Article ID | Journal | Published Year | Pages | File Type |
---|---|---|---|---|
5854360 | Food and Chemical Toxicology | 2009 | 8 Pages |
Abstract
No mutagenicity of PSO was observed in the absence and presence of metabolic activation up to precipitating concentrations of 5000 μg/plate (Ames test) or 333 μg/ml (chromosome aberration test). The acute oral toxicity study revealed no significant findings at 2000 mg PSO/kg body weight. In the 28-day dietary toxicity study PSO was dosed at concentrations of 0, 10,000, 50,000 and 150,000 ppm, which resulted in a mean intake of 0-0, 825-847, 4269-4330 and 13,710-14,214 mg PSO/kg body weight per day in males-females, respectively. At 150,000 ppm dietary exposure to PSO, a much higher dose than the level of PSO that elicits antidiabetic and anti-inflammatory efficacy, increased hepatic enzyme activities determined in plasma (aspartate, alanine aminotransferase and alkaline phosphatase) and increased liver-to-body weight ratios were observed. However, these effects might be the result of a physiological response to exposure to a very high level of a fatty acid which is not part of the normal diet, and are most likely not toxicologically relevant. The no observable adverse effect level (NOAEL) was 50,000 ppm PSO (=4.3 g PSO/kg body weight/day).
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Authors
I.A.T.M. Meerts, C.M. Verspeek-Rip, C.A.F. Buskens, H.G. Keizer, J. Bassaganya-Riera, Z.E. Jouni, A.H.B.M. van Huygevoort, F.M. van Otterdijk, E.J. van de Waart,