Vitamin E Modifies High-Fat Diet-Induced Increase of DNA Strand Breaks, and Changes in Expression and DNA Methylation of Dnmt1 and MLH1 in C57BL/6J Male Mice

• Main Authors: Marlene Remely, Franziska Ferk, Sonja Sterneder, Tahereh Setayesh, Tatjana Kepcija, Sylvia Roth, Rahil Noorizadeh, Martina Greunz, Irene Rebhan, Karl-Heinz Wagner, Siegfried Knasmüller, Alexander Haslberger
• Format: Article
• Language: English
• Published: MDPI AG 2017-06-01
• Series: Nutrients
• Subjects: MLH1; Dnmt1; DNA damage; gene expression; DNA methylation; SCGE assay
• Online Access: http://www.mdpi.com/2072-6643/9/6/607

Obesity is associated with low-grade inflammation, increased ROS production and DNA damage. Supplementation with antioxidants might ameliorate DNA damage and support epigenetic regulation of DNA repair. C57BL/6J male mice were fed a high-fat (HFD) or a control diet (CD) with and without vitamin E supplementation (4.5 mg/kg body weight (b.w.)) for four months. DNA damage, DNA promoter methylation and gene expression of Dnmt1 and a DNA repair gene (MLH1) were assayed in liver and colon. The HFD resulted in organ specific changes in DNA damage, the epigenetically important Dnmt1 gene, and the DNA repair gene MLH1. Vitamin E reduced DNA damage and showed organ-specific effects on MLH1 and Dnmt1 gene expression and methylation. These results suggest that interventions with antioxidants and epigenetic active food ingredients should be developed as an effective prevention for obesity—and oxidative stress—induced health risks.