Tyrosine hydroxylase inhibition in vitro and in vivo by chelating agents

Taylor, Richard T.; Stubbs, C.S.; Ellenbogen, Leon

doi:10.1016/0006-2952(69)90083-5

Cited by 43 publications

(9 citation statements)

References 12 publications

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“…Diethyldithiocarbamate, as reported by Goodchild (1969) and confirmed by our study, increased the concentration of tyrosine in the brain. This effect is probably due to the inhibition of tyrosine hydroxylase by the sudden accumulation of NA precursors as DDC either does not inhibit this enzyme (Nagatsu, Levitt & Udenfriend, 1964) or it is much less effective than the iron chelating agents (Taylor et al, 1969). Though the experiments reported here have proved that exposure to CS2 had the same effect on the NA and DA contents of brain as a single dose of DDC, no change in the brain content of tyrosine was observed after CS2 exposure.…”

Section: Discussionmentioning

confidence: 99%

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The effects of carbon disulphide exposure on brain catecholamines in rats

Magós

1970

British J Pharmacology

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Summary1. Rats exposed to 2-0 mg/i. carbon disulphide (CS2) in the inspired air for 2 days, 4 h a day, showed a 13 % decrease in their brain noradrenaline concentration and a 16 % increase in their brain dopamine concentration. 2. After exposure for 5 or 10 days there was a further decrease in the concentration of noradrenaline in the brain, but brain dopamine returned to the control level. 3. In animals treated intraperitoneally with 2 0 mg/kg reserpine and exposed 2 and 3 days later to 20 mg/I. CS2 for 4 h per day, the brain dopamine concentration showed a 770/o increase compared with the unexposed reserpinized animals, but the noradrenaline concentration remained unchanged. 4. The dopamine concentrations in the adrenals after 10 days' exposure to 2-0 mg/I. CS2 were 67% to 100% higher than in the control animals. In reserpinized rats, 2 days' exposure to CS2 nearly trebled the dopamine content of adrenals. 5. Exposure to CS2 had no effect on the tyrosine concentration in the brain, and there was no change in the brain monoamine oxidase (MAO) activity.Tyrosine in the brain showed a 30 to 96% increase in concentration and MAO activity, using kynuramine as substrate, showed an approximately 5% increase 0-5 to 2 h after the subcutaneous administration of 500 mg/kg sodium diethyldithiocarbamate. 6. CS2 at 10-2M or lower concentrations had no inhibitory effect on the brain MAO activity in vitro. Diethyldithiocarbamate inhibited MAO at 10-2M, but not at 10-3M or lower concentrations. IntroductionCarbon disulphide (CS2) exposure can lead to widely different pathological conditions such as mental aberrations, hypertension, extrapyramidal symptoms and atherosclerosis (Quarelli, 1937; Gordy & Trumper, 1938;McDonald, 1938;Lewey, 1941a;Paluch, 1948;Vigliani & Pernis, 1955 ;Weist, 1957;Magos, 1961;Szobor, 1962). Recently, Tiller, Schilling & Morris (1968) have given statistical evidence on the increased frequency of death from coronary heart disease among viscose workers exposed to CS, and other toxic agents in this country.As catecholamines or drugs acting on catecholamine metabolism can influence brain functions and behaviour

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Section: Discussionmentioning

confidence: 99%

“…However, the effect of DDC is not restricted to dopamine-/3-hydroxylase. There are reports of its action on tyrosine hydroxylase (Taylor, Stubbs & Ellenbogen, 1969) and monoamine oxidase (MAO) (Edington, 1968). The inhibitory effect of CS2 on MAO was also reported (Magistretti & Peirone, 1961).…”

Section: Introductionmentioning

confidence: 89%

The effects of carbon disulphide exposure on brain catecholamines in rats

Magós

1970

British J Pharmacology

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“…To our knowledge there is only one study, where interaction between cyanide and tyrosine hydroxylase has been observed. In vitro incubation of bovine adrenal tyrosine hydroxylase with 1 mM NaCN resulted in a small (15%) inhibition of the enzyme (Taylor et al 1969). Effects of cyanide on brain tyrosine hydroxylase have not been reported.…”

Section: Tablementioning

confidence: 96%

Effects of Acute Lethal Cyanide Intoxication on Central Dopaminergic Pathways

Cassel

Persson

1992

Pharmacology & Toxicology

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In rats treated with sodium cyanide (NaCN), 20 mg/kg intraperitoneally, the striatal dopamine (DA) level was decreased within 60 sec. compared to controls injected with NaCl 0.9%. Treatment with NaCN also increased the naturally occurring L-DOPA in the striatum, but not in the other brain regions studied. Decreased DA levels but increased L-DOPA accumulation were also seen in cyanide-treated animals after inhibition of neuronal L-aromatic amino decarboxylase. In rats given a non-lethal dose of NaCN, 2.5 mg/kg intraperitoneally, 30 min. before sacrifice and L-DOPA, 100 mg/kg intraperitoneally, 25 min. before sacrifice, regional L-DOPA levels were not significantly changed, but the striatal DA levels were diminished compared to controls. Decreased DA levels might indicate that cyanide inhibits the synthesis of brain DA. However, both increased L-DOPA and increased accumulation of L-DOPA after neuronal decarboxylase were observed after cyanide. Furthermore, we have earlier reported that lethal doses of NaCN decreased the DA metabolite HVA in the striatum but did not significantly change the oxidatively deaminated metabolite of DA, DOPAC. Inhibition of L-aromatic amino acid decarboxylase appears to play a minor role in causing decreased striatal DA levels. However, our findings might be compatible with cyanide-produced inhibition of the energy-demanding granular uptake and/or release of DA.

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“…Inhibition of melanogenesis can occur as a consequence of chelation of Cu2+/Fe2+ (Blumenkrantz, 1964;Blumenkrantz & Blomstedt. 1987;Taylor et al, 1969). Although the mothers which received Vantocil added to their feed did not present depigrnentation as their offsprings, the levels of copper in plasma of both groups were lower than their respective controls.…”

Section: Do Not Know If the In Vitro Observation Of Complete Solubilimentioning

confidence: 94%

“…These findings suggest a postnatal alteration in the metabolic transport with deprivation of copper, necessary for some metallo-enzymes, among them tyrosine hydroxylase (Taylor et al, 1969). This enzyme is an aerobic copper-containing oxidase, required for the biosynthesis of melanin, in fact, for the first and the second steps of melanogenesis (Breathnach, 1971;Vijayan et al, 1982).…”

Section: Introductionmentioning

confidence: 99%