의해 cysteine sulfinate로 산화되고 다시 cysteine sulfinate dehydrogenase의 작용에 의해 cysteic acid로 된 다음 cysteic acid decarboxylase의 작용에 의해 taurine으로 전환된다는 설도 있으나 이는 아직까지 많은 부분이 명확하게 밝혀지지 않고 있다. Cysteamine 경로는 cysteine이 여러 단계의 효소작용을 거쳐 cysteamine으로 전환된 후 cysteamine dioxygenase의 작용에 의해 hypotaurine으로 된 다음 taurine으로 전환되는 경로이다.

타우린의 생합성은 조직에 따라 차이는 있으나 전체 생합성량의 약 10% 미만이 cysteamine경로에 의해 생합성되고 대부분이 cysteine sulfinate 경로에 의한 것으로 알려져 있다. Cysteine sulfinate 경로에 작용하는 효소인 cysteine dioxygenase와 cysteine sulfinate decarboxylase의 활성은 동물에 따라 큰 차이를 나타내고 있으며, 같은 종류의 동물 내에서도 먹이 중의 단백질이나 함황아미노산의 함량, 그리고 동물의 발달 단계에 따라서도 영향을 받는 것으로 보고되고 있다. 따라서 동물에 따라 타우린의 생합성 능력은 많은 차이를 나타내고 있다. 특히 cysteine sulfinate decarboxylase의 활성은 쥐나 개에 비하여 인간이나 원숭이, 고양이 등은 매우 낮아 이들 동물에 있어 타우린의 생합성은 극히 제한적이다. ^[3]

Taurine

Taurine is an organic acid with a sulfur in it. It is found in foods, in highest amounts in meats, and is a heart and blood healthy agent that can confer a wide variety of health benefits. Its most well known usage is to reduce cramping caused by fat burners like ephedrine.

1Sources and Structure

1.1Source

Taurine is an amino sulfonic acid that is sometimes referred to as a sulfur containing beta-amino acid due to its structure, although technically not an amino acid due to structural issues. It comprises over 50% of the free amines in cardiac tissue (highly prominent)[1][2] but is located systemically in lower concentrations, particularily the testicles where it is highly prominent.[3][4] In general, taurine is present in excitable tissues more than others[5] although as its transporter is expressed ubiquitously it could be assumed taurine is omnipresent in the human body.[6]

Taurine is not a structural component of any quaternary proteins or peptide bonds and resembles a peptide neurotransmitter (like adrenaline or dopamine) more than classical dietary proteins.[7]

1.2Structure

Taurine is highly water soluble (10.48g/100mL)[8] and, structurally, is an amino group paired to a sulfonic group by two methylene groups in a chain. It is a beta-amino acid (similar to beta-alanine).

Biosynthesis

Taurine is naturally derived from cysteine. Mammalian taurine synthesis occurs in the pancreas via the cysteine sulfinic acid pathway. In this pathway, cysteine is first oxidized to its sulfinic acid, catalyzed by the enzyme cysteine dioxygenase. Cysteine sulfinic acid, in turn, is decarboxylated by sulfinoalanine decarboxylase to form hypotaurine. Hypotaurine is enzymatically oxidized to yield taurine by hypotaurine dehydrogenase.^[10]

Taurine is also produced by the transsulfuration pathway, which converts homocysteine into cystathionine. The cystathionine is then converted to hypotaurine by the sequential action of three enzymes: cystathionine gamma-lyase, cysteine dioxygenase, and cysteine sulfinic acid decarboxylase. Hypotaurine is then oxidized to taurine as described above.^[11]

1.3Biological Significance

Taurine maintains an intracellular concentration of 5-20 µmol/g wet weight,[9][10] and enters cells through its transporter, the Taurine Transporter (TauT) that belongs to the class of sodium-chloride dependent transporters (similar to creatine) and is named SLC6a6; this transporter is expressed in most, if not all, mammalian tissue.[6] Pathological problems are observed when cellular taurine is depleted, and this is observed in as little as 48 hours when the transporter is either blocked by a competitive inhibitor[11] or outright depleted.[12] The reasons for this depletion is that intracellular (within the cell) synthesis of taurine is limited, and cells appear to be dependent on taurine uptake from the blood, and the average serum concentration appears to be 20-100uM (up to 100 fold less than cells), which is reason for the active transport via TauT as taurine uptake works againt a concentration gradient.[12]

