SAM/SAH Mediates Parental Folate Deficiency-Induced Neural Cell Apoptosis in Neonatal Rat Offspring: The Expression of Bcl-2, Bax, and Caspase-3

Research demonstrated that folate deficiency in either the mother or father could impact biological functions of offspring’s neural cells. Folate can also impair methionine cycle, thus contributing to conversion S-adenosylmethionine (SAM) S-adenosylhomocysteine (SAH), which potentially cause damage central nervous system. The study focused on effect parental cell apoptosis offspring neonatal rats and whether it is mediated by levels SAM SAH brains. experimental design was conducted feeding female male Sprague Dawley (SD) with folate-deficient folate-normal diets, sacrificing within 24 h isolating their brain tissue. Rats were divided into four groups: maternal-folate-deficient paternal-folate-deficient (D-D) group; paternal-folate-normal (D-N) maternal-folate-normal (N-D) (N-N) group. There down-regulation B-cell lymphoma 2 (Bcl-2) expression, up-regulation Bcl-2-associated X protein (Bax) Caspase-3 expression cells, pathological changes ultrastructure, as well decreased levels, increased a SAM/SAH ratio rat fetal via deficiency. In conclusion, induce cells rats, while biparental had greatest offspring, unilateral greater mothers than fathers. This process may be brain.