Absorption and metabolism of the food contaminant 3-chloro-1,2-propanediol (3-MCPD) and its fatty acid esters by human intestinal Caco-2 cells

被引:0
作者
Thorsten Buhrke
Rüdiger Weißhaar
Alfonso Lampen
机构
[1] Federal Institute For Risk Assessment,Department of Food Safety
[2] CVUA Stuttgart,undefined
来源
Archives of Toxicology | 2011年 / 85卷
关键词
3-MCPD; 3-MCPD fatty acid ester; Food contaminant; Risk assessment; Caco-2;
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摘要
3-Chloro-1,2-propanediol (3-MCPD) fatty acid esters are formed upon thermal processing of fat-containing foods in the presence of chloride ions. Upon hydrolytic cleavage, these substances could release free 3-MCPD. This compound is toxicologically well characterised and displayed cancerogenic potential in rodent models. Recently, serious contaminations of different food products with 3-MCPD fatty acid esters have been reported. In regard to a risk assessment, the key question is to which degree these 3-MCPD fatty acid esters are hydrolysed in the human gut. Therefore, the aim of the present project was to examine the hydrolysis of 3-MCPD fatty acid esters and the resulting release of free 3-MCPD by using differentiated Caco-2 cells, a cellular in vitro model for the human intestinal barrier. Here, we show that 3-MCPD fatty acid esters at a concentration of 100 μM were neither absorbed by the cells nor the esters were transported via a Caco-2 monolayer. 3-MCPD-1-monoesters were hydrolysed in the presence of Caco-2 cells. In contrast, a 3-MCPD-1,2-diester used in this study was obviously absorbed and metabolised by the cells. Free 3-MCPD was not absorbed by the cells, but the substance migrated through a Caco-2 monolayer by paracellular diffusion. From these in vitro studies, we conclude that 3-MCPD-1-monoesters are likely to be hydrolysed in the human intestine, thereby increasing the burden with free 3-MCPD. In contrast, intestinal cells seem to have the capacity to metabolise 3-MCPD diesters, thereby detoxifying the 3-MCPD moiety.
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页码:1201 / 1208
页数:7
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  • [1] Aoki J(2007)Structure and function of extracellular phospholipase A1 belonging to the pancreatic lipase gene family Biochimie 89 197-204
  • [2] Inoue A(2001)Caco-2 monolayers in experimental and theoretical predictions of drug transport Adv Drug Deliv Rev 46 27-43
  • [3] Makide K(2006)Regulators for blood glucose level affect gene expression of aquaporin 3 Biol Pharm Bull 29 991-996
  • [4] Saiki N(1995)Regulation of tight-junction permeability during nutrient absorption across the intestinal epithelium Annu Rev Nutr 15 35-55
  • [5] Arai H(2002)Interaction between metabolism and transport of benzo[a]pyrene and its metabolites in enterocytes Toxicol Appl Pharmacol 183 168-178
  • [6] Artursson P(2005)Lipid micelles stimulate the secretion of triglyceride-enriched apolipoprotein B48-containing lipoproteins by Caco-2 cells J Cell Physiol 202 767-776
  • [7] Palm K(2008)Carcinogenicity study of 3-monochloropropane-1, 2-diol in Sprague-Dawley rats Food Chem Toxicol 46 3172-3177
  • [8] Luthman K(2008)Subchronic toxicity study of 3-monochloropropane-1,2-diol administered by drinking water to B6C3F1 mice Food Chem Toxicol 46 1666-1673
  • [9] Asai M(1991)A model of human small intestinal absorptive cells. 1. Transport barrier Pharm Res 8 210-216
  • [10] Higuchi S(1991)Mechanism of formation of chloropropanols present in protein hydrolysates J AOCS 68 785-790