Aspartame is a widely used artificial sweetener that was shown to increase brain lipid peroxidation in mice. In the present study the effect administering a high dose of aspartame either alone or in conjunction with vitamin C (Vit. C) or vitamin E (Vit. E) on mouse brain and liver tissue was examined using biochemical and histological methods. Aspartame was given intraperitoneally (i.p.) at the dose 80 mg/kg, alone or in combination with Vit. C (25 mg/kg) or Vit. E (25 mg/kg) once daily for four weeks. Nitric oxide, reduced glutathione and malondialdehyde (lipid peroxidation) were assessed as oxidative stress biomarkers. Haematoxylin and eosin staining was utilised for histological examinations and immunostaining for cleaved caspase-3 was performed to detect signs of cellular apoptosis. Results showed that malondialdehyde and nitric oxide levels in brain and liver tissue significantly increased whilst reduced glutathione levels decreased when aspartame was given at a dose of 40 mg/kg. Histopathological examinations showed cellular infiltration, darkened neuronal nuclei and enhanced caspase-3 immunostaining, all of which indicated that these cells were undergoing apoptosis. Many hepatocytes in the liver displayed apoptosis and vacuolar degeneration and numerous cells had positive caspase-3 immunostaining. Giving vitamins C and E to aspartame-treated mice significantly reduced oxidative stress, histopathological abnormalities and apoptosis in the brain and liver. These results imply that high dosages of the artificial sweetener aspartame may be linked to oxidative stress-mediated brain and liver cell injury, which is treatable with antioxidant vitamins C and E.
Keywords: Aspartame; artificial sweeteners; vitamin C; vitamin E; liver injury; brain injury; oxidative stress; apoptosis; capsace-3 activation
