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Effect of ethanol (EtOH) and dietary histidine (His) on fetal brain histamine (Hm)

Conference · · FASEB Journal (Federation of American Societies for Experimental Biology); (United States)
OSTI ID:5240307
;  [1]
  1. Rutgers-the State Univ., Piscataway, NJ (United States)
The authors have previously shown that gestational EtOH consumption decreased free His in fetal tissues, including the brain. His is the precursor of Hm, a neurotransmitter, and since central nervous system (CNS) dysfunction is frequently observed in the offspring of alcoholic women, experiments were conducted to examine the effects of gestational EtOH consumption on fetal brain Hm. Pregnant Sprague-Dawley rats were fed 35% EtOH-calorie liquid diets with three levels of His from gestation day (GD) 7 to 21. Control rats (LHC, MHC and HHC) were pair-fed with isocaloric sucrose substituted for EtOH. ON GD-21, fetal and maternal tissue were analyzed for His and H. In all tissues examined (fetal brain, plasma and liver, and maternal plasma and liver), His was increased with the increase of dietary His. Hm was also increased in fetal brain and liver in 0.8% dietary His groups. EtOH feeding decreased His in all fetal tissues but increased Hm in fetal brain and liver. The values of fetal brain Hm were: 805 {plus minus} 89 vs 574 {plus minus}47 (LHE vs LHC), 690 {plus minus} 29 vs 446 {plus minus} 32 (MHE vs MHC) and 1,335 {plus minus} 165 vs 938 {plus minus} 72 (HHE vs HHC), an increase of 40-50% by EtOH. Alteration in fetal brain Hm may contribute to the CNS dysfunction.
OSTI ID:
5240307
Report Number(s):
CONF-9104107--
Conference Information:
Journal Name: FASEB Journal (Federation of American Societies for Experimental Biology); (United States) Journal Volume: 5:5
Country of Publication:
United States
Language:
English