Long-term fructose intake reduces oxidative defense and alters mitochondrial performance in mice

Mitochondria are involved in the production of reactive oxygen species and subsequently are very susceptible to oxidative stress. Fructose, a reducing monosaccharide, is widely used as a food ingredient and has a high potential to intensify oxidative stress through the Maillard reaction or autooxidation processes. This study presents a new insight into the long-term effects of fructose consumption on the mouse mitochondria. Examination of carbonyl levels, as a marker of protein oxidative modification, in 17-month-old ICR mice introduced to fructose solutions vs water, showed a significant decrease in hepatic carbonyl levels of fructose-treated animals although no changes in brain and skeletal mitochondria. The activity of manganese superoxide dismutase (MnSOD), the main mitochondrial antioxidative enzyme, was significantly decreased in all the tested tissues after fructose consumption. No correlation was found between the expression levels of MnSOD and its specific activity. These findings suggest that a defense mechanism is activated in hepatic mitochondria of fructose-treated mice, excluding MnSOD as an option. Electron microscopy examination indicated changes in mitochondrial morphology caused by prolonged drinking of fructose solutions. These findings support the concern directed at the extensive use of fructose in the food industry.