Effects Of Taurine Deficiency Research Articles

Taurine, a non-proteinous essential amino acid for human body systems: an overview

PurposeTaurine (2-aminoethane sulfonic acid; C2H7NO3S) is a nonprotein sulfur-containing β-amino acid present in nearly all mammalian tissues and the most ubiquitous free endogenous biomolecule in human cells. Taurine is commonly known as a conditionally essential amino acid because taurine is one of the few amino acids that are not incorporated in protein synthesis. The purpose of this study is to review the existing articles related to taurine and to give an account how useful is taurine to the different body systems. In this thorough overview, taurine is covered in terms of its essentiality, sources, advantages for neonates and the elderly, the effects of taurine deficiency, and the safety and toxicity of taurine supplements.Design/methodology/approachThis is a narrative review into the subject matter. Published articles were searched on different portals like PubMed, EMBASE, Scopus, Google Scholar, PubChem etc. The authors also evaluated the availability of taurine in commercially available energy drinks.FindingsThis comprehensive review, presents the potential clinical benefits and functional properties of taurine as a conditionally essential amino acid. Energy drinks containing taurine (and their concentration) are also reported in this review.Originality/valueThis is the first data that the authors are aware of that shows taurine content in a variety of energy drinks on the market.

Effect of taurine deficiency on adenosine receptor-mediated relaxation of the rat aorta

We recently demonstrated that chronic taurine supplementation or deficiency causes alterations in reactivity of the rat aorta to several vasoactive agents. In the present investigation, we examined the effects β-alanine-induced endogenous taurine deficiency on the mechanical responsiveness of the isolated rat aorta to adenosine receptor stimulation with 2-chloroadenosine (CAD), 5′- N-ethylcarboxyamidoadenosine (NECA), and N 6-cyclopentyladenosine (CPA). The adenosine analogs produced concentration-dependent (1×10 −9−3×10 −3 M) relaxations of aortas from both control and β-alanine-treated rats with the rank order of potencies NECA>CAD>CPA, which was consistent with A 2 receptor identification. CAD and NECA induced both endothelium-dependent and -independent relaxations of the aortas. The endothelium-dependent responses to both agents and the independent responses to CAD were significantly attenuated by β-alanine treatment. The relaxation responses of the aortas from control and taurine-deficient rats to CAD and NECA were markedly antagonized by ZM241385 (10 −5 M), suggesting the involvement of A 2A adenosine receptors. Further, N -nitro- l-arginine methyl ester ( l-NAME; 10 −5 M) significantly attenuated the endothelium-mediated relaxation produced by CAD and NECA in both groups. However, the inhibitory effect of l-NAME was less on the β-alanine-treated tissues, providing evidence that the effect of taurine deficiency was linked to a reduction in nitric oxide generation. As in the aorta, CAD produced both endothelium-dependent and -independent relaxation responses in the rat superior mesenteric artery, and both responses were inhibited by chronic β-alanine treatment, suggesting that not only similar responses can be generated by a given adenosine agonist in different vascular beds, but also β-alanine treatment modulates these responses. On the other hand, while CPA elicited only endothelium-independent aortic relaxation, this response was not altered by taurine deficiency. The results indicate that endogenous taurine deficiency causes differential inhibitory effects on adenosine receptor-mediated vasorelaxation, depending upon the agonists used. Given the recognized role of adenosine in the vasculature, these alterations suggest taurine-mediated modulation of blood flow regulation.

Possible cause of taurine-deficient cardiomyopathy: potentiation of angiotensin II action.

Taurine, an amino acid that exhibits anti-angiotensin II and osmoregulatory activity, is found in very high concentration in the heart. When the intracellular content of taurine is dramatically reduced, the heart develops contractile defects and undergoes an eccentric form of hypertrophy. The development of myocyte hypertrophy has been largely attributed to angiotensin II, whose growth properties are antagonized by taurine. Overt heart failure is usually associated with myocyte death, including death due to angiotensin II-induced apoptosis. However, the effect of taurine deficiency on angiotensin II-induced apoptosis has not been examined. To investigate this effect, taurine-deficient cells, produced by incubating rat neonatal cardiomyocytes with medium containing the taurine transport inhibitor, beta-alanine, were exposed to angiotensin II. The peptide increased terminal deoxynucleotidyl transferase-mediated deoxyuridine triphosphate nick end-labeling (TUNEL) staining and caspase 9 activation more in the taurine-deficient than the normal cell. Angiotensin II also promoted the translocation of protein kinase C (PKC)epsilon and PKCdelta, the expression of Bax, and the activation of c-Jun N-terminal kinase (JNK), effects that were greater in the taurine-deficient cell. However, the data ruled out a role for extracellular signal-related kinase (ERK), Bad, and p38 mitogen-activated protein kinase in the beta-alanine-angiotensin II interaction. Because PKC and JNK affect the expression and phosphorylation state of certain Bcl-2 family members, they appear to contribute to the potentiation of angiotensin II-induced apoptosis by taurine deficiency.

