Effect of acute alcohol ingestion on plasma pyridoxal 5'-phosphate

T. H. Parker, J. P. Marshall, R. K. Roberts, S. Wang, Eugene R Schiff, G. R. Wilkinson, S. Schenker

Research output: Contribution to journalArticle

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Abstract

This study assesses the effect of acute alcohol intake on net plasma pyridoxal 5'-phosphate (PLP) accumulation from pyridoxine and on PLP elimination from plasma. Unanesthetized dogs were given oral alcohol (1 or 3 g/kg as as a 25% solution in normal saline), isocaloric glucose, or were fasted. Two hours later pyridoxine (1 mg/kg i.v.) was given and serial plasma samples were assayed for PLP (enzymatic tyrosine decarboxylase method) over 31 hr. In other dogs, PLP (2.5 mg) was given i.v. and PLP decay monitored over 24 hr. The area under the plasma PLP curve after pyridoxine (i.e., PLP accumulation) and pharmacokinetics of PLP elimination were compared in alcohol and control groups after correcting for the base-line PLP level. Blood alcohol with the 3 g/kg dose averaged about 300 mg/100 ml at 2 hr and fell to 175 mg/100 ml at 16 hr, while with the 1 g/kg dose it was about 85 mg/100 ml at 2 hr and had disappeared in 7 hr. Accumulation of PLP in plasma in 10 controls after pyridoxine was 879.8 ± 101.3 ng/ml per 31 hr (mean ± SE) but only 441.8 ± 86.9 ng/ml per 31 hr in 7 dogs given the high alcohol dose (P < 0.01). By contrast, the low alcohol dose did not alter significantly plasma PLP accumulation. PLP distribution and clearance were comparable in dogs given the high alcohol dose and in control dogs. In conclusion: (1) acute high doses of alcohol in dogs lower plasma PLP accumulation from precursor pyridoxine, (2) this effect can not be accounted for by increased PLP removal from plasma, (3) these composite data indirectly suggest an alcohol-induced abnormality in plasma PLP formation.

Original languageEnglish
Pages (from-to)1246-1252
Number of pages7
JournalAmerican Journal of Clinical Nutrition
Volume32
Issue number6
StatePublished - Dec 1 1979
Externally publishedYes

Fingerprint

pyridoxal phosphate
Pyridoxal Phosphate
alcohols
Eating
Alcohols
ingestion
Pyridoxine
pyridoxine
Dogs
dogs
dosage
Tyrosine Decarboxylase

ASJC Scopus subject areas

  • Medicine (miscellaneous)
  • Food Science

Cite this

Parker, T. H., Marshall, J. P., Roberts, R. K., Wang, S., Schiff, E. R., Wilkinson, G. R., & Schenker, S. (1979). Effect of acute alcohol ingestion on plasma pyridoxal 5'-phosphate. American Journal of Clinical Nutrition, 32(6), 1246-1252.

Effect of acute alcohol ingestion on plasma pyridoxal 5'-phosphate. / Parker, T. H.; Marshall, J. P.; Roberts, R. K.; Wang, S.; Schiff, Eugene R; Wilkinson, G. R.; Schenker, S.

In: American Journal of Clinical Nutrition, Vol. 32, No. 6, 01.12.1979, p. 1246-1252.

