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Taurine in pediatric nutrition: review and update [see comments]
Pediatrics, 83(3):433-42 1989 Mar
Taurine was long considered an end product of the metabolism of the sulfur-containing amino acids, methionine and cyst(e)ine. Its only clearly recognized biochemical role had been as a substrate in the conjugation of bile acids. Taurine is found free in millimolar concentrations in animal tissues, particularly those that are excitable, rich in membranes, and generate oxidants. Various lines of evidence suggest one major nutritional role as protecting cell membranes by attenuating toxic substances and/or by acting as an osmoregulator. The totality of evidence suggests that taurine is nonessential in the rodent, it is an essential amino acid in the cat, and it is conditionally essential in man and monkey. Absence from the diet of a conditionally essential nutrient does not produce immediate deficiency disease but, in the long term, can cause problems. Taurine is now added to many infant formulas as a measure of prudence to provide improved nourishment with the same margin of safety for its newly identified physiologic functions as that found in human milk. Such supplementation can be justified by the finding of improved fat absorption in preterm infants and in children with cystic fibrosis, as well as by salutary effects on auditory brainstem-evoked responses in preterm infants. Experimental findings in animal models and in human cell models provide further justification for taurine supplementation of infant formulas.
Taurine and hyperexcitable human muscle: effects of taurine on potassium-induced hyperexcitability of dystrophic myotonic and normal muscles.
Ann Neurol, 11(3):258-65 1982 Mar
Progressively increasing concentrations of potassium chloride in Evans blue saline were administered to patients affected with myotonic dystrophy and to healthy volunteers before and after parenteral treatment with taurine. Excitability changes of thenar eminence muscles were related to the venous potassium and chloride concentrations. The actual electrolyte concentrations were compared to those to be expected if no infused electrolytes had been transported into cells. The expected concentrations were calculated by means of Evans blue dilution. This method permitted quantification of changes of muscle-excitability in terms of the potassium chloride concentration capable of disturbing the electrical activity of the studied muscles. The method also provided an indirect evaluation of electrolyte movements across muscle membrane in vivo in humans. Dystrophic myotonic muscles appeared highly sensitive to extracellular potassium and, unlike normal muscles, were unable to accumulate potassium-induced muscle hyperexcitability and favored electrolyte accumulation in dystrophic myotonic muscles. The stabilizing effect of taurine is discussed in relation to its ability to increase intracellular potassium concentration, membrane conductance, or both.
Plasma and platelet taurine are reduced in subjects with insulin-dependent diabetes mellitus: effects of taurine supplementation.
Am J Clin Nutr, 61(5):1115-9 1995 May
Plasma and platelet taurine concentrations were assayed in 39 patients with insulin-dependent diabetes mellitus (IDDM) and in 34 control subjects matched for age, sex, and both total and protein-derived daily energy intake. Platelet aggregation induced by arachidonic acid in vitro at baseline and after oral taurine supplementation (1.5 g/d) for 90 d was also studied. Plasma and platelet taurine concentrations (mean +/- SEM) were lower in diabetic patients (65.6 +/- 3.1 mumol/L, or 0.66 +/- 0.07 mol/g protein) than in control subjects (93.3 +/- 6.3 mumol/L, or 0.99 +/- 0.16 mol/g protein, P < 0.01). After oral supplementation, both plasma and platelet taurine concentrations increased significantly in the diabetic patients, reaching the mean values of healthy control subjects. The effective dose (mean +/- SEM) of arachidonic acid required for platelets to aggregate was significantly lower in diabetic patients than in control subjects (0.44 +/- 0.07 mmol compared with 0.77 +/- 0.02 mmol, P < 0.001, whereas after taurine supplementation it equaled the mean value for healthy control subjects (0.72 +/- 0.04 mmol). In in vitro experiments, taurine reduced platelet aggregation in diabetic patients in a dose-dependent manner, whereas 10 mmol taurine/L did not modify aggregation in healthy subjects.
Taurine in human milk: growth modulator or conditionally essential amino acid?