Effects of Taurine Deficiency and Chronic Methanol Administration on Rat Retina, Optic Nerve and Brain Amino Acids and Monoamines

A chronic methanol (MeOH) intoxication scheme (2 g/kg/day ip for 2 weeks) was carried out in Sprague-Dawley rats, previously depleted of folates with methotrexate (MTX). β-Alanine (β-Ala), 5%, was also administered to some animals in the drinking water. Amino acids were determined in plasma, retina, optic nerve, hippocampus and posterior cortex by HPLC with fluorescence detection and monoamines in retina, hippocampus and posterior cortex by electrochemical detection. β-Ala administration reduced taurine (Tau) levels in plasma, hippocampus and posterior cortex, but not in retina and optic nerve. Aspartate (Asp) concentration in the optic nerve was increased in MTX-MeOH treated animals, and the administration of β-Ala did not modify this elevation. The association of β-Ala with MTX-MeOH produced an increase of threonine, and a decrease of 5-hydroxytryptamine (5-HT) in the retina without modifying 5-hydroxyindoleacetic acid, whereas in the hippocampus an elevation of asparagine was observed. We conclude that, in the retina, β-Ala in combination with MTX-MeOH increased serotonin and decreased dopamine (DA) turnover rate, and resulted in changes in the amino acid balance, that could affect glycinergic activity. On the other hand, in the hippocampus, Asp metabolism could be affected by Tau depletion with β-Ala.

Taurine deficiency in dissociated mouse cerebellar cultures affects neuronal migration

The role of taurine in the process of neuronal migration was studied in a microwell cell culture system. Immunocytochemical analysis of the cellular composition of this culture system revealed the presence of the astrocytic marker GFAP in some structures such as the aggregates of neuronal bodies and in those cables used for migration, resembling what is described in vivo. The neuronal marker γ-enolase stained practically all structures, including the aggregates and all cables. The intracellular taurine concentration was reduced by 60% in mouse cerebellar granule cells treated with a blocker of taurine transport, guanidinoethane sulfonate (GES). Under these conditions cell migration was markedly reduced to approximately 50% of that in untrated cultures. Both, taurine depletion and impairment of cell migration induced by GES were prevented by adding taurine to the culture medium. Taurine deficiency similarly affected different morphological parameters such as the number of cables suitable for neuronal migration as well as the number of migrating neurons. The number of aggregates of neuronal bodies was significantly increased, by about 30%, as a consequence of the reduced migration. Taurine alone did not exert any effect on the parameters evaluated. GES treatment of granule cells did not affect mitochondrial metabolism or K+-stimulated Ca2+-dependent [3H]-d-aspartate release. This suggests that the described effects of taurine deficiency were not due to an alteration of neuronal viability and that the action of GES was not simply due to unspecific and deleterious effects. These results are in agreement with those obtained in in vivo studies. This approach represents a useful model to investigate the role played by taurine in the process of neuronal migration.

Effect of taurine deficiency on tissue taurine concentrations and pregnancy outcome in the rat.

Taurine status and pregnancy outcome were assessed in rats fed low dietary taurine and varying doses of guanidinoethyl sulfonate (GES), a structural analogue of taurine. Female Sprague-Dawley rats (225-270 g) were mated overnight and assigned to one of four groups from day 0 to 20 of gestation. Taurine-deficient animals were fed a basal diet containing < 0.001 mumol taurine/g and 0.5 (n = 7), 1.0 (n = 8), or 2.0% (n = 7) GES in their drinking water, ad libitum. Control animals (n = 8) received similar treatment, with 2 mumol taurine/g added to the diet and no GES in their water. Taurine was analyzed by reverse-phase HPLC, using electrochemical detection after precolumn derivatization with ortho-phthalaldehyde. Treatment of rats with varying doses of GES produced a sharp decline in maternal liver and brain taurine to 15 and 55% of that of control levels, and in fetal liver and brain taurine to 75 and 50% of that of control levels, respectively (p = 0.0001; one-way ANOVA). The 2% group had a smaller mean (+/- SEM) litter weight than the control group (35.8 +/- 6.1 vs. 51.9 +/- 2.8 g; p = 0.042) as a result of a smaller litter size. The decrease in litter size was associated with confinement of implantation sites to either the left or right uterine horn in four of seven dams. Taurine deficiency did not result in intrauterine growth retardation or significant external, visceral, or skeletal malformations. Developmental defects were not found in any of the taurine-deficient groups, but reproductive abnormalities were present at the highest dose of the analogue.

Effects of taurine deficiency on arrhythmogenesis and excitation-contraction coupling in cardiac tissue.

