Hepatic S-adenosylmethionine after maternal alcohol exposure on offspring rats

S-adenosylmethionine (SAM) is an universal methyl donor for biological systems in transmethylation reactions. Another metabolic pathway involving S-adenosylmethionine is initiated with the release of -CH3 from the molecule and the formation of S-adenosylhomocysteine and then homocysteine and cysteine, a precursor of the main cellular antioxidant glutathione. Chronic ethanol consumption could affect the bioavailability of amino acids such as methionine. Our purpose was to determine the effect of chronic alcohol feeding during gestation or lactation on hepatic S-adenosyl-methionine, S-adenosylhomocysteine, DNA methylation and homocysteine serum concentration at the end of the lactation period (21-day-old offspring). Wistar dam rats were fed with alcohol during periconceptional, gestation and lactation periods (alcohol-fed rats). This study was conducted with three groups of offspring with different periods of alcohol exposure: control offspring (C), no treatment; and gestation (G) and lactation (L) offspring, exposed to alcohol only during gestation or lactation, respectively. To obtain these last two groups of offspring, on parturition day control newborn rats were cross-fostered to alcohol-fed dams (L) and alcohol new-born rats were cross-fostered to control dams (G). In conclusion, these results indicate that exposure of rats to ethanol during the lactation period affects SAM values more severely than ethanol exposure only during gestation.