Taurine effects on45Ca2+ transport in retinal subcellular fractions

Pasantes‐Morales, Herminia; Ademe, Rosa M.; López-Colomé, Ana Marı́a

doi:10.1016/0006-8993(79)90900-4

Cited by 45 publications

(7 citation statements)

References 20 publications

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“…More recently it was found that taurine fails to reduce lipid peroxidation, although it preserves the membrane organization of isolated rod outer segments and cultured human lymphoblastoid cells exposed to ferrous sulfate and retinoids, respectively [Pasantes-Morales and Cruz, 1984;Pasantes-Morales et al, 19841. These findings support an alternate hypothesis that the protective action of taurine might be related to its action on membrane permeability [Pasantes-Morales, 19861, as its effects on ion transport have been shown in a number of preparations [Gruener and Bryant, 1975;Pasantes-Morales et al, 1979, 1981aPasantes-Morales and Gamboa, 1980;Kruzinger and Hamprecht, 19811. It seems possible, therefore, that taurine plays a role in osmoregulation and protects photoreceptors from excessive influx of ions and water, which seems to result in the swelling of outer segments and mitochondria observed in the present study.…”

Section: Discussionsupporting

confidence: 74%

Retinal degeneration in 3‐month‐old rhesus monkey infants fed a taurine‐free human infant formula

Imaki

Moretz

Wisniewski

et al. 1987

J of Neuroscience Research

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Rhesus monkey infants were raised from birth on a taurine-free soy protein-based human infant formula or on the same formula supplemented with taurine. The monkeys were killed 3 months after birth and the retinas examined by light and electron microscopy. All of the monkeys raised on formula alone showed degenerative ultrastructural changes in photoreceptor outer segments that ranged from swelling and disorientation to fragmentation and disorganization. Cones were more severely affected than rods, and changes were most pronounced in the foveal region. Changes were also noted in the fine structure of the retinal pigment epithelium. These changes were prevented in all but one monkey fed the same formula supplemented with taurine. These results provide further support for the addition of taurine to commercial human infant formulas.

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Section: Discussionsupporting

confidence: 74%

Retinal degeneration in 3‐month‐old rhesus monkey infants fed a taurine‐free human infant formula

Imaki

Moretz

Wisniewski

et al. 1987

J of Neuroscience Research

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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]. Similar results were obtained using a sarcolemma preparation [49] and in synaptosomes [50].…”

Section: Discussionmentioning

confidence: 68%

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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“…Although the physiological significance of this observation remains unclear, some mechanisms relating taurine to the phy siological processes occurring during photoexcitation may be considered. These include an effect of taurine on calcium binding [Pasantes-Morales et al, 1979;Lombardini, 19831, a …”

Section: Discussionmentioning

confidence: 99%

Pharmacological identification of retinal cells releasing taurine by light stimulation

Salazar

Quesada

Campomanes

et al. 1986

J of Neuroscience Research

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The effect of drugs blocking synaptic activity at different retinal levels was examined in this study, in an attempt to identify the origin of the light-stimulated release of 3H-taurine from the chick retina. It was determined by autoradiography that the chick retina accumulates taurine in photoreceptors, in cells from the inner nuclear layer, and in processes of the inner plexiform layer. All these are possible sites for the release of taurine upon illumination. To discriminate among these possibilities, the effects of aspartate, tetrodotoxin, strychnine, picrotoxin, chlorpromazine, tubocurarine, atropine, glutamate diethyl esther, alpha-amino adipate and 2-amino-4-phosphonobutyrate were studied. Aspartate (10 mM), which is known to eliminate the light response of cells postsynaptic to photoreceptors, induced a marked increase of 150% in the resting efflux of 3H-taurine but did not decrease significantly the light-stimulated release. Tetrodotoxin, which blocks amacrine cell responses, decreased 3H-taurine release stimulated by light by less than 20%. The efflux of taurine was unaffected by strychnine, picrotoxin, tubocurarine, atropine, chlorpromazine, and 2-amino-4-phosphonobutyrate, whereas it was increased by glutamate diethyl esther and alpha-amino adipate. These results, all together, point to photoreceptors as the cells releasing 3H-taurine in response to light.

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Taurine effects on45Ca2+ transport in retinal subcellular fractions

Cited by 45 publications

References 20 publications

Retinal degeneration in 3‐month‐old rhesus monkey infants fed a taurine‐free human infant formula

Retinal degeneration in 3‐month‐old rhesus monkey infants fed a taurine‐free human infant formula

The mechanism of neuronal resistance and adaptation to hypoxia

Pharmacological identification of retinal cells releasing taurine by light stimulation

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