Ascorbic acid-like effect of the soluble fraction of rat brain on adenosine triphosphatases and its relation to catecholamines and chelating agents

Schaefer, András; Seregi, András; Komlós, Márta

doi:10.1016/0006-2952(74)90555-3

Cited by 78 publications

(24 citation statements)

References 35 publications

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“…in the absence of the brain soluble fraction depends on the presence of an inhibitory contaminant in commercial ATP preparations. This observation, however, does not exclude the possibility that the physiological role of noradrenaline is to remove the inhibition of the enzyme by an endogenous inhibitor present in the cytoplasm, an idea suggested by different authors (Hexurn, 1977;Schaefer et al, 1972;Schaefer et al, 1973;Schaefer et al, 1974). Further supports for this suggestion has been forthcoming from our experiments on noradrenaline stimulation when it was shown that in homogenate where cytoplasmic factor is present 10 -4 M noradrenaline is effective in increasing enzyme activity from 9.26_+0.56 to 17.1+1.5 Pi/mg protein/hour (p <0.001, n = 8) although contaminating vanadium was not present in the mixture.…”

Section: Discussionmentioning

confidence: 67%

“…While stimulation of membrane ATPase by noradrenaline occurs in homogenates, this was not the case when the synaptosomes were used in the medium. In addition, the fact that the enzyme activity of the homogenate, is significantly lower than those of synaptosomal fraction indicates that a cytoplasmic inhibitory factor should be present (Hexurn, 1977;Schaefer et al, 1972;Schaefer et al, 1973;Schaefer et al, 1974) in the tissue used.…”

Section: Discussionmentioning

confidence: 96%

“…In addition this preparation seemed to be interesting since it has been suggested (Paton et al, 1971;Vizi, 1972;Gilbert et al, 1975 ;Vizi, 1977) that nerve terminal Na+K +-ATPase may play a role in the release mechanism of transmitters (Vizi, 1978) and that the presynaptic inhibitory effect of catecholamines on transmitter release (Gilbert et al, 1975;Vizi, 1978) is associated with the stimulation of this enzyme (Godfraind et al, 1974;Schaefer et al, 1972;Schaefer et al, 1973;Yoshirnura, 1973;Schaefer et al, 1974;Logan and O'Donovan, 1976;Lee and Phillis, 1977;Hexum, 1977;Wu and Phillis, 1978). All the data concerning stimulatory effect of noradrenaline on ATPase activity were obtained with ATP contaminated with vanadate, therefore we studied its effect using both vanadium containing and vanadium-free ATP as well.…”

Section: Introductionmentioning

confidence: 97%

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Effect of noradrenaline and vanadium on Na+K+-activated ATPase in rat cerebral cortex synaptosomal preparation

Ádám-Vizi

Ördögh

Horváth

et al. 1980

J. Neural Transmission

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The effect of l-noradrenaline and vanadate on the activity of Na+K+-activated ATPase was studied on synaptosomal brain cortex preparation. Using neutron activation analysis it was found that the rat cerebral cortex synaptosomal preparation contains 0.16 microM vanadium. The concentration of vanadium needed to reduce enzyme activity by 50% proved to be 2 x 10(-6) M. Evidence has been provided that the increase by noradrenaline of enzyme activity in synaptosomal preparation depends on the presence of an inhibitory contaminant in commercial ATP preparations. In homogenate, however, noradrenaline was able to enhance enzyme activity even when vanadium-free ATP was used. This fact indicates that noradrenaline removes the inhibitory effect of cytoplasmic factor thereby stimulating enzyme activity.

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Section: Discussionmentioning

confidence: 67%

Section: Discussionmentioning

confidence: 96%

Section: Introductionmentioning

confidence: 97%

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Effect of noradrenaline and vanadium on Na+K+-activated ATPase in rat cerebral cortex synaptosomal preparation

Ádám-Vizi

Ördögh

Horváth

et al. 1980

J. Neural Transmission

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“…Controversal reports have implicated different mechanisms concerning biogenic amine stimulation of Na + ;K + ATPase in various brain preparations (Hexum, 1977;Schaefer et al, 1974;Svoboda and Mosinger, 1981). According to these authors, the catecholamines enhanced the activity of Na+,K+ATPase by chelating inhibitory divalent cations or by preventing lipid peroxidation.…”

Section: Neurochemical Pathologymentioning

confidence: 98%

Effect of lead on Na+,K+ ATPase activity in the developing brain of intra-uterine growth-retarded rats

Chanez

Giguère

Flexor

et al. 1986

Neurochemical Pathology

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Lead (Pb) intoxication in developing mammals, including humans, produces serious brain damage. In addition, it is known that nutritional status influences the susceptibility to Pb toxicity. We developed an in utero undernutrition model based on restriction of blood supply to fetuses on d 17 of pregnancy (IUGR rats). The aim of this study was to investigate in vitro the possible effect of Pb on Na+, K+ATPase activity in the brain of developing IUGR and control rats from 6 to 60 d after birth. In addition, we measured the stimulation of Na+, K+ATPase by the monoamines noradrenaline and serotonin. Our results show that: The neurotoxic effect of Pb is an age-related phenomenon. Both IUGR and control rats were more sensitive to Pb in the first week of life. In adults, Pb had a weak inhibitory potency; the delayed matured brain in IUGR animals seemed less sensitive to Pb when compared to age-paired control rats; in the IUGR group, at 15 and 22 d, low doses of Pb had a stimulatory effect on Na+, K+ATPase instead of an inhibitory effect; noradrenaline and serotonin stimulated Na+, K+ATPase activity to an equivalent extent, but this was greater in IUGR than control rats; and at low Pb concentrations, the studied monoamines reversed Pb-induced inhibition.

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“…Ascorbic acid prevented this but did not affect the results, so it seems improb able that it had any effect apart from stabilis ing noradrenaline. In other experiments, as corbic acid has been reported not to affect (Na+, K+)-ATPase [16,25], to stimulate it by antagonising the effect of vanadate [13,21] or to inhibit it directly [26], according to the conditions.…”

Section: Effect Of Potassium Concentration On Optimum Phmentioning

confidence: 99%

The Optimum pH of Renal Adenosine Triphosphatase in Rats: Influence of Vanadate, Noradrenaline and Potassium

Ar¹,

Ea²

1982

Enzyme

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In the presence of vanadate, the optimum pH of renal (Na^+, K^+)-ATPase in rats is reduced and lies in the range of intracellular pH. This explains the difference in optimum pH observed with ATP extracted from equine muscle. Removal of vanadate from such ATP (with noradrenaline) raises the optimum to the accepted range obtained with synthetic ATP. Changes in the sensitivity of the enzyme to potassium concentration contribute to the alterations in optimum pH. The optimum pH of Mg-ATPase is unaffected by vanadate. Since vanadate may be an intracellular regulator of (Na^+, K^+)-ATPase changes of optimum pH in relation to intracellular pH could well contribute to the regulation of sodium pump activity.

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Ascorbic acid-like effect of the soluble fraction of rat brain on adenosine triphosphatases and its relation to catecholamines and chelating agents

Cited by 78 publications

References 35 publications

Effect of noradrenaline and vanadium on Na+K+-activated ATPase in rat cerebral cortex synaptosomal preparation

Effect of noradrenaline and vanadium on Na+K+-activated ATPase in rat cerebral cortex synaptosomal preparation

Effect of lead on Na+,K+ ATPase activity in the developing brain of intra-uterine growth-retarded rats

The Optimum pH of Renal Adenosine Triphosphatase in Rats: Influence of Vanadate, Noradrenaline and Potassium

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