Prenatal cigarette smoke exposure selectively alters protein kinase C and nitric oxide synthase expression within the neonatal rat brainstem

被引:19
|
作者
Hasan, SU
Simakajornboon, N
MacKinnon, Y
Gozal, D [1 ]
机构
[1] Univ Calgary, Div Neonatal Med, Dept Pediat, Fac Med, Calgary, AB T2N 1N4, Canada
[2] Tulane Univ, Sch Med, Dept Pediat, Constance S Kaufman Pediat Pulm Res Lab, New Orleans, LA 70112 USA
[3] Univ Louisville, Kosair Childrens Hosp,Sch Med, Inst Res, Dept Pediat, Louisville, KY 40202 USA
[4] Univ Louisville, Kosair Childrens Hosp,Sch Med, Inst Res, Dept Pharmacol, Louisville, KY 40202 USA
[5] Univ Louisville, Kosair Childrens Hosp,Sch Med, Inst Res, Dept Toxicol, Louisville, KY 40202 USA
关键词
cigarette smoke; protein kinase C; nitric oxide synthase; respiratory control; hypoxia; newborn; nicotine; fetus; sudden infant death syndrome;
D O I
10.1016/S0304-3940(01)01624-X
中图分类号
Q189 [神经科学];
学科分类号
071006 ;
摘要
Maternal smoking is a major risk factor for sudden infant death syndrome. Protein kinase C (PKC) and neuronal nitric oxide synthase (NOS) activities within the dorsocaudal brainstem (DB) mediate critical components of respiratory drive and could be implicated in SIDS. Thus, exposure to smoking during fetal life could modify the expression of these kinases in the DB. Rats were exposed to cigarette smoke or room air (Sham) from day 2 to 22 of pregnancy. Immunoblots of DB lysates at 2 days postnatally revealed no differences in PKC-alpha, PKC-beta, and endothelial NOS expression. However, PKC-gamma, PKC-delta, and neuronal NOS immunoreactivities were reduced in the cigarette smoke group. We conclude that gestational smoking is associated with selective reductions in PKC and NOS isoforms within the DB, which could decrease respiratory drive and lead to enhanced hypoxic vulnerability in infants of smoking mothers. (C) 2001 Elsevier Science Ireland Ltd. All rights reserved.
引用
收藏
页码:135 / 138
页数:4
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