Abstract：
:There has been an intensive debate whether dietary exposure to acrylamide could increase the risk of human cancer since the first description of the presence of acrylamide in food in 2002. As the intestinal mechanisms of acrylamide absorption are poorly investigated we studied the transport of acrylamide in differentiated Caco-2 cells and its effects on biotransformation enzymes (CYP2E1 and glutathione S-transferase) and glutathione levels. We found that the apparent permeability of [1-(14)C] acrylamide from the basal to the apical compartment was approximately 20% higher compared to that in the opposite direction. No differences were detected for apical-basal transport against a basal gradient. Transport rates from the apical to the basal chamber at 4 degrees C were about 50% lower than at 37 degrees C. Concentration dependent transport from apical to basal was linear. Predominantly, basal to apical transport was decreased when energy metabolism of the cells was inhibited by application of sodium azide and 2-deoxy-d-glucose. Finally, more acrylamide was transported at luminal pH 6 compared to pH 7.4 from basal to the apical direction. Increasing levels of acrylamide showed no effects on the activity of glutathione S-transferase but resulted in a depletion of total glutathione concentrations. In conclusion transport of acrylamide in the intestine is mediated primarily by passive processes possibly combined with a modest energy- and pH-dependent active secretory component. Depletion of cellular glutathione levels may be one potential mechanism for acrylamide (geno)toxicity.
journal_name
Toxicologyjournal_title
Toxicologyauthors
Zödl B,Schmid D,Wassler G,Gundacker C,Leibetseder V,Thalhammer T,Ekmekcioglu Cdoi
10.1016/j.tox.2006.12.014subject
Has Abstractpub_date
2007-03-22 00:00:00pages
99-108issue
1-2eissn
0300-483Xissn
1879-3185pii
S0300-483X(06)00757-8journal_volume
232pub_type
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