Cellular accumulation of Taurine is dependent almost exlusively on the SLC6a6 transporter, and avoiding pathological conditions of Taurine deficiency are dependent on having taurine in the cell

1.4Taurine Deficiency

In non-human species who cannot synthesize taurine, it is an essential nutrient. The primary example of a species that is taurine-dependent is all feline species (cat family) where a lack of dietary taurine results in cardiopathology, impaired muscular function, and ocular degeneration.[13][14] These side-effects may occur to humans if a taurine deficiency exists, but this assumes an error in inborn metabolism impairing one's ability to synthesis taurine. The average human would not need to worry about outright taurine deficiency and its clinical manifestations.

Cats need taurine like a vitamin, these same deficiency conditions may exist with humans but since we synthesize taurine we are not outright dependent on it. Thus its status as 'conditionally essential'

It is possible to be 'deficiency' in taurine despite it being classified as a non-essential amino acid, and deficiency states can be induced experimentally with overfeeding of beta-alanine which competes at the level of the transporter due to being structured similarily.[1] Guanidinoethane sulfonate (GES) may also be used to inhibit taurine uptake.[15]

Knocking out the taurine transporter (TauT, also known as SLC6a6) genetically, and preventing its uptake into cardiomyocytes and skeletal muscle, can lead to cardiomyopathy and reduction in exercise performance coupled with a loss of body weight.[12]

Taurine deficiency in skeletal muscle is a bit difficult to assess as the two ways to inhibit uptake influence muscle function, as guanidinoethane sulfonate itself enhances response to Ca2+ in muscle cells[16] as does beta-alanine which is a proven ergogenic aid. Studies using genetic knock-out mice without the transporter at all note that weight-loaded swimming test performance was reduced from 118+/-2.3m to 10+/-2.5min,[17] treadmill running endurance is reduced by over 80%,[18] and the skeletal muscle itself undergoes atrophy with some cells actually displaying necrosis.[12]

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2Pharmacology

2.1Absorption

In the stomach, taurine seems to be safe from stomach acid and does not undergo changes.[19]

Taurine does not appear to undergo any changes in the environment of the stomach

In the intestines, pancreatin can reduce levels of detectable food-bound taurine by almost 40%.[19] However, this study noted that the taurine was not broken into metabolites but somehow became 'inaccessible', which may be due to the taurine being from meat.[19]

It has been hypothesized that taurine may enhance the absorption of lipid-soluble components,[20] based on its ability to conjugate with bile acids to promote water solubility secondary to formation of taurocholic acid (as seen with tauroursodeoxycholic acid[2] and in the general process of aiding phospholipid absorption from the intestines to the liver[21]) and its ability to enhance the water solublility of retinal (an aldehyde of vitamin A) which is also fat soluble as well as endogenously occurring.[22][23]

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3Neurology

3.1Regulation and Transport

Taurine has been noted to be taken up into synaptosomes via a high-affinity uptake system.[24]

3.2Glutaminergic Neurotransmission

Taurine has been noted to potentiate signalling via presynaptic NMDA receptors (EC50 19µM) in a manner that is blocked by co-administration with glycine.[25] Presynaptic NMDA receptors are those located prior to the synapse[26][27] and appear to promote release of glutamate[28][29] and GABA[30] into the synapse, they also require an agonist at the glycine binding site to work.[25]

Taurine has been found to not significantly alter fEPSPs in postsynaptic neurons (via NMDA) in one study[25] although others contrast this.[31] Taurine has been found to interact with the postsynaptic receptor at 100µM[32] and it appears to work via hindering how much agonists at the polyamine binding site (ie. spermidine) can increase affinity at the MK-801 binding site.[32]

Taurine has also been noted to diminish the affinity of glycine to the NMDA receptor.[32]

