Role of taurine in organs' dysfunction and in their alleviation

Abstract Taurine, a sulphur amino acid found endogenously in human and in several others. It is significantly in higher concentration in mammals and has a number of physiological and pharmacological actions and also used in the therapy of important organ dysfunctions. It is essential for cat and conditional for humans. A patient on parenteral nutrition (PN) may develop taurine deficiency which may hamper proper growth and development. Taurine biosynthesis is limited to early stages and with advancing of age, synthetic capability further reduced to negligible, providing diet as only alternative source. Most of the marine and meat products generally contains considerable high amount of taurine but it is almost absent in plants, thus vegetarian may constitute a risk group. Its beneficial effects range from cardiotonic to antiprovide the answers [1,2]. Now, we know taurine is essential for cats, and conditionally essential for humans. It is regarded as preventive medicine and also behaves as a vitamin- like molecule. The involvement of taurine to cell welfare started even in the embryonic developmental stage where taurine deficiencies have been linked to various lessons, e.g. cardiomyopathy, retinal degeneration, growth retardation, disease of fetus origin like diabetes, making taurine as an essential amino acid for neonates. Taurine supplementation seems to be working well for neonates on PN [3,4]. However, significance of it is not confined to neonates only, it is further extended to children, adults, and elderly, due to its greater involvement in bile salt formation for reducing some symptoms associated with aging. On the clinical front, taurine utility has been patented for many; to name a few, epilepsy, congestive heart failure, hypertension, anti-alcoholic and antismoking; currently it is a part eye/ear drops, health drinks, antiaging and antidiabetic supplements. Perhaps taurine is the only endogenous biomolecule involved in so many actions to prevent and protect variety of organs, such as brain, eye, heart, and liver. In this mini review, we have tried to see every aspect where taurine has a role. From the Department of Pharmacology, School of Dentistry, Kyung Hee University, Seoul, Korea (Drs. Ramesh C. Gupta and Sung-Jin Kim). Address requests for reprints to: Sung-Jin Kim, Ph.D., Chair, Department of Pharmacology, School of Dentistry, Kyung Hee University, Seoul, KOREA 130-701. Tel. 82-2-961-0868; Fax: 82-2-957-5309 E-mail: convulsant and protection of retina to liver from diseases. Being a constituent of bile salt, taurine also helps in reducing cholesterol content. It helps in alleviating hypertension, too. Taurine has been found to be effective in metabolic diseases like diabetes and metabolic bone diseases. Taurine has special role in preterm neonate care, and so also linked to disease of fetus origin. Apart from its special role in neonates and PN, taurine is a part of combination therapy as a nutritional supplement, in varieties of diseases. As everyone hate to like aging, the happiest addition is that taurine has a role in alleviating aging symptoms. Taurine along with its analogues may provide a hope to cope with this situation. Hence, taurine having this much beneficial action deserves to be compiled and reviewed, yet requires regular update.




