Aspartame Metabolism in Human Subjects

Stegink, L. D.; Filer, L. J.; Baker, George L.; Brummel, Marvin C.; Tephly, Thomas R.

doi:10.1159/000402697

Cited by 9 publications

(7 citation statements)

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“…Aspartic acid is mostly eliminated through the lungs in the form of CO 2 . In humans, plasma level of aspartic acid does not increase significantly following oral administration of aspartame at a dose of 34 mg/ kg (Stegink, 1984). However, some of the phenylalanine formed in the intestine following ingestion of ASP is excreted in the form of CO 2 , most of it is incorporated into the pool of amino acids and contributes to protein synthesis (Stegink and Filer, 1996;Trefz and Bickel, 1996).…”

Section: Discussionmentioning

confidence: 99%

Effect of aspartame on some oxidative stress parameters in liver and kidney of rats

Iman¹

2011

Afr. J. Pharm. Pharmacol.

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Aspartame is one of the most widely used artificial sweeteners in over 90 countries worldwide. It is a highly intensity sweetener added to a large variety of food, most commonly found in low calorie beverages, desserts and table top sweeteners added to tea or coffee. The present study examined whether the daily oral administration of ASP (40 mg/kg) for 2, 4 and 6 weeks induce oxidative stress in the liver and kidney of male albino rats. Lipid peroxidation (LPO), glutathione reduced (GSH) levels as well as the activities of superoxide dismutase (SOD), glutathione-S-transferase (GST) and catalase (CAT) enzymes were determined. A significant increase in LPO levels was obtained in the liver tissue after 4 and 6 weeks of ASP administration while there was a significant decrease in LPO level after 2 weeks followed by a significant increase in the renal tissue at the end of the 6 weeks. SOD activity significantly decreased in the liver tissue after 2, 4 and 6 weeks of treatment. Also, there was a significant decrease in SOD activity after 2 and 4 weeks in the renal tissue. CAT activity significantly decreased in the liver tissue after 2 and 4 weeks of ASP administration. Regarding to GSH content, there was a significant decrease in the liver tissue after 2, 4 and 6 weeks which was accompanied by a significant increase in GST activity after 4 and 6 weeks of ASP administration. In conclusion, ASP may induce an oxidative stress in the liver and kidney of male albino rats.

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Section: Discussionmentioning

confidence: 99%

Effect of aspartame on some oxidative stress parameters in liver and kidney of rats

Iman¹

2011

Afr. J. Pharm. Pharmacol.

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“…Aspartame doses of 100, 150, and 200 mg/kg body wt were administered as a single bolus in orange juice to normal adult volunteers (3). Such intakes represent situations of abuse or accidental ingestion comparable with a daily intake of >20 L of an aspartame-sweetened beverage or a 10-kg 1-yr-old ingesting the entire contents of an aspartame coffee-sweetener bottle (100 tablets of 20 mg each).…”

Section: Methodsmentioning

confidence: 99%

“…For the average 70-kg adult or 20-kg 4-yr-old, aspartame intake under these amounts would approximate 3-10 mg/kg body wt. The Market Research Corporation of America (MRCA) has projected the 99th percentile of daily intake of aspartame at 34 mg/kg body wt (3). Accordingly, the clinical studies highlighted in this review bracket aspartame intakes that range from 4 to 200 mg/kg body wt.…”

mentioning

confidence: 99%

Aspartame Metabolism in Normal Adults, Phenylketonuric Heterozygotes, and Diabetic Subjects

