Physiological actions of taurine

Background: Experimental models and observational studies suggest that vitamin E supplementation may prevent cardiovascular disease and cancer. However, several trials of high-dosage vitamin E supplementation showed non–statistically significant increases in total mortality. Purpose: To perform a meta-analysis of the dose–response relationship between vitamin E supplementation and total mortality by using data from randomized, controlled trials. Patients: 135 967 participants in 19 clinical trials. Of these trials, 9 tested vitamin E alone and 10 tested vitamin E combined with other vitamins or minerals. The dosages of vitamin E ranged from 16.5 to 2000 IU/d (median, 400 IU/d). Data Sources: PubMed search from 1966 through August 2004, complemented by a search of the Cochrane Clinical Trials Database and review of citations of published reviews and metaanalyses. No language restrictions were applied. Data Extraction: 3 investigators independently abstracted study reports. The investigators of the original publications were contacted if required information was not available. Data Synthesis: 9 of 11 trials testing high-dosage vitamin E (>400 IU/d) showed increased risk (risk difference > 0) for allcause mortality in comparisons of vitamin E versus control. The pooled all-cause mortality risk difference in high-dosage vitamin E trials was 39 per 10 000 persons (95% CI, 3 to 74 per 10 000 persons; P 0.035). For low-dosage vitamin E trials, the risk difference was 16 per 10 000 persons (CI, 41 to 10 per 10 000 persons; P > 0.2). A dose–response analysis showed a statistically significant relationship between vitamin E dosage and all-cause mortality, with increased risk of dosages greater than 150 IU/d. Limitations: High-dosage (>400 IU/d) trials were often small and were performed in patients with chronic diseases. The generalizability of the findings to healthy adults is uncertain. Precise estimation of the threshold at which risk increases is difficult. Conclusion: High-dosage (>400 IU/d) vitamin E supplements may increase all-cause mortality and should be avoided.

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Meta-Analysis: High-Dosage Vitamin E Supplementation May Increase All-Cause Mortality

Lang, Florian, Gillian L. Busch, Markus Ritter, Harald Volkl, Siegfried Waldegger, Erich Gulbins, and Dieter Haussinger. Functional Significance of Cell Volume Regulatory Mechanisms. Physiol. Rev. ...

Functional Significance of Cell Volume Regulatory Mechanisms

Astrocytes become activated (reactive) in response to many CNS pathologies, such as stroke, trauma, growth of a tumor, or neurodegenerative disease. The process of astrocyte activation remains rather enigmatic and results in so-called "reactive gliosis," a reaction with specific structural and functional characteristics. In stroke or in CNS trauma, the lesion itself, the ischemic environment, disrupted blood-brain barrier, the inflammatory response, as well as in metabolic, excitotoxic, and in some cases oxidative crises--all affect the extent and quality of reactive gliosis. The fact that astrocytes function as a syncytium of interconnected cells both in health and in disease, rather than as individual cells, adds yet another dimension to this picture. This review focuses on several aspects of astrocyte activation and reactive gliosis and discusses its possible roles in the CNS trauma and ischemia. Particular emphasis is placed on the lessons learnt from mouse genetic models in which the absence of intermediate filament proteins in astrocytes leads to attenuation of reactive gliosis with distinct pathophysiological and clinical consequences.

Astrocyte activation and reactive gliosis

The ability to control cell volume is pivotal for cell function. Cell volume perturbation elicits a wide array of signaling events, leading to protective (e.g., cytoskeletal rearrangement) and adap...

Physiology of cell volume regulation in vertebrates.

Free amino acids of chicken and rat retina.

Taurine protection of lymphoblastoid cells from iron-ascorbate induced damage.

https://www.amjmed.com/article/S0002-9343(06)00488-8/pdf

Mechanisms of Cell Volume Regulation in Hypo-osmolality

Cultured astrocytes superfused with isosmotic solutions containing high concentrations of potassium, i.e., 25, 56, 75, and 100 mM, showed a proportional increase in cell volume corresponding to 25, 36, 57, and 75% greater than the cell volume in physiological solutions. This volume increase was abolished in low chloride or hypertonic solutions. The release of 3H-taurine previously accumulated by astrocytes was stimulated by potassium at all concentrations examined. During 4-minute exposure to 25, 56, 75, or 100 mM of potassium, cells released 13.5, 15.6, 20.2, or 36.2%, respectively, of the total labeled taurine accumulated during the preloading period. The potassium-stimulated release of 3H-taurine was calcium-independent and insensitive to BaCl2 and bumetanide. Substitution of chloride by gluconate to concentrations necessary to maintain the K+ X Cl- product constant abolished the potassium-stimulated release of 3H-taurine. Superfusion with solutions made hypertonic with sucrose also decreased the potassium-elicited efflux of 3H-taurine. In both conditions, the depolarizing effect of potassium measured with 3H-TPP+ was unchanged. High potassium concentrations and hyposmotic solutions released 3H-taurine by a nonadditive mechanism. These results indicate that in cultured astrocytes high concentrations of potassium produce both swelling and depolarization, but only swelling elicits the release of taurine. These observations suggest an involvement of taurine in cell-volume regulation in astrocytes.

Herminia Pasantes-Morales

Papers

Free amino acids of chicken and rat retina.

Taurine protection of lymphoblastoid cells from iron-ascorbate induced damage.

Mechanisms of Cell Volume Regulation in Hypo-osmolality

Release of taurine from astrocytes during potassium-evoked swelling.

Taurine and hypotaurine inhibit light-induced lipid peroxidation and protect rod outer segment structure.