Taurine may be an indirect suppressor of NMDA signalling, and while it can also stimulate both glutamate and GABA release from the synapse it ultimately seems to reduce excitatory transmission

The suppressive effect of taurine on glutaminergic signalling seen with the NDMA receptors does not appear to extend to the kainate nor AMPA receptors.[32]

AMPA and Kainate are not known to be highly affected by taurine

Glutamic acid decarboxylase (GAD65 and GAD67) appears unaffected by chronic taurine intake at doses that are neuroactive.[33][34]

3.3GABAergic Neurotransmission

Taurine is one of the major inhibitory amino acid neurotransmitters in the brain, alongside GABA and Glycine,[35][36] and while the latter two amino acids have their own signalling systems (GABAergic and Glycinergic) taurine is thought to act vicariously as a neuromodulator of these two systems.[37]

Taurine is known to bind to both GABAA[38] and GABAB[39] receptors

At 1µM, taurine is able to enhance NMDA-dependent phosphatidylinositol hydrolysis by 80.4+/-3.5%, which is due to its actions at the GABAB receptors.[40] 

GABA transaminase (the enzyme that degrades GABA[41]) is not affected by taurine.[24]

Taurine is unable to prevent picrotoxin-induced seizures (antagonizing GABA receptors[42]).[8]

3.4Glycinergic Neurotransmission

Taurine is able to act on glycine receptors.

Glycinergic signalling mediates anxiolytic effects of taurine.[8]

3.5Memory and Learning

Both Akt and GSK3β phosphorylation (the PI3K/Akt cascade) are enhanced in the hippocampus of rats fed around 230-460mg/kg daily for four weeks, while CAMKII phosphorylation was increased at only the higher dose and protein content itself was unaffected.[33][34]

3.6Anxiety

200mg/kg taurine (but not 100mg/kg) given to mice 60 minutes before anxiety tests was able to reduce anxiety to a degree greater than the reference drug thiopental (25mg/kg) but lesser than midozolam (1.2mg/kg).[8] This anxiolytic effect was mediated by interactions with glycine receptors as they were abolished by antagonists of this receptor.[8]

Taurine has shown anti-anxiety actions following oral ingestion

3.7Depression

Taurine appears to be involved in depression as the concentrations of taurine in the rat brain appear to be altered (13% increase) in response to experimentally induced stress;[43] it was hypothesized to be released in order to attenuate the depressive/stressful response, since taurine itself at a cellular level depresses neuronal firing.[44]

Oral taurine (around 230-460mg/kg) has been noted to increase hippocampal phosphorylation of ERK1, ERK2, and CREB in rats over four weeks without affecting protein content;[33][34] a cascade (MAPK-CREB) thought to play a role in depression.[45][46]

In diabetic rats (diabetics being more prone to depression[47]) injected with taurine (100mg/kg) over 30 days have experienced an increase in hippocampal BDNF mRNA when compared to saline and an increase in the mRNA for the GABAA α2 receptor subunit.[48] Diabetic rats with depression are known to have lower levels of GABA[49] while rats without that particular receptor subunit (GABAA α2) experience depression,[50] suggesting a mechanism for the actions of taurine in diabetics. When this taurine injection was tested in nondiabetic rats there was no increase in GABAA α2 mRNA, and the increase in BDNF normalized the diabetic rats relative to nondiabetic control (BDNF is reduced in the blood of diabetics[51]) and did not affect nondiabetic rats.[48]

Taurine has some mechanisms, potentially associated with GABA and BDNF signalling, suggesting it may have antidepressant properties. It is possible that this antidepressant effect is more relevant in diabetic subjects

Taurine at 45mM/kg of the diet to rats over four weeks (ended up eating 462.8mg/kg bodyweight) has shown antidepressant effects in a forced swim test when compared to a control diet, whereas half this taurine dose did not differ from control.[33]

This antidepressant effect has been noted with 100mg/kg taurine injections in the forced swim test in diabetic rats[48] and elsewhere at the same dose and a lower dose of 25mg/kg intraperitoneal injection.[52]

When tested in rodents there appears to be a minor antidepressant effect of taurine supplementation when compared to control, which requires a relatively high dose (estimated 75mg/kg bodyweight in humans or 5 grams for a 150lb person)

In free living adults, dietary taurine intake does not appear to be associated with depressive-like symptoms[53] and while one study has noted an association between dietary taurine intake and life stress in college-age students[54] two later studies failed to find an association.[55][56]

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4Interactions with Cardiovascular Health

4.1Mechanisms

Taurine acts as both a cell protecting agent by modulating the cell membranes fluidity and health, as well as exerting anti-oxidant like effects.

