Nicotine-induced cessation of embryonic development is reversed by γ-tocotrienol in mice.

Abstract

BackgroundThis study aimed to evaluate the adverse effects of various doses of nicotine and protective effects of different concentrations of γ-tocotrienol (γ-TCT) on in vitro embryonic development and lipid peroxidation in mice.Material/MethodsA) Effects of various doses of nicotine on in vitro embryonic development: Female mice were treated with 1.0, 3.0, or 5.0 mg/kg/day nicotine for 7 consecutive days. Animals were superovulated, cohabited overnight, and sacrificed. Embryos were cultured in vitro. Plasma was assayed. B) Effects of concomitant treatment of nicotine concurrently with various doses of γ-TCT on in vitro embryonic development: Female mice were treated with nicotine (5.0 mg/kg/day), gavaged γ-TCT of 30, 60, or 90 mg/kg/day or nicotine concurrently with γ-TCT of 3 different doses for 7 consecutive days. Animals were superovulated, cohabited overnight, and sacrificed. Embryos were cultured and plasma was assayed.ResultsA) Effects of various doses of nicotine on in vitro embryonic development: Number of hatched blastocysts decreased in 1.0 and 3.0 mg/kg/day nicotine groups. Nicotine at 5.0 mg/kg/day stopped embryo development at morula. MDA concentrations increased following all nicotine doses. B) Effects of concomitant treatment of nicotine concurrently with various doses of γ-TCT on in vitro embryonic development: Embryo development was completed in all groups. MDA concentration increased only in the group treated with nicotine concurrently with 30 mg/kg/day γ-TCT.ConclusionsNicotine impairs in vitro embryo development and increases MDA in plasma. The deleterious impact of nicotine on embryo development is reversed by supplementing γ-TCT concurrently with nicotine.