Brain nitric oxide synthase levels increase in response to antenatal ethanol exposure.
OBJECTIVE
Our previous in vitro data have indicated that ethanol can increase nitric oxide synthase (NOS) expression. Thus, the Aims of this study were to determine whether ethanol produces the same effect in vivo.


METHODS
To accomplish this, we utilized the well-established prenatal ethanol (EtOH) exposure model in the guinea pig to examine the effect on brain NOS expression and activity.


RESULTS
Brain homogenates isolated from offspring of guinea pigs fed EtOH exhibited an increase in NOS protein expression and NOS activity compared to controls. Increased expression of neuronal NOS was observed only in soluble fractions of brain homogenates (P < 0.05 vs. control). Increased expression of a approximately 60 kDa band was detected in the soluble fraction that was immunoreactive against an antiserum raised against inducible NOS. In addition, an immunoreactive band of the correct predicted molecular weight for iNOS was found in the particulate fraction although the expression was unchanged between control and EtOH-treated animals. Endothelial NOS protein expression could not be detected in either soluble or particulate fractions from control or EtOH-treated animals.


CONCLUSIONS
These results suggest that EtOH may exert its toxic effects antenatally via a mechanism of altered nitric oxide availability from NOS.
Department of Pediatrics, Northwestern University, Chicago, IL, USA.
Maria L V
ML
Dizon
Lou Ann
LA
Brown
Stephen M
SM
Black
D000818:Animals; D001921:Brain / Q000187:drug effects* / Q000201:enzymology; D000431:Ethanol / Q000494:pharmacology*; D005260:Female; D015971:Gene Expression Regulation, Enzymologic / Q000187:drug effects / Q000502:physiology; D006168:Guinea Pigs; D019001:Nitric Oxide Synthase / Q000096:biosynthesis* / Q000235:genetics; D011247:Pregnancy; D011297:Prenatal Exposure Delayed Effects
D000431:Ethanol; D019001:Nitric Oxide Synthase