It may exert anti-oxidant like effects by binding free ions (Fe2+, Cu2+) and oxidant metalloproteins the blood[57] which would then act as pro-oxidants in situations of high blood glucose.[58] Taurine may also exert anti-oxidant like effects over time by preventing pro-oxidative effects associated with insulin resistance via it's insulin sensitizing actions.[59]

Taurine, at a concentration of 1mM, significantly reduces oxidative stress on cardiac muscle tissue in the presence of oxidative stress[60] and can protect against damage from ischaemia-reperfusion injury in cardiac tissue.[61]

4.2Angiogenesis

Angiogenesis is the process of forming new blood vessels, and is of concern to both cardiovascular health (microcirculation) and cancer metabolism (fuelling tumor cells). Taurine appears to be able to activate angiogenesis (via Akt and via PI3K, FAK via Src, and ERK via MEK) and accelerate endothelial cell proliferation (via Cyclin D1/B), and angiogenesis appears to mediated from outside the cell as inhibiting taurine uptake with beta-alanine actually increased these effects.[62]

4.3Interventions

One study on type I diabetic smokers with higher rates of endothelial dysfunction who were given taurine supplementation, 2 weeks of 1,500mg taurine supplementation was able to return these parameters to the levels of control and improve both blood flow (assessed by flow-mediated vasodilation and brachial flow).[63]

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5Interactions with Glucose Metabolism

Many of the in vivo studies to follow were conducted in experimental procedures of fructose-induced insulin resistance.

Taurine may hold promise in treating insulin resistance by modifying the post-receptor (intracellular) effects of insulin signalling[64] as well as regenerating intrinsic antioxidants, reducing lipid peroxidation, and ameliorating insulin resistance in fructose-induced insulin resistance.[59] Taurine can also control glucose levels to a degree via improved acute insulin action.[65]

This anti-diabetic effect may be (in part) specific to fructose-induced insulin resistance (both hepatic and peripheral) due to the interactions with post-receptor intermediates (and subsequent receptor transcription) rather than receptor desensitization; as has been shown in fructose feedings.[66]

5.1Diabetes

Outside of the previous benefits established in glucose metabolism, eye health, kidney health and endothelial health (all of which are systems that are potentially damaged in diabetics), taurine has other mechanisms which lead it to be a great conjunct treatment to diabetes management.

Taurine can aid in diabetic-induced joint pain by alleviating the glycation and physiological changes of collagen[67] via donating amino groups to glycating agents in a sacrificial manner[68] although the effect was only seen in those with compromised health. This is the same mechanism of actions seen to protect the retinas from glycation.

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6Interactions with Physical Performance

6.1Muscle Soreness

One study using 2,000mg taurine paired with 3,200mg BCAAs (to be taken thrice daily for two weeks prior to physical testing and four days after) noted that combination therapy, but neither placebo nor either supplement in isolation, was able to reduce muscle soreness.[69]

6.2Aerobic Exercise

Fat oxidation during submaximal activity has been noted to be increased with an acute dose of 1,660mg taurine supplementation in trained cyclists, although this did not impact performance.[70]

Taurine at 1,000mg taken 2 hours prior to exercise has been implicated in improving performance on a 3km time trial in trained athletes, improving time by 1.7% without significantly affecting heart rate or oxygen uptake.[71] Trained cyclists given 1,660mg taurine an hour before cycling (nonmaximal cycling for 90 minutes followed by a time trial) failed to find an improvement in time trial performance with supplementation.[70]

