Parkinsonism developed later, and respiratory failure occurred terminally. Sleep disturbances, exhaustion, and marked weight loss were features. The earliest and most prominent symptom was mental depression not responsive to antidepressant drugs or electroconvulsive therapy. Symptoms began late in the fifth decade in 6 affected persons and death occurred after 4 to 6 years. OMIM 168605, an unusual neuropsychiatric disorder inherited in an autosomal dominant fashion through 3 generations of a family.If molybdenum is deficient, uric acid levels are reduced, xanthine is increased and aldehyde detoxification is impaired (aldehyde intolerance). In this condition, there is increased urinary sulfites and decreased sulfates. The uncommon condition of overall taurine excess (hypertaurinuria with hypertyrosinemia) usually is an insufficiency of sulfite oxidase activity, possibly due to molybdenum deficiency.Renal wasting of taurine can be medically significant if it affects one or more of taurine many important functions. In molybdenum deficiency or sulfite oxidase impairment, elevated urine taurine results as a mode of sulfur excretion. Wasting can also occur when the similarly-structured amino acid beta-alanine is elevated or is present in kidney tubules. Urinary wasting can be secondary to generally increase renal clearance or nephrotic syndromes.Magnesium deficiency may cause fatigue, depression, muscle tremor, and hypertension. Urinary magnesium wasting can result from taurine insufficiency. Increased resistance to aggregation of blood platelets and decreased thromboxane release if aggregation does occur. Deficient taurine may result in increased cellular calcium and sodium and reduced magnesium. Mediation of the flux of electrolyte elements at the plasma membrane of cells. Conjugation of cholesterol (as cholylcoenzyme A) to form taurocholic acid, an important component of bile and a major utilization of cholesterol.Therapeutic applications of taurine to eye disease are likely to be forthcoming. Taurine deficiency in experimental animals produces degeneration of light-sensitive cells. Low levels of taurine are found in retinitis pigmentosa.It is often difficult to distinguish compensatory changes in human biochemistry from true metabolic or deficiency disease. One reason that the findings are not entirely clear is that taurine is often elevated in the blood of epileptics who need it. Taurine levels have been found to decrease significantly in many depressed patients.Cysteine and B6 are the nutrients most directly involved in taurine synthesis. The amino acids alanine and glutamic acid, as well as pantothenic acid, inhibit taurine metabolism while vitamins A and B6, zinc, and manganese help build taurine. Taurine in the brain is usually associated with zinc or manganese.Acts as a neurotransmitter that inhibits anxiety. Xenobiotic chemicals including aldehydes, alcohols, amines, petroleum solvents, and chlorine or chloride (bleach).Taurine scavenges excess hypochlorite ion, OCl-, in leukocytes and facilitates effective phagocytosis by enhancing survival of leukocytes.ĭeficient taurine may lead to an increased inflammatory response to:.Taurine has many diverse biological functions serving as a neurotransmitter in the brain, a stabilizer of cell membranes and a facilitator in the transport of ions such as sodium, potassium, calcium, and magnesium.Adults can synthesize their own taurine, yet are probably depends in part on dietary taurine.Taurine is an essential amino acid in pre-term and newborn infants of humans and many other species.It is a lesser-known amino acid because it is not incorporated into the structural building blocks of protein.Taurine is a sulfur amino acid like methionine, cystine, cysteine, and homocysteine.Taurine is one of the few known naturally occurring sulfonic acids. Taurine is a derivative of the sulfur-containing (sulfhydryl) amino acid, cysteine.It is the most abundant found in the heart. For normal functioning of the heart, brain, gallbladder, breast, kidney, eyes and vascular system.
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