Effect of pyridoxine on the depletion of tissue pyridoxal phosphate by carbidopa.

@article{Airoldi1978EffectOP,
  title={Effect of pyridoxine on the depletion of tissue pyridoxal phosphate by carbidopa.},
  author={Luisa Airoldi and Carol J. Watkins and J F Wiggins and Richard J. Wurtman},
  journal={Metabolism: clinical and experimental},
  year={1978},
  volume={27 7},
  pages={
          771-9
        }
}

Pyridoxal 5′-phosphate levels in brain after treatments which impair cerebral glucose metabolism

PLP levels in brain were unchanged, or were increased (in hepatectomized rats) and in animals treated withl-dopa or with 5-hydroxytryptophan alone or with inhibitors of MAO or ofl-aromatic amino acid decarboxylase.

Regulation and function of pyridoxal phosphate in CNS

  • M. Ebadi
  • Biology, Medicine
    Neurochemistry International
  • 1981

Dietary influence of tyrosine and phenylalanine on the response of B16 melanoma to carbidopa-levodopa methyl ester chemotherapy.

It is shown that concomitant dietary tyrosine-phenylalanine restriction enhances the antitumor activity of carbidopa-levodopa methyl ester against B16 melanoma.

The Parkinson’s disease death rate: carbidopa and vitamin B6

The only indication for carbidopa and benserazide is the management of L-3,4-dihydroxyphenylalanine (L-dopa)-induced nausea, and carbidopa is postulated to contribute to the increasing Parkinson's disease death rate and to the classification of Parkinson’s as a progressive neurodegenerative disease.

Neurobiology of pyridoxine.

More direct evidence has accumulated to confirm both a neurotransmitter role for GABA in the vertebrate CNS and the regulation of its synthesis by pyridoxal phosphate (PALP).

Development of a scleroderma-like illness during therapy with L-5-hydroxytryptophan and carbidopa.

The data and studies in the literature suggest that two factors may be important in the pathogenesis of some scleroderma-like illness: high plasma serotonin and the abnormality associated with elevated kynurenine.

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Levodopa and Pyridoxine

To the Editor.— Recent reports inThe Journalhave clearly indicated the negative effects of pyridoxine on the therapeutic response of patients with parkinsonism to levodopa.1,2Blood dopa levels have

Effect of chronic levodopa treatment on pyridoxine metabolism

Chronic administration of levodopa may result in an adaptive alteration in the decarboxylase system with an increased cellular ability to synthesize pyridoxal-5-phosphate from pyriridoxine, possibly through enzyme induction.

METABOLISM OF CARBIDOPA [L-(-)-α-HYDRAZINO-3,4-DIHYDROXY-α-METHYLHYDROCINNAMIC ACID MONOHYDRATE], AN AROMATIC AMINO ACID DECARBOXYLASE INHIBITOR, IN THE RAT, DOG, RHESUS MONKEY, AND MAN

Radioactivity in the rat showed that after 1 hr radioactivity was concentrated relative to the plasma in the kidney, lungs, small intestine, and liver, and Unchanged carbidopa was excreted in the urine of man, monkey, dog, and rat.

L‐DOPA: Effect on cerebral pyridoxal phosphate content and coenzyme activity

The present report describes studies in vivo to assess certain effects of the administration of L-DOPA on the vitamin B6 coenzyme, pyridoxal phosphate, in the brain.

Blocking the negative effects of pyridoxine on patients receiving levodopa.

It was noted that diurnal variations in performance could be controlled with orally administered combinations of inhibitor and levodopa and that such combinations have diminished the striking postprandial reemergence of symptoms otherwise experienced by some of the authors' patients.

Potentiation and inhbition of some central actions of L(-)-dopa by decarboxylase inhibitors.

It is concluded that decarboxylase inhibitors can either inhibit or potentiate the central actions of i.-dopa depending upon whether they reach the brain sites where L-dopa acts.

Enhancement of the anti-hypertensive effect of methyldopa and other anti-hypertensive drugs by carbidopa in spontaneously hypertensive rats.

Biochemical studies support the assumption that carbidopa is likely to reduce sympathetic nervous system activity, and enhance the anti-hypertensive effects of methydopa, hydrallazine, guanethidine and clonidine, and, to a lesser extent, reserpine and hydrochlorothiazide.

Evaluation of the biochemical effects produced in vivo by inhibitors of the three enzymes involved in norepinephrine biosynthesis.

The lowering of norepinephrine levels in guinea pig tissues by α-methyltyrosine was found to be directly related to the degree of inhibition of tyrosine hydroxylase.

Suppression of noradrenaline synthesis in sympathetic nerves by carbidopa, an inhibitor of peripheral dopa decarboxylase

Evidence is presented that the administration to rats of carbidopa (MK-486; α-methyl-L-dopa-hydrazine), a peripherally acting inhibitor of AAAD3, not only blocks the decarboxylation of exogenous L- dopa, but also suppresses the decarate of endogenous dopa formed from 3H-tyrosine within cardiac sympathetic nerve terminals.