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7Interactions with Hormones

7.1Testosterone

Taurine is investigated for its interactions with testosterone due to being the most prominent free amino acid localized in the testicles of males. It has been detected in Leydig cells, vascular endothelial cells, and other interstitial cells of testis, epithelial cells of the efferent ducts by immunohistochemical methods.[72] In the testes, taurine acts mostly as an anti-oxidant compound and protect the testes and localized structures from oxidative stress. This does appear to attenuate reductions of testosterone from other agents which may reduce testosterone via pro-oxidation, and this has been shown with nicotine,[73] arsenic,[74] cadmium,[75] and doxorubicin.[76]

Another state in which taurine may prevent oxidation-mediated reductions in testosterone is diabetes. Excess glucose and pro-oxidants in the blood of diabetic rats negatively influence testicular function, which is attenuated by taurine[77] and testicular anti-oxidants in general.[78] One study to measure testicular anti-oxidant enzymes also found they were increased, with increases in superoxide dismutase (SOD) and glutathione with more efficacy in aged rats;[4] young rats had a remarkable increase in sorbitol dehydrogenase, and both groups experienced a slight increase in testicular Nitric Oxide levels.[4]

Maternal consumption of taurine also appears to beneficially influence androgen levels of the offspring, when measuring serum testosterone when the mother consumed 1% taurine in drinking water (rats).[4]

General protective effects of taurine on oxidant-induced decreases in testosterone, which is linked to taurine acting as an anti-oxidant and being highly concentrated in the testicles

One study in healthy 2-month old rats given 0.5, 1, and 1.5% taurine in the drinking water for 5 weeks noted increases in serum testosterone (as well as FSH and LH) with 1% being most significant and elevating testosterone in both serum and the testes from around 50ng/dL to 80ng/dL, a 60% increase.[79] These results were later replicated with 1% Taurine in the diet of adult and aged male rats, where an increase in testosterone and LH were noted in both groups but to a more significant degree in older rats.[4]

The mechanism, as assessed in vitro, appears to be enhancement of HCG-induced testosterone secretion at 10-100ug/mL (and also progresterone induced testosterone secretion) while 1ug/mL or less had no effect and 400ug/mL had a suppressive effect.[79] Secretion of testosterone was attenuated when cysteine sulfinate decarboxylase (CSD) was inhibited as well, suggesting that locally produced taurine also plays a role.[79]

The only human study on taurine (1500mg) was confounded with creatine (5g) and glucuronolactone (350mg) as well as caffeine (110mg) and 19g Branched Chain Amino Acids (Amino Shooter, Champion Nutrition) and failed to show any significant influence on testosterone different than placebo.[80] The lack of response from creatine in increasing testosterone may be due to creatine's instability in solution, and the selected product being a ready-to-drink formulation (and thus no active creatine, only creatinine).[80]

Two studies have shown taurine supplementation to increase testosterone in otherwise healthy rats, no current human studies with similar design; one human study showing no effects of 1,500mg taurine acutely with other ingredient confounds

7.2Estrogen

1% of the diet as taurine to adult or aged male rats does not appear to significantly influence estrogen levels.[4]

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8Interaction with Oxidation

8.1Mechanism

Taurine is an anti-oxidant compound with relatively unique mechanisms as it is directly unable to scavenge any free radical,[81] yet one of the events of taurine deficiency is tied into dysregulated oxidation.[82] One in vitro study noted that taurine deficiency (via beta-alanine incubation) was associated with increased oxidative stress (measured by aconitase and glutathione redox couplet) yet the 10% increase in taurine levels after incubation with taurine alone was not paired with any alteration and coincubation of the two also resulted in no significant differences with control cells (incubated with neither) and similar trends were seen in the mitochondria when measuring the activity of Complex I and III.[83] Beta-alanine resulted in an impaired electron-transport chain function (due to either beta-alanine per se or merely a deficiency of taurine), which tends to cause increases in superoxide production[84] due to spare electrons being diverted to other accepting molecules such as oxygen;[85] it appears that taurine prevents this increase in oxidation by attenuating its own deficiency at times.[83] These effects have been hypothesized elsewhere, and it was expanded that taurine may play a role in mitochondrial tRNA conjugation where its deficiency and the relative lack of conjugation produced oxidation via the aforementioned electron chain impairment.[86] This study hypothesized a lack of 5-taurinomethyluridine as the first step of mitochondrial impairment, but a later study failed to note this despite a decrease in mitochondrial protein synthesis.[11]

A cellular deficiency of taurine results in cellular death by pro-oxidative means, and indirectly dietary taurine can prevent oxidation by preventing its own deficiency

Taurine has also been found to upregulate thioredoxin interacting protein (TXNIP) mRNA levels, which is dependent on cellular accumulation of taurine.[87] As TXNIP regulates oxidation via thioredoxin, this is a plausible mechanism for anti-oxidative effects.

