Toxicological evaluation of aspartame against Madin–Darby canine kidney cells

Aspartame is most widely used as artificial sweeteners in more than 6000 food varieties. Aspartame digested into aspartic acid, phenylalanine, and methanol, and several peroxides, superoxide molecules also generated together. The kidney is the secondary site for the cellular metabolism. The present study examined whether the treatment of aspartame induces oxidative stress in the Madin–Darby kidney cells (MDCK). The effects of aspartame on MDCK cell viability were investigated by the sulphorhodamine-B assay and flow cytometry. Morphology of MDCK cells following aspartame exposure was observed. Mitochondria-derived reactive oxygen species (ROS) was also determined using 2′,7′-dichlorodihydrofluorescein diacetate. Lipid peroxidation (LPO), glutathione reduced (GSH) levels and activities of superoxide dismutase (SOD), and catalase enzymes were also determined. Cell viability was significantly altered following aspartame exposure. Morphology of MDCK cells did not change significantly. However, there was a marginal morphological change, including rounding, sporadic distribution and loss of adherence were observed at higher doses of aspartame exposure. Mitochondria-derived ROS was increased in a dose-dependent manner following aspartame exposure. A significant increase in LPO levels, whereas GSH level was reduced after 48 and 72 h of aspartame exposure. SOD and catalase enzyme activities were significantly reduced in a dose- and time-dependent manner. Taking all these data together, it is concluded that aspartame may induce oxidative stress in the MDCK cells.