J Pediatr Gastroenterol Nutr, 2 Suppl 1(Suppl 1):S266-71 1983
Deficiency of this ubiquitous and abundant small molecule, which is not metabolized under ordinary circumstances, can cause retinal damage not only in the cat but also in the monkey and in man. Its deficiency also is capable of producing growth retardation in the monkey. It seems prudent, therefore, to examine this problem further in order better to understand the role of such growth modulators in infant nutrition. This may be especially so in countries such as India where the vegetarian diet, one which is low in taurine because of the relatively small amounts of taurine in most plants (7), might prove of particular importance.
Effect of taurine on the fatty liver of children with simple obesity.
Adv Exp Med Biol, 403(Obinata K):607-13 1996
This study elucidated the effect of taurine on fatty liver in simple obesity. Taurine was orally administered to 10 children with fatty liver. During taurine administration, the CT numbers of the liver, which were low in the beginning, increased. Serum ALT levels were improved, especially in those children whose weight was well controlled. Even in those who failed in weight control, serum ALT levels were slightly recovered. Ratios of glycine/taurine-conjugated bile acids were decreased. Thus, taurine was effective in treating fatty liver of children with simple obesity regardless of the success/failure of weight control. Taurine administration is considered to be helpful as an adjuvant therapy for fatty liver.
Taurine supplementation prevents hyperaminoacidemia in growing term infants fed high-protein cow's milk formula.
Acta Paediatr, 403(12):1403-7 1996 Dec
Blood urea nitrogen (BUN) and plasma and urine amino acid concentrations were compared between three cohorts of healthy growing term infants who were breast-fed (BF) or randomly assigned to one of two formulas either taurine non-supplemented (FF) or taurine supplemented (FF + T). The infants were studied from 2 to 12 weeks of age. Weight gain and growth in length was normal and similar in all three feeding groups during the study interval. At 12 weeks BUN was significantly higher in the FF group than in the BF and FF + T groups, 16.5 mg/dl vs 7.0 and 7.3 mg/dl, respectively. Total plasma amino acids (FF group: 240.5 +/- 110.1 mumoles/dl; BF group 180.1 +/- 28.7 mumoles/dl; FF + T group: 182.3 +/- 89.4 mumoles/dl) and total essential amino acids (FF group: 89.8 +/- 37.3 mumoles/dl; BF group: 56.1 +/- 16.3 mumoles/dl; FF + T group: 53.0 +/- 24.2 mumoles/dl). The urine amino acid concentrations reflected the plasma levels in all groups. These results indicate that taurine supplementation to a high protein formula lowers BUN levels and the plasma urine amino acid concentrations by some yet unknown mechanism to concentrations similar to those found in breast-fed infants with a much lower protein intake.
Protective effect of taurine on hypoxia and reoxygenation-induced damage of human colon cells (HT 29).
Adv Exp Med Biol, 403(213-22):213-22 1996
In this experimental model, taurine administered during hypoxia markedly reduced the cell damage due to O2 deficiency, and the beneficial effect outlasted the period of reoxygenation. The mechanisms for the improved survival rates are postulated to be a reduced osmoregulatory disturbance of cellular integrity, improved Ca2+ homeostasis and induction of accelerated cellular growth processes. In our simplified cell culture model the UW solution seems to be the most appropriate solution for the cold (hypoxic) preservation of human colon cells. We conclude, that within this experimental model and under these experimental conditions, taurine supplementation of the conventionally used preservation solutions improved the solutions markedly. Considering our previous studies, taurine seems to be a potent endogenous protective agent against cellular deterioration due to hypoxia and reoxygenation.
Protective effect of taurine on indomethacin-induced gastric mucosal injury.
