Cytochrome P-450 expression in sudden infant death syndrome

Treluyer, JM; Cheron, G; Sonnier, M; Cresteil, T

HERO ID

730587

Reference Type

Journal Article

Year

1996

Language

English

PMID

8687505

HERO ID 730587
In Press No
Year 1996
Title Cytochrome P-450 expression in sudden infant death syndrome
Authors Treluyer, JM; Cheron, G; Sonnier, M; Cresteil, T
Journal Biochemical Pharmacology
Volume 52
Issue 3
Page Numbers 497-504
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 epoxyeicosatrienoic acids in the neonate, believed to act as relaxant of pulmonary smooth muscles. Its consequence might be the induction of fatal apnea in SIDS.
Doi 10.1016/0006-2952(96)00253-5
Pmid 8687505
Is Certified Translation No
Dupe Override No
Is Public Yes
Language Text English
Is Qa No