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9Interactions with Organ Systems

9.1Eyes

In cats and monkeys (known to be reliant on dietary taurine due to low endogenous synthesis), a deficiency of dietary taurine can result in significantly reduced taurine concentrations in the retina (up to a 50% reduction)[88] associated with retinal degeneration and impaired vision,[89][90][91] similar symptoms being shown in rats (adequate synthesis in the liver) treated with guanidinoethane sulfonate (transportation antagonist to taurine in the retina[92]) which has also resulted in retinal degeneration.[93]

On a mechanistic level, taurine is known to form conjugates with vitamin A (retinol) in the eye as a molecule known as all-trans retinylidene taurine or tauret. Tauret is synthesized within the retina[94] where it either plays a role in regenerating rhodopsin[95] and photoreceptors[96] (supported by channels into rods specialized for tauret[23]) or through binding to all-trans retinal (a prooxidant produced by light stimulation) and sequestering its prooxidative effects to a degree.

Taurine also exerts osmolytic properties in the retina[97] which may be mechanically protective of retinal rod outer segments by regulating hydration and pressure of these organelles.[98]

Taurine appears to have vital roles in the eyes for all tested mammalian species including primates. This protection and growth promoting properties seen with taurine are hypothesized to either be due to a stimulatory effect on photoreceptors and rhodopsin (a pigment vital for sight) or secondary to controlling prooxidative stressors within the eye that are a result of light stimulation

Taurine may also help protect the eyes from other stressors such as elevated glucose concentrations in retinal tissues[99][100] (a consequence of diabetes that may lead to diabetic retinopathy) and its efficacy in this model has been shown to be comparable to effective concentrations of the combination of Vitamin E and Selenium.[100]

The protective effects of taurine, at least in vitro, have been noted to extend towards elevated glucose concentrations in medium (a model for diabetic retinopathy)

9.2Kidneys

Similar to the heart, taurine supplementation can protect against ischemia/reperfusion injury in the kidneys[101] and protect against toxin-induced oxidative stress[102][103] in addition to general diet-induced oxidative stress[104]

9.3Lungs

Taurine may also protect the lungs from oxidant induced stress (as occurs with smoking) via acting in a sacrificial manner and producing N-chlorotaurine via reactions with hypochlorous acid (HOCl) rather than having HOCl react in alternate methods to induce inflammation responses which then cause damage.[105]

9.4Liver

Taurine can protect the liver from acetominophen induced toxicity at a level slightly less potent than N-acetylglutathione.[106] It may also exert protective effects against other toxins in general.[107]

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10Interactions with Aesthetics

10.1Skin

In isolated skin cells treated with UV(A) radiation, whereas the cells normally take up a variety of osmolytes (inositol and TMG as well) it is noted that all osmolytes are increased in their cellular uptake with taurine having a 69% increase (but TMG having the largest increase at 170%);[108] however, it seems that taurine exclusively was capable of suppressing the increase in IL-6 secreted from the radiation.[108]

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11Safety and Toxicity

11.1General

The observed safety limit, the highest dose for which one can be relatively assured that no side effects will occur over a lifetime, has been suggested to be 3g of taurine in supplemental form (in addition to food intake) a day.[109] Higher doses have been tested and well tolerated, but not enough evidence is available to suggest lifelong safety of said doses.

There is a notion that taurine causes heart damage, which is currently unsupported (and contrary to a fair bit of evidence). This appears to be due to a misunderstanding of why serum taurine levels are elevated during cardiac failure (which is from taurine leakage from cells).

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