Current interest
in fructose metabolism and chemical properties has arisen because of its
increased use in the food industry in the crystalline form and as high-fructose
corn syrup. During the last decades, the importance of mitochondria as a major
contributor to various types of diseases and to aging has become apparent. This
research was undertaken to find and characterize the possible metabolic events,
induced by fructose as compared to glucose in the mitochondria. We performed an
extensive analysis of different parameters at three molecular levels: mtDNA,
RNA and protein. Cytotoxicity experiments in muscle cell culture suggested that
carbohydrate effects were dose- and time-dependent. The estimation of the mtDNA
susceptibility to reducing sugars demonstrates that fructose consumption causes
minor modifications to the mtDNA. Following 17 months drinking of fructose
solutions we observed a significant decrease in the activity of the main
mitochondrial antioxidant - manganese superoxide dismutase. Various genes
expression patterns reflected the attempts of nuclear regulation machinery to
balance the non-desirable changes in mitochondrial functioning in a tissue
dependent manner. The results indicated that the liver is the main target of
fructose influence, although there are minor alterations in postmitotic tissue
(skeletal muscles and brain). Electron microscopy analysis of skeletal muscles
obtained from mice maintained on fructose solutions, revealed some pathological
alterations in their mitochondrial morphology. Taking all together, these
findings implicate that fructose has a negative impact on the biological
machinery of the mammalian mitochondria, pointing out the need for
reconsideration fructose extensive use in food industry.
