(814.5) Effect of Short-Term and Long-Term Exposure to Sucrose on Protein Expression and Oxidative Modification of Glutathione-S-Transferase Mu 1 (GSTM1) in Liver of Wild Type Mice

Poster Board Number: A376

Debra Boyd-Kimball (University of Mount Union), Elise Chojnacki (University of Mount Union), Santino Diaz-Palma (University of Mount Union), Shelby Graham (University of Mount Union), Andrew McMillen (University of Mount Union), Brett Scheib (University of Mount Union), Benjamin Trenka (University of Mount Union), Alaina Metzler (University of Mount Union), Katelyn Gonczy (University of Mount Union), Ashlyn Paxton (University of Mount Union)

High dietary sugar intake is an environmental risk factor for the development of metabolic syndrome (MS), type 2 diabetes (T2D), and non-alcoholic fatty liver disease (NAFLD).  All three of these conditions are associated with oxidative stress and a high sugar diet has been shown to affect the protein expression and activity of antioxidant and detoxification enzymes including glutathione-S-transferase (GST).  In this study, the effect of short-term (ST) 2-month and long-term (LT) 8-month sucrose exposure on the protein expression and oxidative modification of GST mu 1 (GSTM1) in liver of wild type mice was assessed.  It was hypothesized that sucrose exposure would result in a decrease in GSTM1 protein expression and an increase in oxidative modification of GSTM1 as indexed by protein-bound 4-hydroxy-2-trans-nonenal (HNE). It was determined that the protein expression of GSTM1 was significantly increased in the ST sucrose exposed mice, but significantly decreased in the LT control mice compared to the ST control mice.  Additionally, GSTM1 was found to be significantly oxidatively modified by protein-bound HNE in the LT sucrose exposed mice compared to the ST control mice, the ST sucrose exposed mice, and the LT control mice. These results suggest that a high sugar diet may impair the antioxidant status of the liver by oxidatively modifying detoxification enzymes such as GSTM1.