Mitochondria-Derived Oxidative Stress Associated with Aspartame Effect on Kidney Cells

Abstract

Aspartame is a low calorie sugar that is widely used in artificial sweeteners. Although different studies indicated associated health symptoms to it, it continues to be controversial. Studies have also shown consumption of aspartame caused neurological deficits and mitochondrial mediated activation of apoptosis was observed as a long-term effect of aspartame in rat brain. In this study, the biochemical responses of distal tubular kidney cells upon short-term exposure to aspartame were measured. MDCK Type II (kidney) cells were exposed to 50 µg/ml to 250 µg/ml aspartame for 30 mins. Mitochondrial linked biochemical responses such as oxidative stress and energy production was measured. Overall increase in dehydrogenase activity together with increased production of ATP was observed. This was accompanied by an overall increase in mitochondria derived oxidative stress. However, mitochondrial membrane potential and cellular NAD/NADH ratio in the aspartame exposed cells remained unchanged. These results indicate that while aspartame did not cause significant changes in the mitochondrial activity, the elevated activity of the mitochondria shown through the increase in ATP production and oxidative stress indicate the involvement of the mitochondria in aspartame-mediated cellular response. More studies would need to be done to clarify the mechanism by which aspartame increases oxidative stress via the mitochondria.