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J Chem Neuroanat. 2016 Dec;78:42-56. doi: 10.1016/j.jchemneu.2016.08.006. Epub 2016 Aug 24.

Alterations in behaviour, cerebral cortical morphology and cerebral oxidative stress markers following aspartame ingestion.

Author information

1
Department of Anatomy, Faculty of Basic Medical Sciences, College of Health Sciences, Ladoke Akintola University of Technology, Ogbomosho, Oyo State, Nigeria; Department of Anatomy and Cell Biology, Faculty of Basic Medical Sciences, Obafemi Awolowo University, Ile-Ife, Osun State, Nigeria. Electronic address: adegbayibiy@yahoo.com.
2
Department of Pharmacology and Therapeutics, Faculty of Basic Medical Sciences, College of Health Sciences, Ladoke Akintola University of Technology, Oshogbo, Osun State, Nigeria. Electronic address: olakunleonaolapo@yahoo.co.uk.
3
Department of Anatomy and Cell Biology, Faculty of Basic Medical Sciences, Obafemi Awolowo University, Ile-Ife, Osun State, Nigeria.

Abstract

OBJECTIVE:

The study evaluated changes in open field behaviours, cerebral cortical histomorphology and biochemical markers of oxidative stress following repeated administration of aspartame in mice.

METHODOLOGY:

Adult mice were assigned into five groups of twelve each. Vehicle (distilled water), or aspartame (20, 40, 80 and 160mg/kg body weight) were administered orally for 28days. Horizontal locomotion, rearing and grooming were assessed after the first and last dose of aspartame. Sections of the cerebral cortex were processed and stained for general histology, and also examined for neuritic plaques using the Bielschwosky's protocol. Glial fibrillary acidic protein (GFAP) and neuron specific enolase (NSE) immunoreactivity were assessed using appropriate antibodies. Aspartate and antioxidant levels were also assayed from cerebral cortex homogenates. Data obtained were analysed using descriptive and inferential statistics.

RESULTS:

Body weight and food consumption decreased significantly with aspartame consumption. Locomotion, rearing and grooming increased significantly after first dose, and with repeated administration of aspartame. Histological changes consistent with neuronal damage were seen at 40, 80 and 160mg/kg. Neuritic plaque formation was not evident; while GFAP-reactive astrocytes and NSE-reactive neurons increased at 40 and 80mg/kg but decreased at 160mg/kg. Superoxide dismutase and nitric oxide increased with increasing doses of aspartame, while aspartate levels showed no significant difference.

CONCLUSION:

The study showed morphological alterations consistent with neuronal injury and biochemical changes of oxidative stress. These data therefore supports the need for caution in the indiscriminate use of aspartame as a non-nutritive sweetener.

KEYWORDS:

Cerebral cortex; Glial fibrillary acid protein; Histology; Neuron specific enolase; Oxidative stress

PMID:
27565676
DOI:
10.1016/j.jchemneu.2016.08.006
[Indexed for MEDLINE]

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