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

Med Sci Monit Basic Res. 2013 Mar 6:19:87-92. doi: 10.12659/MSMBR.883822.

Abstract

Background: This study aimed to evaluate the adverse effects of various doses of nicotine and protective effects of different concentrations of gamma-tocotrienol (gamma-TCT) on in vitro embryonic development and lipid peroxidation in mice.

Material and methods: A) 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 gamma-TCT on in vitro embryonic development: Female mice were treated with nicotine (5.0 mg/kg/day), gavaged gamma-TCT of 30, 60, or 90 mg/kg/day or nicotine concurrently with gamma-TCT of 3 different doses for 7 consecutive days. Animals were superovulated, cohabited overnight, and sacrificed. Embryos were cultured and plasma was assayed.

Results: A) 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 gamma-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 gamma-TCT.

Conclusions: Nicotine impairs in vitro embryo development and increases MDA in plasma. The deleterious impact of nicotine on embryo development is reversed by supplementing gamma-TCT concurrently with nicotine.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Blastocyst / pathology
  • Chromans / pharmacology*
  • Disease Models, Animal
  • Dose-Response Relationship, Drug
  • Embryo Culture Techniques / methods
  • Embryonic Development / drug effects*
  • Female
  • Lipid Peroxidation*
  • Malondialdehyde / blood
  • Mice
  • Nicotine / pharmacology
  • Thiobarbituric Acid Reactive Substances / analysis
  • Time Factors
  • Vitamin E / analogs & derivatives*
  • Vitamin E / pharmacology

Substances

  • Chromans
  • Thiobarbituric Acid Reactive Substances
  • Vitamin E
  • plastochromanol 8
  • Malondialdehyde
  • Nicotine