Cytochrome P-450 expression in sudden infant death syndrome

doi:10.1016/0006-2952(96)00253-5

Biochemical Pharmacology

Volume 52, Issue 3, 9 August 1996, Pages 497-504

https://doi.org/10.1016/0006-2952(96)00253-5 Get rights and content

Abstract

In the human liver, the major rise of the cytochrome P-450 isoform content occurs during the first months following birth (e.g., the high vulnerability period to sudden infant death syndrome (SIDS), a syndrome frequently associated with viral infection and drug hypersensitivity. We examined the expression of individual P-450 isoforms in liver samples collected postmortem from SIDS infants and compared values with those of control adults and children of the same age suffering from various pathologies. Hepatic microsomes were prepared and examined for their content in total P-450, the level of individual isoforms (CYP1A2, CYP2E1, CYP4A, CYP3A, and CYP2C) determined with specific antibodies and for their enzymatic activities. Total RNA was extracted and probed with several CYP cDNAs and oligomers. The overall hepatic P-450 content was not modified in SIDS infants. Among cytochrome P-450 isoforms, only CYP2C was markedly increased. This rise resulted from an accumulation of RNA encoding CYP2C and was associated with a stimulation of diazepam demethylation. The precocious expression of CYP2C in SIDS could result in a higher production of epoxye-icosatrienoic acids in the neonate, believed to act as relaxant of pulmonary smooth muscles. Its consequence might be the induction of fatal apnea in SIDS.

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^☆: This study was supported by a grant from the Délegation á la Recherche Clinique de l'Assistance Publique-Hôpitaux de Paris (912001).

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Research paperCytochrome P-450 expression in sudden infant death syndrome☆

Abstract

J Pediatr

Biochem Biophys Res Commun

Biochem Pharmacol

Biochem Pharmccol

Biochem Pharmacol

J Biol Chem

Biochim Biophys Acta

Biochem Pharmacol

Biochem Biophys Res Commun

Biochem Pharmacol

Arch Biochem Biophys

Lancet

Postneonatal mortality, sudden infant death syndrome: factors preventing the decline of infant mortality in France from 1973 to 1985

Paediatr Perinatal Epidemiol

Sudden infant death syndrome: seasonality and a biphasic model of pathogenesis

J Epidemiol Community Health

SIDS and near-SIDS

N Engl J Med

Morts subites au berceau. Expérience d'un centre de référence, 1986–1991

Arch Fr Pediatr

Cytokine release from human peripheral blood leucocytes incubated with endotoxin with and without prior infection with influenza virus: relevance to the sudden infant death syndrome

Int J Exp Path

Sudden infant death syndrome victims show local immunoglobulin M response in tracheal wall and immunoglobulin A response in duodenal mucosa

Pediatr Res

Phenothiazines and sudden death infant syndrome

Pediatrics

Potentiation and suppression of mouse liver cytochrome P450 isoforms during the acute-phase response induced by bacterial endotoxin

Eur J Biochem

The P450 superfamily: update on new sequences, gene mapping, accession numbers, early trivial names of enzymes and nomenclature

DNA and Cell Biol

Immunoquantification of epoxide hydrolase and cytochrome P-450 isoenzymes in fetal and adult human liver microsomes

Eur J Biochem

Fetus-specific expression of a form of cytochrome P-450 in human livers

Biochemistry (USA)

Expression of CYP2D6 in the developing human liver

Eur J Biochem

Research paper
Cytochrome P-450 expression in sudden infant death syndrome☆