Effects of taurine on heart calcium in the cardiomyopathic hamster

McBroom, James; Welty, Joseph D.

doi:10.1016/s0022-2828(77)80061-8

Cited by 65 publications

(12 citation statements)

References 13 publications

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“…These findings confirm and extend previous studies, in which when taurine was given orally for 1 month prior to the appearance of lesions, there was decreased accumulation of calcium by the heart (McBroom and Welty, 1977).…”

Section: -November 1980supporting

confidence: 92%

“…Such conformational changes result in alteration in ion flux and cation affinity. Thus, McBroom and Welty (1977) have shown taurine to decrease calcium overload in cardiomyopathic hamsters. This work is designed to establish the site for calcium overload, the involvement of other ions beside calcium in the cardiomyopathy, and the effect of taurine in controlling calcium overload and necrotic lesion severity in advance stages of cardiomyopathy.…”

Section: Introductionmentioning

confidence: 98%

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Taurine Decreases Lesion Severity In the Hearts of Cardiomyopathy Hamsters

Azari

Brumbaugh

Barbeau

et al. 1980

Can. j. neurol. sci.

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Section: -November 1980supporting

confidence: 92%

Section: Introductionmentioning

confidence: 98%

Taurine Decreases Lesion Severity In the Hearts of Cardiomyopathy Hamsters

Azari

Brumbaugh

Barbeau

et al. 1980

Can. j. neurol. sci.

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“…Much attention has been focused on the potential role of elevated intracellular calcium in the initiation of myocellular dysfunction and structural damage (Fleckenstein et al, 1974;Lossnitzer et al, 1975;Wrogemann and Pena, 1976 be a valuable link in the debate of this important hypothesis. This report emphasizes degenerative changes that develop concurrent with maximum calcium excess (McBroom and Welty, 1977) during the acute phase of active myolysis but prior to cardiac hypertrophy and congestive heart failure (Strobeck et al, 1979). Myopathic animals of other ages were examined to study the course of myocardial involvement through all disease stages to permit a comprehensive comparison with the spectrum of structural changes reported by other investigators (Nakao et al, 1970;Onishi et al, 1970;Buchner, 1971;Nadkarni et al, 1972;Paterson et al, 1972;Schwartz et al, 1972;Lazarus et al, 1976;Wada et al, 1976Wada et al, , 1977Wada et al, , 1978Jasmin and Eu, 1979;Strobeck et al, 1979;Galle et al, 1981;Kidd et al, 1981).…”

Section: Introductionmentioning

confidence: 70%

“…Although definitive evidence of calcium deposition in prenecrotic cardiocytes has not been obtained in this or previous investigations of hamster dystrophy, the possibility remains that increased ionic calcium levels my exist prior to the formation of insoluble calcium precipitates. Chemical analyses have shown elevation of tissue and mitochondrial calcium in skeletal and cardiac muscle of the dystrophic hamster (Lossnitzer et al, 1975;Wrogemann and Pena, 1976;McBroom and Welty, 1977;Palmieri et al, 1981;Bhattacharya et al, 1982). Necrotic muscle contains one order of magnitude more calcium than normal-appearing muscle from the same animal (Wrogemann et al, 1979); and two mitochondrial populations have been identified-a minor fraction with a 50-fold increase of calcium and a major fraction with close to normal values (Mezon et al, 1974).…”

Section: Discussionmentioning

confidence: 99%

Ultrastructure of cardiocyte degeneration and myocardial calcification in the dystrophic hamster

Burbach

1987

Am. J. Anat.

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The myocardium of the Bio 14.6 cardiomyopathic hamster was examined with the electron microscope to identify cellular and organelle changes during the acute lesioning stage, a period typified by concomitant cardiocyte destruction and calcium elevation. Most cardiocytes retained their normal histologic and ultrastructural features, but scattered foci of altered and necrotic cells were observed in association with degenerative calcifying lesions. Prenecrotic alterations of myocytes included cellular edema; varying degrees of distension of sarcoplasmic reticulum and T-tubules; contraction bands and other myofibrillar abnormalities; mitochondrial clustering and hyperplasia; a wide spectrum of mitochondrial changes such as altered sizes, shapes, and cristal patterns, and increases in the number and size of osmiophilic matrix inclusions. Morphologic features consistent with substantial calcium excess were not observed in most altered but prenecrotic cells. Instead, calcium deposition within extruded mitochondria and upon degenerating organelle debris was observed only after cardiocyte disruption. Some calcifying cell remnants were phagocytized by macrophages, whereas large calcified plaques and other deposits remained in the interstitium. Mitochondrial calcification in vascular smooth muscle cells and fibroblasts was evident in highly calcified lesions. These observations suggest that most of the morphologically identifiable calcium deposition present in this cardiomyopathy results from secondary calcification subsequent to sarcolemmal disruption.

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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: 98%

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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Effects of taurine on heart calcium in the cardiomyopathic hamster

Cited by 65 publications

References 13 publications

Taurine Decreases Lesion Severity In the Hearts of Cardiomyopathy Hamsters

Taurine Decreases Lesion Severity In the Hearts of Cardiomyopathy Hamsters

Ultrastructure of cardiocyte degeneration and myocardial calcification in the dystrophic hamster

The mechanism of neuronal resistance and adaptation to hypoxia

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