Adv Exp Med Biol, 403(-TI-):147-55 1996
It has been suggested that oxygen-derived free radicals play an important role in the pathophysiology of acute gastric ulceration induced by NSAIDs and ischemia-reperfusion. Taurine is hypothesized to exert its protective effect on NSAIDs-induced gastric injury by its antioxidant properties. The protective effect of taurine on indomethacin-induced gastric mucosal lesion and its protective mechanism were investigated. Intragastric administration of 25 mg/kg of indomethacin induced hemorrhagic lesions on the glandular stomach in rats. Pretreatment with 0.25 or 0.5 g/kg of taurine one day before or for 3 days significantly reduced gastric lesion formation and inhibited the elevation of lipid peroxide level in gastric mucosa. Both resting and FMLP-induced luminol-dependent chemiluminescence of rat peritoneal neutrophils increased immediately after treatment with indomethacin. Taurine (5-20 mM) inhibited chemiluminescence of neutrophils activated by FMLP. Human neutrophils (polymorphonuclear leukocytes) adhered to the confluent monolayer of human umbilical vein endothelial cells (HUVEC) after coincubation with indomethacin. This neutrophil adhesion induced by indomethacin to HUVEC was prevented by taurine in a dose-dependent manner. These results indicate that the protective effect of taurine against NSAIDs-induced gastric mucosal injury is due to its antioxidant effect, which inhibits lipid peroxidation and neutrophil activation.
The beneficial effect of taurine on the prevention of human endothelial cell death.
Shock, 6(5):331-8 1996 Nov
This study was designed to test the hypothesis that the antioxidant taurine may modulate human endothelial cell (EC) death (apoptosis versus necrosis). Sodium arsenite (80 microM) alone and in combination with tumor necrosis factor-alpha (25 ng/mL) caused EC apoptosis after 24 h of treatment. Taurine (.5 mg/mL) added at 0 and 6 h could significantly attenuate EC apoptosis, and oxidative state in response to lipopolysaccharide and tumor necrosis factor-alpha stimulation. EC necrosis was induced by activated neutrophils (PMNs). Taurine reduced PMN-mediated EC necrosis in a dose-dependent manner. Moreover, treatment of ECs with a calcium ionophore, A23187 (1.0-4.0 microM), resulted in both EC apoptosis and necrosis. Taurine significantly abrogated A23187-mediated intracellular calcium elevation and EC death. These data indicate that taurine, possibly through its antioxidant activity and regulation of intracellular calcium flux, can prevent EC dysfunction and cell death, which may have implications for the application of this amino acid in the amelioration of acute lung injury during systemic inflammatory response syndrome.
Evidence of taurine depletion and accumulation of cysteinesulfinic acid in chronic dialysis patients.
Kidney Int, 6(5):1713-7 1996 Nov
Methionine, taurine and cysteinesulfinic acid (CSA) were determined by reversed-phase high-performance liquid chromatography (RP-HPLC) in plasma from ten patients treated with hemodialysis (HD) and eight patients treated with continuous ambulatory peritoneal dialysis (CAPD). The patients' data were compared with data obtained from ten healthy controls. Significant reductions in plasma taurine levels were observed in the HD patients (34 +/- 13 mumol/liter, mean +/- SD) and the CAPD patients (47 +/- 12 mumol/liter) compared to the controls (66 +/- 5 mumol/liter), while the CSA levels were markedly higher in the HD patients (9.1 +/- 2.8 mumol/liter) and the CAPD patients (9.1 +/- 2.4 mumol/liter) than in the controls (0.79 +/- 0.15 mumol/liter). A single HD treatment significantly reduced the plasma taurine and CSA concentrations (P < 0.01 and P < 0.001), respectively. The plasma methionine levels were normal in both patient groups. The finding of a low plasma taurine level and a large accumulation of CSA suggests that the metabolic conversion of CSA to taurine is impaired in uremic patients and this metabolic abnormality may cause taurine depletion.
Antioxidant dietary status and genetic cardiovascular risk, or how an adequate intake of a-tocopherol, selenium, taurine, magnesium and various other natural antioxidants may overcome the deleterious metabolic consequences related to the E4-4 type of apolipoprotein E [editorial]
Magnes Res, 6(5):139-41 1996 Jun
Effects of taurine on depletion of erythrocyte membrane Na-K ATPase activity due to ozone exposure or cholesterol enrichment.
