Effects of gestational and lactational choline deprivation on brain antioxidant status, acetylcholinesterase, (Na(+),K(+))- and Mg(2+)-ATPase activities in offspring rats.
BACKGROUND
Choline plays an important role in brain development. Choline-deficient diet (CDD) is known to produce (among other effects) a decrease in acetylcholine in rat brains. The aim of our study was to investigate how CDD administration during gestation and lactation could affect total antioxidant status (TAS) and activities of acetylcholinesterase (AChE), (Na(+),K(+))- and Mg(2+)-ATPase in the brains of both male and female newborn and suckling (21-day-old) rats.


METHODS
Three different experiments were performed. Whole brains were obtained from: (a) newborn rats following gestational CDD (experiment I); (b) 21-day-old rats following gestational but not lactational CDD (experiment II); and (c) 21-day-old rats following gestational and lactational CDD (experiment III). Enzyme activities and TAS were measured spectrophotometrically.


RESULTS
In choline-deprived (CD) newborn rats, TAS and AChE and Na(+),K(+)-ATPase activities were significantly reduced by 23%, 24% and 50%, respectively, in the brains of both sexes. Gestational CDD caused only a decrease in TAS (-27%, p<0.001) in suckling rat brains in both sexes. No changes were observed for the other enzyme activities. Moreover, gestational and lactational CDD also led only to a decrease in TAS (-24%, p<0.001) in the suckling rat brains of both sexes. Mg(2+)-ATPase activities showed no changes after any of the experimental procedures.


CONCLUSIONS
Our data suggest that the lower enzyme activities in newborn CD brains were restored to normal after 21 days of either normal or CDD lactation, possibly due to novel synaptogenesis, endogenous neuroregulation, and/or to other substances acquired by lactation. The increase in homocysteine concentration due to choline deficiency reported in the literature may be the cause of the low antioxidant capacity observed in offspring rat brains. Brain Na(+),K(+)-ATPase inhibition (induced by CDD) could result in modulations of neural excitability, metabolic energy production and neurotransmission.
Liapi
Charis
C
Department of Experimental Pharmacology, Medical School, University of Athens, Athens, Greece.
Feskou
Irini
I
Zarros
Apostolos
A
Galanopoulou
Panagiota
P
Tsakiris
Stylianos
S
D000110:Acetylcholinesterase / Q000378:metabolism; D000818:Animals; D000831:Animals, Newborn; D000975:Antioxidants / Q000032:analysis*; D001921:Brain / Q000254:growth & development / Q000378:metabolism*; D017301:Ca(2+) Mg(2+)-ATPase / Q000378:metabolism; D002796:Choline Deficiency / Q000378:metabolism*; D005260:Female; D006710:Homocysteine / Q000378:metabolism; D006867:Hydrolases / Q000378:metabolism*; D007774:Lactation / Q000378:metabolism*; D008297:Male; D011247:Pregnancy / Q000378:metabolism*; D051381:Rats; D000254:Sodium-Potassium-Exchanging ATPase / Q000378:metabolism
D000975:Antioxidants; D006710:Homocysteine; D006867:Hydrolases; D000110:Acetylcholinesterase; D017301:Ca(2+) Mg(2+)-ATPase; D000254:Sodium-Potassium-Exchanging ATPase