Ethanol-induced increased endogenous homocysteine levels and decreased ratios of SAM/SAH are only partially attenuated by exogenous glycine in developing chick brains

The effects of exogenous ethanol (EtOH) and/or glycine on chick (Gallus gallus) embryo viability, brain apoptosis (caspase-3 activities), and the endogenous levels of brain homocysteine (HoCys), S-adenosylmethionine (SAM), S-adenosylhomocysteine (SAH), and SAM/SAH were studied. Embryonic EtOH exposure caused decreased embryo viability as measured by EtOH-induced reductions in % living embryos at theoretical stage 37, EtOH-induced reductions in embryo masses, and EtOH-induced reductions in brain caspase-3 (Casp-3) activities. Exogenous glycine failed to attenuate EtOH-induced decreased embryo viability and EtOH-induced increased brain Casp-3 activities. Embryonic EtOH exposure caused elevated levels of endogenous HoCys, decreased levels of SAM, increased levels of SAH, and decreased SAM/SAH ratios in embryonic chick brains. While exogenous glycine failed to attenuate EtOH-induced increased HoCys levels, exogenous glycine attenuated EtOH-induced decreased levels of SAM, increased levels of SAH, and decreased SAM/SAH levels in embryonic chick brains.