J Nutr Sci Vitaminol (Tokyo), 6(6):627-34 1995 Dec
The objective of this study was to investigate the interrelationship between taurine and erythrocyte-membrane Na-K ATPase activity. A comparison was conducted to test whether taurine or uric acid (a water-soluble scavenger of free radicals) prevents or recovers the depletion in membrane ouabain-sensitive Na-K ATPase activity resulting from ozone exposure or cholesterol enrichment of the erythrocyte membrane. A depletion of 44% and 27% in ouabain-sensitive Na-K ATPase activity was respectively caused by ozone exposure and cholesterol enrichment. Taurine as well as uric acid partially prevented the activity loss from ozone exposure. In addition, taurine at high concentrations (from 1.5 to 4.5 mM) restored the depletion of erythrocyte-membrane Na-K ATPase activity due to ozone exposure and prevented the depletion of the enzyme activity due to cholesterol enrichment. In contrast, although the same high concentrations were used, uric acid failed to show either of the above effects. These results suggest that taurine acts (1.5-4.5 mM) polyvalently as not only an antioxidizing agent but also as a membrane stabilizer to maintain the functions of membrane Na-K ATPase, a membrane-bound protein.
Complementary vascular-protective actions of magnesium and taurine: a rationale for magnesium taurate.
Med Hypotheses, 6(2):89-100 1996 Feb
By a variety of mechanisms, magnesium functions both intracellularly and extracellularly to minimize the cytoplasmic free calcium level, [Ca2+]i. This may be the chief reason why correction of magnesium deficiency, or induction of hypermagnesemia by parenteral infusion, exerts antihypertensive, anti-atherosclerotic, anti-arrhythmic and antithrombotic effects. Although the amino acid taurine can increase systolic calcium transients in cardiac cells (and thus has positive inotropic activity), it has other actions which tend to reduce [Ca2+]i. Indeed, in animal or clinical studies, taurine lowers elevated blood pressure, retards cholesterol-induced atherogenesis, prevents arrhythmias and stabilizes platelets--effects parallel to those of magnesium. The complex magnesium taurate may thus have considerable potential as a vascular-protective nutritional supplement, and might also be administered parenterally, as an alternative to magnesium sulfate, in the treatment of acute myocardial infarction as well as of pre-eclampsia. The effects of magnesium taurate in diabetes deserve particular attention, since both magnesium and taurine may improve insulin sensitivity, and also may lessen risk for the micro- and macrovascular complications of diabetes.
Taurine in pediatric nutrition.
Pediatr Clin North Am, 6(4):879-97 1995 Aug
The past 20 years have seen the status of taurine change from an end product of methionine and cysteine metabolism and substance conjugated to bile acids to that of an important, and sometimes essential, nutrient. It is now added to most synthetic human infant formulas and pediatric parenteral solutions throughout the world. This article describes the research that led to this end.
Taurine in development.
J Nutr, 118(10):1169-76 1988 Oct
Taurine is a ubiquitous dietary constituent of most mammals and is present in especially high concentrations in the tissues of developing mammals. Research to date indicates that taurine plays an important role in the development of the nervous system and the process of migration in particular. It is speculated that taurine uptake and release, in conjunction with glutamate uptake and release, may represent one form of communication between neurons and glial cells. The need of taurine by the body is emphasized by the ability of the kidney to curtail taurine excretion to conserve taurine in the face of a low dietary taurine intake. The evidence for a special role of taurine in development is considered and discussed.
Taurine: an overview of its role in preventive medicine.
Prev Med, 18(1):79-100 1989 Jan
Taurine (2-aminoethanesulfonic acid), well known for its role in bile salt synthesis, is also involved in a number of crucial physiological processes including modulation of calcium flux and neuronal excitability, osmoregulation, detoxification, and membrane stabilization. With the exception of cow's milk, taurine is widely distributed in foods from many animal, but not plant, sources. Although taurine is synthesized from sulfur-containing amino acids, concern has been expressed about the adequacy of endogenous sources, especially in neonates. Accordingly, proprietary milk formulas are now supplemented with taurine. Retinal dysfunction occurs in taurine-deficient animals. A milder form of this condition has been observed in children on long-term total parenteral nutrition. Preliminary evidence suggests a possible role for taurine administration in congestive heart disease, acute hepatitis, cystic fibrosis, and myotonia. Further studies are required before taurine can be routinely advocated for use in these and other disorders. Recent discoveries concerning taurine's role in cellular proliferation and membrane protection underscore its physiological significance. In this context, taurine's interaction with other nutrients, biochemicals, and xenobiotics warrants extensive exploration. As a conditionally essential nutrient, taurine has several important preventive medical applications.
