By Margareta Törnqvist (auth.), Mendel Friedman, Don Mottram (eds.)
Reports that warmth processing of meals induces the formation of acrylamide heightened curiosity within the chemistry, biochemistry, and defense of this compound. Acrylamide-induced neurotoxicity, reproductive toxicity, genotoxicity, and carcinogenicity are capability human overall healthiness hazards in line with animal experiences. simply because publicity of people to acrylamide can come from either exterior resources and the vitamin, there exists a necessity to enhance a greater knowing of its formation and distribution in foodstuff and its function in human overall healthiness. To give a contribution to this attempt, specialists from 8 international locations have awarded information at the chemistry, research, metabolism, pharmacology, and toxicology of acrylamide.
Specifically coated are the next elements: publicity from the surroundings and the nutrition; biomarkers of publicity; possibility evaluate; epidemiology; mechanism of formation in foodstuff; organic alkylation of amino acids, peptides, proteins, and DNA through acrylamide and its epoxide metabolite glycidamide; neurotoxicity, reproductive toxicity, and carcinogenicity; safety opposed to adversarial results; and attainable ways to lowering degrees in meals. Cross-fertilization of rules between a number of disciplines within which an curiosity in acrylamide has built, together with foodstuff technology, pharmacology, toxicology, and drugs, will offer a greater figuring out of the chemistry and biology of acrylamide in meals, and will bring about the advance of nutrition procedures to diminish the acrylamide content material of the diet.
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Extra info for Chemistry and Safety of Acrylamide in Food
Or oral (gavage, drinking water) route. ) and route (inhalation. LoPachin 24 dermal, oral) of exposure. Clearly, future studies are needed to characterize neurotoxic potential of AA in lower dose-rate models and to discern the potential long-term cumulative effects of AA. 20 30 days of exposure Figure 1. Effects of AA on mean gait scores. AA was administered to groups of rats (n = 810 per group) at a daily dose rate of either 50 or 21 mg/kg per day. p. injections. To assess gait scores rats were placed in a clear Plexiglas box and observed for three minutes.
05 - 2 mg/kg/d) that are, in accordance with the cumulative neurotoxicity of AA, conducted over appropriately long experimental durations. Such studies would accurately determine the lowest observed and no observed adverse effect levels (LOAEL and NOAEL, respectively), which are important parameters for risk characterization. Table 1. Density (mean iSEM) of nerve terminal degeneration in spinal cord gray matter of AA intoxicated rats. 4 lumbar Ll-4 L5-7 L8-9 area 10 The density of degeneration was rated according to the following scale: 0=None, l=Rare, 2=Occasional, 3=Slight, 4=Moderate or 5=Heavy.
1994; Mastrogiacomo and Gundersen, 1995; Rothman, 1994). , 1994). , 2002a, 2003). Acrylamide Neurotoxicity 7. 31 SUMMARY Exposure of both laboratory animals and humans to AA produces neurotoxicity characterized by ataxia and skeletal muscle weakness. Reproductive toxicity and carcinogenicity are also potential human health concerns based on substantial data from animal studies. , French fries, potato chips, and some breads. , different dose-rates produce equivalent neurotoxic effects that differ with respect to onset and development.