Taurine is the major constituent of the free amino acid pool of mammalian myocardium, but its precise function is little understood. There is little biosynthesis of taurine within the heart; instead its mM levels are determined by active transmembrane transport by a specific carrier. It is not found in proteins, neither is it a substrate for metabolism. Taurine deficiency, however, produces cardiac electrophysiological and mechanical abnormalities (Lake et al., 1987; 1990) and life-threatening dilated cardiomyopathy documented by echocardiography in cats and foxes (Pion et al., 1987; Moise et al., 1989). Novotny et al. (1991) have recently described deficits in left ventricular systolic pressure development in such cats. Taurine supplements can reverse these conditions, and are also beneficial in the treatment of human congestive heart failure of many etiologies (Azuma et al., 1985) and a rabbit model of this condition (Azuma et al., 1984). The sites of action of most of these effects are unknown. The majority of studies have described the pharmacological effects of exogenous taurine in doses which far exceed the micromolar levels normally found in the plasma. Interactions with calcium (Ca) are suggested by the observations that taurine administration has positive inotropic effects (Huxtable, 1976), prevents Ca paradox (Kramer et al., 1981) and delays the onset of Ca accumulation which causes necrotic lesions in genetic cardiomyopathic hamsters (McBroom and Welty, 1977).

Effects of taurine deficiency on immune function in mice.

The role of the sulfur-containing amino acid, taurine, in immune function has received scant attention until recently. In the past few years reports have described its adjuvant effect for viral antigens in mice and human subjects (Kuriyama et al., 1988; Ishizaka et al., 1990), its reversal of age-related immune decline in mice (Nishio et al., 1990) and a decline in polymorphonuclear cell function in severely taurine-deficient cats (Schuller-Levis et al., 1990).

High dietary taurine and feline reproduction.

Taurine is now well established as an essential nutrient for cats and may also be a conditionally essential nutrient for some other species, especially during development (Sturman, 1988). There is now a large body of literature dealing with the effects of taurine deficiency (Hayes, 1988; Sturman, 1988; Hayes and Trautwein, 1989; Sturman, 1990). Little attention has been paid to potential effects of taurine supplementation, however. In humans and cynamolgus monkeys which conjugate bile acids with taurine and glycine, the proportion of bile acids conjugated with taurine increases as the amount of taurine in the diet is increased (Sjovall, 1960; Haslewood, 1967; Hofmann and Small, 1967; Schersten, 1971; Sturman et al., 1975; Hayes et al., 1980). Such changes influence absorption from the gut, and beneficial effects of dietary taurine supplementation have been reported in chronic and acute hepatitis (Matsuyama et al., 1983; Nakashima et al., 1983), drug-induced liver disease (Attili et al., 1984), cirrhosis (Kroll and Lund, 1966), myotonia (Durelli et al., 1983), cystic fibrosis (Darling et al., 1985; Belli et al., 1987; Colombo et al., 1988; Thompson, 1988) and epilepsy (Barbeau and Donaldson, 1973; Barbeau and Donaldson, 1974; Bergamini et al., 1974; Fukuyama and Ochiai, 1982) although not in retinitis pigmentosa (Reccia et al., 1980). In addition, taurine has been added to commercial infant formulas and pediatric parenteral solutions in recent years because of mounting evidence of subtle abnormalities in visual function resulting from its absence (Sturman, 1986). A recent study reported adverse effects in the guinea pig comprising of fatty changes in the liver accompanied by changes in the lipid content after 14 days of oral administration of taurine (Cantafora et al., 1986).

Elevation of Retinol Levels and Suppression of Alanine Aminotransferase Activity in the Liver of Taurine-Deficient Kittens

In taurine-deficient cats, the secretion of bile acids is impaired, and this impairment may reduce intestinal uptake of lipophilic vitamins. It was therefore hypothesized that retinol deficiency is involved in the generation of retinal lesions in taurine-deficient kittens. To this end, the concentration of retinol in plasma and liver was determined in taurine-deficient kittens. Further, the effects of taurine deficiency on amino acid concentrations of heart, liver and kidney were investigated. To see whether taurine deficiency adversely affects the liver, hepatic enzymes were measured in plasma and liver of kittens suffering from taurine deficiency. In addition, liver morphology, growth and food intake were studied. Taurine was the only amino acid whose concentration was consistently decreased in plasma of the experimental group. Unexpectedly, retinol level was increased in plasma and liver from taurine-depleted kittens. Several alterations were noted in amino acid concentrations in liver and kidney, but not in heart. Plasma alanine aminotransferase activity was diminished, probably reflecting decreased activity in the liver. Perivenular steatosis was found in both groups. Controls grew linearly, in contrast to deficient animals, which nevertheless consumed more food. The results demonstrate that retinol deficiency is not involved in taurine-deficiency retinopathy. Moreover, taurine is required for linear growth of juvenile cats and for the maintenance of hepatic and renal pools of certain amino acids.