The treatment of myotonia: evaluation of chronic oral taurine therapy.
Neurology, 33(5):599-603 1983 May
A double-blind, single crossover study of chronic oral taurine administration versus placebo was conducted on nine patients with dystrophia myotonica. The severity of myotonia was assessed by clinical and electromyographic criteria and by testing the sensitivity of myotonic muscles to the intra-arterial infusion of potassium chloride. Confirming the antimyotonic effect of acute parenteral taurine, chronic treatment induced significant improvement of myotonia and a decreased sensitivity to the arterial potassium load as well as an enhancement of electrolyte movements across the membrane of the studied muscles. No significant side effects were noted.
Protective effect of taurine, zinc and tocopherol on retinol-induced damage in human lymphoblastoid cells.
J Nutr, 114(12):2256-61 1984 Dec
Cultured human lymphoblastoid cells exposed for short times to retinol and retinoic acid, undergo a time- and dose-dependent decrease in viability, accompanied by cell swelling. The presence of taurine (5-20 mM) and zinc (50-100 microM) protected cells from retinol-induced injury. Taurine 20 mM and zinc 100 microM added simultaneously abolished cell swelling and increased cell viability from 7 to 55%. Tocopherol (200 microM) was also effective in protecting these cells from retinol. The three compounds together afforded complete protection. The effects of retinol and of taurine, zinc or tocopherol seem to be unrelated to lipid peroxidation. A membrane stabilizer action is proposed as the mechanism underlying the protective effect of taurine and zinc or of tocopherol.
Therapy of congestive heart failure with orally administered taurine.
Clin Ther, 5(4):398-408 1983
The clinical efficacy of 2 gm BID of oral taurine (2-aminoethane sulfonic acid) was studied in 24 patients with congestive heart failure (CHF). We expressed the severity of CHF by a score based on clinical signs and symptoms and on roentgenographic data. The maximum possible score, corresponding to the worst CHF, was 23 points. How much the 24 patients improved after receiving taurine for four or eight weeks was estimated by the difference between their pretreatment and posttreatment scores. In 19 of the 24 patients, taurine was effective. In the group as a whole, mean (+/- SEM) scores fell significantly, from 7.3 +/- 0.6 before treatment to 4.4 +/- 0.5 after treatment. Thirteen of the 15 patients who were designated as New York Heart Association (NYHA) functional class III or IV before receiving taurine could be designated as class II after they completed the study. This pilot study should prompt further investigation into the possible use of taurine in the treatment of patients with CHF.
Taurine: retinal function.
Brain Res Brain Res Rev, 16(2):151-69 1991 May-Aug
The status and potential functions of taurine in the retina have been reviewed. Taurine is present in high concentrations in the retina of all species tested, while the retinal concentrations of the enzymes necessary to synthesize taurine are presumed to vary among those species. The documented low activity of cysteinesulfinic acid decarboxylase, a key enzyme in taurine biosynthesis, in the livers of the cat, monkey and human possibly reflect low activity in their retinas, indicating reliance on the diet as an important source of taurine. Both high- and low-affinity binding proteins and uptake systems have been described for taurine in retinal tissue. Evoked release of taurine by light and other depolarizing stimuli have been well documented. Retinal pathologies including diminished ERGs and morphologic changes have been reported for animals and man deficient in taurine. Possible functions for taurine in the retina include: (1) protection of the photoreceptor - based on the shielding effects of taurine on rod outer segments exposed to light and chemicals; (2), regulation of Ca2+ transport - based on the modulatory effects of taurine on Ca2+ fluxes in the presence and absence of ATP; and (3) regulation of signal transduction - based on the inhibitory effects of taurine on protein phosphorylation.
