Abstract

Aspartame (L- aspartyl- L-phenylalanine methyl ester) is one of the most widely artificial sweeteners consumed in so many products worldwide in various countries which added to a large variety of food, most commonly found in low calorie beverages. On metabolism in humans and experimental animals, aspartame is rapidly and completely metabolized to aspartic acid (40%), phenylalanine (50%) and methanol (10%). Methanol, a toxic metabolite is primarily metabolized by oxidation to formaldehyde and then to formate; these processes are accompanied by the formation of superoxide anion and hydrogen peroxide. This study focus is to understand whether the oral administration of aspartame (40 mg/kg b.w) for 15, 30 and 90 days have any effect on the antioxidant status (enzymatic and non-enzymatic) in immune organs such as the spleen, thymus, lymph nodes and bone marrow of rats. To mimic human methanol metabolism, folate deficient rats were used. After 15 days of aspartame administration, animals showed a significant increase in free radical production as indicated by the increase in both enzymatic (superoxide dismutase, catalase, glutathione peroxidase) and non-enzymatic (reduced glutathione and vitamin C) antioxidant level along with the marked increase in lipid peroxidation and nitric oxide level. However, after repeated long term administration (30 and 90 days), the generation of reactive free radicals overwhelmed the antioxidant defense as indicated by an increase in lipid peroxidation with the decrease in antioxidants level. This study concludes that administration of aspartame even at the Food and Drug Administration permitted level its repeated exposure causes oxidative stress by altering the oxidant/antioxidant balance in immune organs of the rats and its effects also reflected in the histology of the spleen and lymph nodes Key words: Aspartame, folate- deficient, immune organs, oxidative stress.

Highlights

  • Aspartame marketed as nutra sweet, candrelel or equal was serendipitously discovered in 1965 by JamesSchlatter, a chemist working for G.D

  • Aspartame (L- aspartyl- Lphenylalanine methyl ester) is one of the most widely artificial sweeteners consumed in so many products

  • According to Britton et al (1992), it may be due to methanol, a metabolite of aspartame which stimulates norepinephrine to act on corticotrophin releasing factor (CRF) neurons in the paraventicular nucleus of hypothalamus to directly stimulate CRF release to act on pituitary to release adrenocorticotropic hormone (ACTH)

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Summary

Introduction

Aspartame marketed as nutra sweet, candrelel or equal was serendipitously discovered in 1965 by JamesSchlatter, a chemist working for G.D. Aspartame marketed as nutra sweet, candrelel or equal was serendipitously discovered in 1965 by James. Aspartame (L- aspartyl- Lphenylalanine methyl ester) is one of the most widely artificial sweeteners consumed in so many products. After oral administration to humans and experimental animals, aspartame is rapidly and completely metabolized to 40% aspartic acid, 50%. Phenylalanine and 10% methanol (Karim and Burns, 1996; Stegink and Filer, 1996). It forms methanol when the methyl group of aspartame encounters the enzyme chymotrypsin in the small intestine (Stegink et al, 1981). A relatively small amount of aspartame can significantly increase plasma methanol levels (Davoli, 1986). In an update on the safety in use of aspartame, the European

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