Filer

Stegink

1989

Diabetes Care

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This study reviews clinical studies testing the effects of various doses of aspartame on blood levels of phenylalanine, aspartate, and methanol in normal subjects and known phenylketonuric heterozygotes. The effect of aspartame on the phenylalanine-to-large neutral amino acid ratio under various feeding situations is shown. The clinical studies of aspartame in diabetic subjects are limited to observations of its effects on blood levels of glucose, lipids, insulin, and glucagon. These studies clearly demonstrate the safety of this high-intensity sweetener for use by humans. Diabetes Care 12:67-74, 1989 I n the United States the prevalence of diabetes, both insulin dependent (IDDM) and non-insulin dependent (NIDDM), involves 2.7% of women and 2.0% of men (1). In 1976, it was projected that the incidence of diabetes was increasing at a rate of 6%/yr (2). The association of NIDDM with the degree and duration of obesity suggests one reason why high-intensity sweeteners, nutritive and nonnutritive, may be a component of foods eaten by diabetic individuals. The natural interest of humans in the sweet taste modality provides another rationale for incorporation of high-intensity sweeteners into the diet of diabetic individuals. Currently, the most widely consumed high-intensity sweetener is aspartame, a dipeptide methyl ester (L-aspartyl-L-phenylalanine methyl ester).On the basis of total pounds of aspartame sold to food and beverage processors, it has been estimated that as- Daily intake can be calculated and amounts to 104 mg/day or 1.5 mg/kg body wt for a 70-kg individual. Aspartame is rarely consumed alone but is usually ingested in conjunction with varying proportions of carbohydrate, protein, and fat. Unless a person drinks an aspartame-sweetened beverage, carbonated or still, as a refreshment, the intake usually involves other foods. Aspartame-containing carbonated soft drinks provide 150-200 mg of aspartame per serving (12 oz or 360 ml). Noncarbonated beverages usually contain 140 mg per serving (8 oz or 240 ml). For the average 70-kg adult or 20-kg 4-yr-old, aspartame intake under these amounts would approximate 3-10 mg/kg body wt. The Market Research Corporation of America (MRCA) has projected the 99th percentile of daily intake of aspartame at 34 mg/kg body wt (3). Accordingly, the clinical studies highlighted in this review bracket aspartame intakes that range from 4 to 200 mg/kg body wt. These studies largely represent single-bolus doses of aspartame given to normal adult subjects, known adult phenylketonuric (PKU) heterozygotes, or normal 1-yr-olds. Aspartame was administered in orange juice, in a noncarbonated beverage, as part of a hamburger and milk shake meal, or in a beverage ingested at repeated intervals. Aspartame doses >50 mg/kg body wt were considered to represent abuse doses; i.e., 100-200 mg/kg body wt. Based on the relative sweetness of aspartame to sucrose, abuse intakes of this magnitude represent an acute intake of sweetness equivalent to 3-6 Ib of sucrose. Participants in the latter clinica...

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“…Subsequent research by Black et al (72) showed that THF concentration in monkey livers was 59% of that in rats; the ratio of THF concentrations was similar to the ratio of their maximal formate oxidation rates. Several human studies show that even methanol exposures not saturating the folate pathway produce small amounts of formate in blood and urine (73)(74)(75). However, background blood formate levels varied in these studies, masking subtle differences methanol exposure may have caused.…”

Section: Toxicokineticsmentioning

confidence: 99%

Acute toxicity of gasoline and some additives.

Reese

Kimbrough

1993

Environ Health Perspect

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The acute toxicity of gasoline; its components benzene, toluene, and xylene; and the additives ethanol, methanol, and methyl tertiary butyl ether are reviewed. All of these chemicals are only moderately to mildly toxic at acute doses. Because of their volatility, these compounds are not extensively absorbed dermally unless the exposed skin is occluded. Absorption through the lungs and the gastrointestinal tract is quite efficient. After ingestion, the principal danger for a number of these chemicals, particularly gasoline, is aspiration pneumonia, which occurs mainly in children. It is currently not clear whether aspiration pneumonia would still be a problem if gasoline were diluted with ethanol or methanol. During the normal use of gasoline or mixtures of gasoline and the other solvents as a fuel, exposures would be much lower than the doses that have resulted in poisoning. No acute toxic health effects would occur during the normal course of using automotive fuels.

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Aspartame Metabolism in Human Subjects

Cited by 9 publications

References 0 publications

Effect of aspartame on some oxidative stress parameters in liver and kidney of rats

Effect of aspartame on some oxidative stress parameters in liver and kidney of rats

Aspartame Metabolism in Normal Adults, Phenylketonuric Heterozygotes, and Diabetic Subjects

Acute toxicity of gasoline and some additives.

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