Myocardial failure in cats associated with low plasma taurine: a reversible cardiomyopathy.
Science, 237(4816):764-8 1987 Aug 14
Thousands of pet cats die each year with dilated cardiomyopathy, the cause of which is unknown. Although taurine is present in millimolar concentrations in the myocardium of all mammals, taurine depletion has not previously been associated with a decrease in myocardial function in any species. In this study, low plasma taurine concentrations associated with echocardiographic evidence of myocardial failure were observed in 21 cats fed commercial cat foods and in 2 of 11 cats fed a purified diet containing marginally low concentrations of taurine for 4 years. Oral supplementation of taurine resulted in increased plasma taurine concentrations and was associated with normalization of left ventricular function in both groups of cats. Since myocardial concentrations of taurine are directly related to plasma concentrations and low plasma concentrations were found to be associated with myocardial failure in cats, a direct link between decreased taurine concentration in the myocardium and decreased myocardial mechanical function is proposed.
Effects of increased adrenomedullary activity and taurine in young patients with borderline hypertension.
Circulation, 75(3):525-32 1987 Mar
Recent studies showed that taurine, a sulphonic amino acid, could decrease blood pressure and increase sympathoadrenal tone in DoCA-salt-treated hypertensive rats. To determine whether taurine exerts its antihypertensive action in man in a similar fashion, we studied the effect of oral administration of taurine (6 g for 7 days) on blood pressure and plasma catecholamines in 19 young patients with borderline hypertension in a double-blind, placebo-controlled fashion. Systolic blood pressure in the 10 patients who were treated with taurine decreased by 9.0 +/- 2.9 mm Hg (mean +/- SE; p less than .05 by paired t test), compared with a 2.7 +/- 2.3 mm Hg decrease (NS) in the nine patients treated with placebo and diastolic blood pressure in the taurine-treated patients decreased by 4.1 +/- 1.7 mm Hg (p less than .05) compared with 1.2 +/- 3.0 mm Hg (NS) in the placebo-treated subjects. In the patients receiving taurine plasma epinephrine (E) decreased significantly, with a negligible decrease in plasma norepinephrine (NE). The effect of taurine on plasma catecholamines and the response of plasma E after the stimulation with glucagon was also studied in 12 borderline hypertensive and nine age-matched normotensive subjects. Basal plasma E was significantly higher in borderline hypertensive than in normal subjects, but basal plasma NE did not differ in the two groups.
The role of taurine in infant nutrition.
Adv Exp Med Biol, 442():463-76 1998
The importance of taurine in the diet of pre-term and term infants has not always been clearly understood and is a topic of interest to students of infant nutrition. Recent evidence indicates that it should be considered one of the "conditionally essential" amino acids in infant nutrition. Plasma values for taurine will fall if infants are fed a taurine-free formula or do not have taurine provided in the TPN solution. Urine taurine values also fall, which is indicative of an attempt by the kidney to conserve taurine. The very-low-birth-weight infant, for a variety of reasons involving the maturation of tubular transport function, cannot maximally conserve taurine by enhancing renal reabsorption and, hence, is potentially at greater risk for taurine depletion than larger pre-term or term infants, and certainly more than older children who have taurine in their diet. Taurine has an important role in fat absorption in pre-term and possibly term infants and in children with cystic fibrosis. Because taurine-conjugated bile acids are better emulsifiers of fat than glycine-conjugated bile acids, the dietary (or TPN) intake has a direct influence on absorption of lipids. Taurine supplementation of formulas or TPN solutions could potentially serve to minimize the brain phospholipid fatty acid composition differences between formula-fed and human milk-fed infants. Taurine appears to have a role in infants, children, and even adults receiving most ( 75%) of their calories from TPN solutions in the prevention of granulation of the retina and electroencephalographic changes. Taurine has also been reported to improve maturation of auditory-evoked responses in pre-term infants, although this point is not fully established. Clearly, taurine is an important osmolyte in the brain and the renal medulla. At these locations, it is a primary factor in the cell volume regulatory process, in which brain or renal cells swell or shrink in response to osmolar changes, but return to their previous volume according to the uptake or release of taurine. While there is a dearth of clinical studies in man concerning this volume regulatory response, studies in cats, rats, and dog kidney cells indicate the protective role of taurine in hyperosmolar stress. The infant depleted of taurine may not be able to respond to hyper- or hyponatremic stress without massive changes in neuronal volume, which has obvious clinical significance. The fact that the brain content of taurine is very high at birth and falls with maturation may be a protective feature, or compensation for renal immaturity Defining an amino acid as "conditionally essential" requires that deficiency result in a clinical consequence or consequences which can be reversed by supplementation. In pre-term and term infants, taurine insufficiency results in impaired fat absorption, bile acid secretion, retinal function, and hepatic function, all of which can be reversed by taurine supplementation. Therefore, this small beta-amino acid, taurine, is indeed conditionally essential.
