Taurine Decreases Lesion Severity In the Hearts of Cardiomyopathy Hamsters

Azari, Jamshid; Brumbaugh, P. F.; Barbeau, A.; Huxtable, Ryan J.

doi:10.1017/s0317167100023027

Cited by 18 publications

(10 citation statements)

References 20 publications

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“…Taurine also prevents myocardial necrotic lesions associated with calcium overload [45][46][47]. Accumulation of 45Ca by retinal subcellular fractions isolated from the chick retina was decreased when taurine was present in the incubation medium [48].…”

Section: Discussionmentioning

confidence: 99%

The mechanism of neuronal resistance and adaptation to hypoxia

Schurr

Rigor

1987

FEBS Letters

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In this work we provide a theoretical explanation for the observations that: (i) young animals are more resistant to hypoxia than adult ones and (ii) repeated exposure to a hypoxic insult increases the tolerance of young animals and isolated brain tissue to that insult. Considered here is the role of taurine, a putative Ca 2+ transport modulator, in attenuating Ca 2+ influx and overload in brain tissue upon hypoxia. It is proposed that the higher resistance of young animals to hypoxia stems from their higher brain content of taurine as compared with adults. The increased resistance to lack of oxygen upon re-exposure to hypoxia may occur as a result of protein and coenzyme A (CoA) breakdown which leads to the accumulation of products like cystine, cysteine, cysteamine and other sulfur-containing compounds. Upon reoxygenation, these compounds are oxidized to form taurine, which in turn attenuates neuronal Ca 2+ accumulation. The sulfurcontaining compounds are considered to be natural scavengers of oxygen-derived free radicals which are formed upon reoxygenation and have been implicated as a major component in the process leading to ischemic/hypoxic brain damage. Repeated hypoxic insults bring about the formation of higher levels of taurine and hence the observed adaptation to oxygen lack. The hypothesis presented here is supported by experimental observations in our laboratory and those of others.

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Section: Discussionmentioning

confidence: 99%

The mechanism of neuronal resistance and adaptation to hypoxia

Schurr

Rigor

1987

FEBS Letters

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“…Studies of animal models have found that orally administered taurine significantly reduces myocardial damage induced by the calcium paradox, doxorubicin, isoproterenol, or in hamster cardiomyopathy [61,62]. It has also been found to increase survival in rabbits with aortic insufficiency [63] and to have a protective effect in the murine model of iron overload cardiomyopathy [64].…”

Section: Taurine and The Regulation Of Intracellular Calciummentioning

confidence: 99%

The management of conditioned nutritional requirements in heart failure

2006

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Patients suffering from congestive heart failure exhibit impaired myocardial energy production, myocyte calcium overload and increased oxidative stress. Nutritional factors known to be important for myocardial energy production, calcium homeostasis and the reduction of oxidative stress, such as thiamine, riboflavin, pyridoxine, L-carnitine, coenzyme Q10, creatine and taurine are reduced in this patient population. Furthermore, deficiencies of taurine, carnitine, and thiamine are established primary causes of dilated cardiomyopathy. Studies in animals and limited trials in humans have shown that dietary replacement of some of these compounds in heart failure can significantly restore depleted levels and may result in improvement in myocardial structure and function as well as exercise capacity. Larger scale studies examining micronutrient depletion in heart failure patients, and the benefits of dietary replacement need to be performed. At the present time, it is our belief that these conditioned nutritional requirements, if unsatisfied, contribute to myocyte dysfunction and loss; thus, restoration of nutritional deficiencies should be part of the overall therapeutic strategy for patients with congestive heart failure.

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“…Hypertrophic cardiomyopathy is a disease of unknown etiology which is characterized by cardiac hypertrophy and disarrays of myocardial fiber and fibrils (1,2). Although half of the patients with hypertrophic cardiomyopathy show an apparent family history, and mutations in the ␤-myosin heavy chain gene have been identified in these patients (2)(3)(4), the molecular and genetic bases of the disease remain unclear.…”

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confidence: 99%

Opioid Peptide Gene Expression in the Primary Hereditary Cardiomyopathy of the Syrian Hamster

Ventura

Pintus

Fiori

et al. 1997

Journal of Biological Chemistry

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Prodynorphin gene expression was investigated in adult ventricular myocytes isolated from normal (F1B) or cardiomyopathic (BIO 14.6) hamsters. Prodynorphin mRNA levels were higher in cardiomyopathic than in control myocytes and were stimulated by treatment of control cells with the protein kinase C (PKC) activator 1,2-dioctanoyl-sn-glycerol. Both chelerythrine and calphostin C, two PKC inhibitors, abolished the stimulatory effect of the diglyceride and significantly reduced prodynorphin gene expression in cardiomyopathic myocytes. Nuclear run-off experiments indicated that the prodynorphin gene was regulated at the transcriptional level and that treatment of nuclei isolated from control cells with 1,2-dioctanoyl-sn-glycerol increased prodynorphin gene transcription, whereas chelerythrine or calphostin C abolished this transcriptional effect. Direct exposure of nuclei isolated from cardiomyopathic myocytes to these inhibitors markedly down-regulated the rate of gene transcription. The expression of PKC-␣, -␦, and -⑀, as well as PKC activity, were increased in nuclei of cardiomyopathic myocytes compared with nuclei from control cells. The levels of both intracellular and secreted dynorphin B, a biologically active product of the gene, were higher in cardiomyopathic than in control cells and were stimulated or inhibited by cell treatment with 1,2-dioctanoyl-sn-glycerol or PKC inhibitors, respectively.

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Taurine Decreases Lesion Severity In the Hearts of Cardiomyopathy Hamsters

Cited by 18 publications

References 20 publications

The mechanism of neuronal resistance and adaptation to hypoxia

The mechanism of neuronal resistance and adaptation to hypoxia

The management of conditioned nutritional requirements in heart failure

Opioid Peptide Gene Expression in the Primary Hereditary Cardiomyopathy of the Syrian Hamster

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