RESUMO
A hypothesis that acrylamide is formed by/upon cooking was confirmed in experimental animals by a verification of the identity of the acrylamide adduct in hemoglobin [Hb]. This was comprehensively approved by GC/MS analysis and the demonstration that the increased adduct levels were compatible with expectation from the contents of acrylamide determined in fried feeds. A significant dependence of acrylamide formation on temperature was demonstrated. Extensive efforts were made to assess the human exposure to acrylamide by monitoring several metabolites excreted in the urine as well as products resulting from biological alkylation by acrylamide. The results from in vivo studies conducted on rats explored that dermal absorption ranged from approximately 14 to 61% of the applied dose. Meanwhile, it was obvious that acrylamide was widely distributed in all tissues of the body. The major metabolite formed from acrylamide via the cytochrome P450 pathway was glycidamide. Conjugation to reduced glutathione [GSH] catalyzed by glutathione S-transferase [GST] and excretion as mercapturic acid is a major pathway for the metabolism of acrylamide. Experiments revealed neuro and reproductive toxicity of acrylamide. The International Agency of Research on Cancer [IARC] has classified acrylamide as probably carcinogenic to humans. Acrylamide in foods can be determined by GC/MS, HPLC and liquid chromatography-mass spectrometry [LC-MS] using the MS/MS mode. For the GC/MS and HPLC methods, the achieved detection level of acrylamide was 5 mug/kg; while, for LC-MS/MS method, it was 10 mug/kg. The latter method is simple and preferable for routine analysis