Annatto (Bixa orellana) δ-TCT Supplementation Protection against Embryonic Malformations through Alterations in PI3K/Akt-Cyclin D1 Pathway

Biomolecules. 2019 Jan 10;9(1):19. doi: 10.3390/biom9010019.

Abstract

Protective action by annatto-derived delta-tocotrienol (δ-TCT) and soy-derived alpha-tocopherol (α-TOC) through the regulation of the PI3K/Akt-cyclin D1 pathway against nicotine-induced DNA damage is the focus of the present study. Nicotine, which has been widely reported to have numerous adverse effects on the reproductive system, was used as a reproductive toxicant. 48 female balb/c mice (6⁻8 weeks) (23⁻25 g) were randomly divided into eight groups (Grp.1⁻Grp.8; n = 6) and treated with either nicotine or/and annatto δ-TCT/soy α-TOC for seven consecutive days. On Day 8, the females were superovulated and mated before euthanization for embryo collection (46 h post-coitum). Fifty 2-cell embryos from each group were used in gene expression analysis using Affymetrix QuantiGene Plex2.0 assay. Findings indicated that nicotine (Grp.2) significantly decreased (p < 0.05) the number of produced 2-cell embryos compared to the control (Grp.1). Intervention with mixed annatto δ-TCT (Grp.3) and pure annatto δ-TCT (Grp.4) significantly increased the number of produced 2-cell embryos by 127% and 79%, respectively compared to Grp.2, but these were lower than Grp.1. Concurrent treatment with soy α-TOC (Grp.5) decreased embryo production by 7%. Supplementations with δ-TCT and α-TOC alone (Grp.6-Grp.8) significantly increased (p < 0.05) the number of produced 2-cell embryos by 50%, 36%, and 41%, respectively, compared to control (Grp.1). These results were found to be associated with alterations in the PI3K/Akt-Cyclin D1 genes expressions, indicating the inhibitory effects of annatto δ-TCT and soy α-TOC against nicotinic embryonic damage. To our knowledge, this is the first attempt in studying the benefits of annatto δ-TCT on murine preimplantation 2-cell embryos.

Keywords: annatto delta-tocotrienol; murine preimplantation embryos; nicotine; reproductive toxicant; tocopherols; vitamin E.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Bixaceae / metabolism*
  • Cyclin D1 / genetics
  • Cyclin D1 / metabolism
  • Dietary Supplements
  • Embryo, Mammalian / drug effects
  • Embryo, Mammalian / metabolism
  • Embryonic Development / drug effects
  • Female
  • Gene Expression Regulation, Developmental / drug effects
  • Glycine max / metabolism
  • Mice
  • Mice, Inbred BALB C
  • Nicotine / pharmacology
  • Phosphatidylinositol 3-Kinases / genetics
  • Phosphatidylinositol 3-Kinases / metabolism
  • Proto-Oncogene Proteins c-akt / genetics
  • Proto-Oncogene Proteins c-akt / metabolism
  • Signal Transduction / drug effects*
  • Superovulation / drug effects
  • Tocotrienols / pharmacology*
  • Vitamin E / analogs & derivatives*
  • Vitamin E / pharmacology

Substances

  • Tocotrienols
  • Cyclin D1
  • Vitamin E
  • tocotrienol, delta
  • Nicotine
  • tocotrienol, alpha
  • Phosphatidylinositol 3-Kinases
  • Proto-Oncogene Proteins c-akt