Hyperglycemia and neuronal damage in cerebral ischemia and beyond

Abstract The aggravation of cerebral ischemic neuronal damage by preischemic hyperglycemia has been lauded as the proof that lactic acidosis is a major detrimental factor in such damage. This phenomenon has steered clinicians to attenuate blood glucose levels as a means of brain protection against the risk of ischemia during cardiopulmonary bypass surgery and neurosurgical procedures. Researchers who use in vivo models of ischemia have repeatedly confirmed this paradoxical phenomenon where the only energy substrate capable of supporting ATP formation in the absence of oxygen must be avoided. Consequently, lactate, too, acquired a bad reputation among clinicians and researchers alike. The only investigators to defend glucose as a possible neuroprotectant have been those who use in vitro modelevated intraischemic lactic acidosis that exacerbates postischemic brain damage. Several highly cited studies [12- 14] demonstrated that normal preischemic brain levels of glucose fell drastically and those of lactate rose sharply by the end of cerebral ischemia/hypoxia. However, shortly after the onset of reperfusion/reoxygenation, brain glucose levels were significantly higher than the preischemic levels [12,13]. Despite the huge increase in lactate concentration after 10 min of hypoxia, the rate of its efflux from the brain to the venous blood remained unchanged from the very low control levels before hypoxia [12]. The postischemic increase in brain glucose level was accompanied by a rapid decrease in lactate level, termed by the investigators themselves as “lactate utilization” [14]. An oxidative utilization of lactate upon reperfusion would explain such postischemic decline in the monocarboxylate concentration and a concomitant rise in glucose to above its preischemic level [15] as the latter remains mostly unused, at least for a while. Other studies reported similar outcome [16], notwithstanding their claim of providing evidence for a damaging role of lactic acidosis following hyperglycemic ischemia [17]. A closer examination of these studies shows that aerobic lactate utilization had occurred postischemia. Nonetheless, almost a quarter of a century later [18] it was argued that hyperglyce- Brain Attack Research Laboratory, Department of Anesthesiology, University of Louisville School of Medicine, Louisville, KY 40292, USA (Drs Avital Schurr and Ralphiel S. Payne) Address requests for reprints to: Avital Schurr, Ph.D., Brain Attack Research Laboratory, Department of Anesthesiology, University of Louisville School of Medicine, Louisville, KY 40292, USA Tel: 502-852-6544, Fax: 502-852-6056 E-mail: els of ischemia/hypoxia, where the higher the glucose concentration preischemia, the lower the degree of neuronal damage postischemia. Nevertheless, after almost three decades since the inception of the lactic acidosis hypothesis of cerebral ischemia, no direct proof has been presented in its support. Recent studies in our laboratory provide evidence that refutes the lactic acidosis hypothesis of cerebral ischemia and offer a different explanation for the glucose paradox of cerebral ischemia in which hyperglycemia-induced increase in the release of the stress hormone corticosterone, not lactic acidosis, is responsible for the aggravation of the ischemic damage. These studies led us to explore the role of stress hormones in diabetic hyperglycemia and neuropathy.




Central Diabetes Insipidus Complicating Near-Drowning

Central diabetes insipidus (DI) is a very rare sequela of near-drowning. We report this case to add to the limited existing knowledge of this highly unusual complication in this group of patients. A young female rescued from fresh water submersion developed polyuria associated with hypernatremia 4 days after the accident. Desmopressin (DDAVP) was used to control the inappropriate diuresis and stabilize her intravascular volume and tonicity. Despite satisfactory re- sponse to DDAVP, she remained in a comatose state and cardiac arrest supervened 18 days after the accident. Central DI should be considered in near-drowning patients with polyuria, and needs to be treated even in those with a dismal prognosis as this would facilitate the diagnosis of brain death. This might be of relevance to communities and medical institutions where the lawful procurement of human organs in optimal conditions for transplantation is a clinical priority.





For much of medical history, the precise mechanism of sudden cardiac arrest was assumed to be the abrupt cessation of activity in diastole. Not until the nineteenth century was ventricular fibrillation recognized as the causative entity, and not until the late twentieth were practical electrical defibrillators developed for terminating this dysrhythmia. Timely defibrillation is considered by many to be the most important single factor in successful cardiac arrest resuscitation. The likelihood of survival is directly related to the duration of cardiac arrest and the time that elapses before the first defibrillation attempt occurs. Over the past two decades, automatic external defibrillators have been developed and improved to provide more rapid defibrillation for victims of cardiac arrest. Their development has been considered the most important recent advance for improving outcome in out-of-hospital sudden death. The internal microprocessor-based system contained in the automatic defibrillator detects VF and prepares the machine to deliver a shock. It has been recommended that these devices be made available for use by basic rescue responders, lay bystanders with a minimal amount of training, and family members of high-risk patients. Public access defibrillation is increasingly seen as a logical extension of the automatic external defibrillator concept.