Research output: Contribution to journalArticle

Parker, TH, Marshall, JP, Roberts, RK, Wang, S, Schiff, ER, Wilkinson, GR & Schenker, S 1979, 'Effect of acute alcohol ingestion on plasma pyridoxal 5'-phosphate', American Journal of Clinical Nutrition, vol. 32, no. 6, pp. 1246-1252.
Parker TH, Marshall JP, Roberts RK, Wang S, Schiff ER, Wilkinson GR et al. Effect of acute alcohol ingestion on plasma pyridoxal 5'-phosphate. American Journal of Clinical Nutrition. 1979 Dec 1;32(6):1246-1252.
Parker, T. H. ; Marshall, J. P. ; Roberts, R. K. ; Wang, S. ; Schiff, Eugene R ; Wilkinson, G. R. ; Schenker, S. / Effect of acute alcohol ingestion on plasma pyridoxal 5'-phosphate. In: American Journal of Clinical Nutrition. 1979 ; Vol. 32, No. 6. pp. 1246-1252.
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abstract = "This study assesses the effect of acute alcohol intake on net plasma pyridoxal 5'-phosphate (PLP) accumulation from pyridoxine and on PLP elimination from plasma. Unanesthetized dogs were given oral alcohol (1 or 3 g/kg as as a 25{\%} solution in normal saline), isocaloric glucose, or were fasted. Two hours later pyridoxine (1 mg/kg i.v.) was given and serial plasma samples were assayed for PLP (enzymatic tyrosine decarboxylase method) over 31 hr. In other dogs, PLP (2.5 mg) was given i.v. and PLP decay monitored over 24 hr. The area under the plasma PLP curve after pyridoxine (i.e., PLP accumulation) and pharmacokinetics of PLP elimination were compared in alcohol and control groups after correcting for the base-line PLP level. Blood alcohol with the 3 g/kg dose averaged about 300 mg/100 ml at 2 hr and fell to 175 mg/100 ml at 16 hr, while with the 1 g/kg dose it was about 85 mg/100 ml at 2 hr and had disappeared in 7 hr. Accumulation of PLP in plasma in 10 controls after pyridoxine was 879.8 ± 101.3 ng/ml per 31 hr (mean ± SE) but only 441.8 ± 86.9 ng/ml per 31 hr in 7 dogs given the high alcohol dose (P < 0.01). By contrast, the low alcohol dose did not alter significantly plasma PLP accumulation. PLP distribution and clearance were comparable in dogs given the high alcohol dose and in control dogs. In conclusion: (1) acute high doses of alcohol in dogs lower plasma PLP accumulation from precursor pyridoxine, (2) this effect can not be accounted for by increased PLP removal from plasma, (3) these composite data indirectly suggest an alcohol-induced abnormality in plasma PLP formation.",
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N2 - This study assesses the effect of acute alcohol intake on net plasma pyridoxal 5'-phosphate (PLP) accumulation from pyridoxine and on PLP elimination from plasma. Unanesthetized dogs were given oral alcohol (1 or 3 g/kg as as a 25% solution in normal saline), isocaloric glucose, or were fasted. Two hours later pyridoxine (1 mg/kg i.v.) was given and serial plasma samples were assayed for PLP (enzymatic tyrosine decarboxylase method) over 31 hr. In other dogs, PLP (2.5 mg) was given i.v. and PLP decay monitored over 24 hr. The area under the plasma PLP curve after pyridoxine (i.e., PLP accumulation) and pharmacokinetics of PLP elimination were compared in alcohol and control groups after correcting for the base-line PLP level. Blood alcohol with the 3 g/kg dose averaged about 300 mg/100 ml at 2 hr and fell to 175 mg/100 ml at 16 hr, while with the 1 g/kg dose it was about 85 mg/100 ml at 2 hr and had disappeared in 7 hr. Accumulation of PLP in plasma in 10 controls after pyridoxine was 879.8 ± 101.3 ng/ml per 31 hr (mean ± SE) but only 441.8 ± 86.9 ng/ml per 31 hr in 7 dogs given the high alcohol dose (P < 0.01). By contrast, the low alcohol dose did not alter significantly plasma PLP accumulation. PLP distribution and clearance were comparable in dogs given the high alcohol dose and in control dogs. In conclusion: (1) acute high doses of alcohol in dogs lower plasma PLP accumulation from precursor pyridoxine, (2) this effect can not be accounted for by increased PLP removal from plasma, (3) these composite data indirectly suggest an alcohol-induced abnormality in plasma PLP formation.

AB - This study assesses the effect of acute alcohol intake on net plasma pyridoxal 5'-phosphate (PLP) accumulation from pyridoxine and on PLP elimination from plasma. Unanesthetized dogs were given oral alcohol (1 or 3 g/kg as as a 25% solution in normal saline), isocaloric glucose, or were fasted. Two hours later pyridoxine (1 mg/kg i.v.) was given and serial plasma samples were assayed for PLP (enzymatic tyrosine decarboxylase method) over 31 hr. In other dogs, PLP (2.5 mg) was given i.v. and PLP decay monitored over 24 hr. The area under the plasma PLP curve after pyridoxine (i.e., PLP accumulation) and pharmacokinetics of PLP elimination were compared in alcohol and control groups after correcting for the base-line PLP level. Blood alcohol with the 3 g/kg dose averaged about 300 mg/100 ml at 2 hr and fell to 175 mg/100 ml at 16 hr, while with the 1 g/kg dose it was about 85 mg/100 ml at 2 hr and had disappeared in 7 hr. Accumulation of PLP in plasma in 10 controls after pyridoxine was 879.8 ± 101.3 ng/ml per 31 hr (mean ± SE) but only 441.8 ± 86.9 ng/ml per 31 hr in 7 dogs given the high alcohol dose (P < 0.01). By contrast, the low alcohol dose did not alter significantly plasma PLP accumulation. PLP distribution and clearance were comparable in dogs given the high alcohol dose and in control dogs. In conclusion: (1) acute high doses of alcohol in dogs lower plasma PLP accumulation from precursor pyridoxine, (2) this effect can not be accounted for by increased PLP removal from plasma, (3) these composite data indirectly suggest an alcohol-induced abnormality in plasma PLP formation.

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