Nutritional requirement for taurine in patients receiving long-term parenteral nutrition.
N Engl J Med, 312(3):142-6 1985 Jan 17
Animals fed diets lacking the amino acid taurine have low plasma and tissue levels of taurine and ultimately have retinal dysfunction. Since parenteral nutrition does not ordinarily provide taurine, we looked for evidence of taurine deficiency in 21 children and 23 adults undergoing long-term parenteral nutrition at home for an average of 27 +/- 23 (S.D.) months. The fasting plasma taurine level was reduced in children as compared with controls (26 +/- 13 vs. 57 +/- 16 mumol per liter, P less than 0.001). In adults with less than 25 per cent intestinal absorption of the recommended caloric intake, the plasma taurine level was also significantly reduced and correlated inversely with the duration of parenteral nutrition. Electroretinograms were abnormal in each of eight children who were examined. Addition of taurine to the intravenous solutions restored plasma levels to normal in four children; the electroretinograms of three of these children also became normal. The plasma taurine level became abnormally low again in two of three children one year after the intravenous taurine was discontinued. We conclude that children and possibly adults receiving long-term parenteral nutrition have a nutritional requirement for taurine.
Rapid isolation of muscle and heart mitochondria, the lability of oxidative phosphorylation and attempts to stabilize the process in vitro by taurine, carnitine and other compounds.
Mol Cell Biochem, 312(1-2):61-6 1997 Sep
We modified the isolation procedure of muscle and heart mitochondria. In human muscle, this resulted in a 3.4 fold higher yield of better coupled mitochondria in half the isolation time. In a preparation from rat muscle we studied factors that affected the stability of oxidative phosphorylation (oxphos) and found that it decreased by shaking the preparation on a Vortex machine, by exposure to light and by an increase in storage temperature. The decay was found to be different for each substrate tested. The oxidation of ascorbate was most stable and less sensitive to the treatments. When mitochondria were stored in the dark and the cold, the decrease in oxidative phosphorylation followed first order kinetics. In individual preparations of muscle and heart mitochondria, protection of oxidative phosphorylation was found by adding candidate stabilizers, such as desferrioxamine, lazaroids, taurine, carnitine, phosphocreatine, N-acetylcysteine. Trolox-C and ruthenium red, implying a role for reactive oxygen species and calcium-ions in the in vitro damage at low temperature to oxidative phosphorylation. In heart mitochondria oxphos with pyruvate and palmitoylcarnitine was most labile followed by glutamate, succinate and ascorbate. We studied the effect of taurine, hypotaurine, carnitine, and desferrioxamine on the decay of oxphos with these substrates. 1 mM taurine (n = 6) caused a significant protection of oxphos with pyruvate, glutamate and palmitoylcarnitine, but not with the other substrates. 5 mM L-carnitine (n = 6), 1 mM hypotaurine (n = 3) and 0.1 mM desferrioxamine (n = 3) did not protect oxphos with any of the substrates at a significant level. These experiments were undertaken in the hope that the in vitro stabilizers can be used in future treatment of patients with defects in oxidative phosphorylation.
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