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Glycidyl fatty acid esters (GEs), one of the main contaminants in processed oils, are mainly formed during the deodorization step in the refining process of edible oils and therefore occur in almost all refined edible oils. GEs are potential carcinogens, due to the fact that they readily hydrolyze into the free form glycidol in the gastrointestinal tract, which has been found to induce tumors in various rat tissues. Furthermore, glycidol has already been identified as a "possible human carcinogen'' (group 2A) by the Intl. Agency for Research on Cancer (IARC). Therefore, significant effort has been devoted to inhibit and eliminate the formation of GEs. The aim of this review is to provide a comprehensive summary on the following topics: (i) GE occurrence data for different edible oils and oil-based food products, (ii) precursors of GEs, (iii) factors influencing the formation of GEs, (iv) potential reaction mechanisms involving the leaving group and reaction intermediates, and (v) analytical methods, including the indirect and direct methods. More importantly, the various elimination methods for GEs in refined edible oils are being reviewed with focus on 3 aspects: (i) inhibition and removal of reactants, (ii) modification of reactive conditions, and (iii) elimination of GE products.

Premise The natural population size of Huperzia serrata (Lycopodiaceae) has dramatically decreased and the species has become endangered due to overexploitation. Here, we developed simple sequence repeat (SSR) markers for H. serrata to survey both its genetic diversity and population structure. Methods and results Based on 177 individuals, 120 SSR primer pairs were developed and optimized from five regions of the H. serrata transcriptomic data. Of these primer pairs, 20 were successfully amplified and 10 showed obvious polymorphism. These polymorphic loci were investigated to study the genetic diversity of H. serrata. Two to 11 alleles per locus were identified, the level of observed heterozygosity ranged from 0.00 to 1.00, and the level of expected heterozygosity ranged from 0.19 to 0.79. All loci were successfully amplified in H. crispata, H. sutchueniana, and H. selago. Conclusions The 10 polymorphic primer pairs developed here will be valuable for studies of the endangered H. serrata and other related species.

Breakdown of membrane phospholipids is a causative event leading to irreversible cell injury after ischemia and reperfusion insults, which might be one mechanism leading to liver tumor cell death after repeated arterial ischemia as well. After 2 hr of hepatic dearterialization followed by 30 min of reperfusion tumor phospholipid was measured chromatographically, glutathione (GSH) analyzed by determining nonprotein sulfhydryl and activity of glutathione-S-transferase (GST) determined spectrophotometrically using 1-chloro-2,4-dinitrobenzene (CDNB) as the subtrate. A transient, arterial ischemia for 2 hr induced a substantial decrease of phosphatidylserine (PS) and phosphatidylinosital (PI) compared with sham treatment (P < 0.01). Although phosphatidylcholine (PC) and phosphatidylethanolamine (PE) did not significantly decline after a single arterial ischemia for 2 hr, they dropped dramatically following repeated arterial ischemia for 2 hr during 5 days (P < 0.01 and P < 0.05 respectively). GSH was depleted in tumors after both a single (P < 0.01) and repeated arterial ischemia (P < 0.05) and GST was inactivated as well (P < 0.001). By contrast, neither liver phospholipid nor liver GSH or GST was significantly changed. Tumor growth was significantly retarded in rats subjected to repeated arterial ischemia compared with sham treatment (P < 0.01). Repeated arterial ischemia facilitated degradation of tumor membrane phospholipids and induced depletion of GSH and inactivation of GST without affecting the normal liver. Thus, ischemia/reperfusion induced depletion of membrane phospholipids and of GSH might represent two mechanisms by which repeated arterial ischemia led to tumor growth delay. (C) 1996 Wiley-Liss, Inc.

Background. Conflicting results have been obtained regarding blood flow distribution to liver tumors. The emphasis on portal vein perfusion has had a great impact on the design of treatment protocols. Methods. Double microsphere technique with reference organ sampling was used for the measurement of hepatic artery and portal vein blood flow of an implanted liver tumor in 42 rats after permanent dearterialization and repeated dearterialization (2 hours/day) compared with untreated sham-operated controls. Results. Portal veinous blood flow constituted 16% of total tumor blood flaw and slightly increased after permanent and repeat dearterializations, though the elevation was not statistically significant as compared with sham-treatment (P> 0.05). In another 3 groups, the treatment was extended to 10 days, and tumor blood flow was measured in central and peripheral parts separately. Arterial blood flow further decreased in tumor periphery and was still lower in the tumor center (P 0.05). Furthermore, portal supply increased neither in tumor periphery nor in tumor center after both permanent and repeated dearterialization (P > 0.05). Conclusion. The authors' results showed that portal blood flow did contribute to tumor circulation, but made up only 16% of blood flow when tumors were small and declined to 4% of entire tumor blood supply when tumors became large. Portal perfusion also declined as tumors grew larger and did not compensate for the withdrawal of tumor arterial blood supply after dearterialization. Cancer 1994:74:2454-9.

The present study aimed at modifying the surface of biliary drain material to reduce bacterial adherence. The adherence of cells of seven E. coli strains to rubber slices treated with phosphatidylcholin (PC) or phosphatidylinositol (PI) and the adherence of cells of E. coli strain NG7C to PC- or PI-treated rubber slices implanted in the common bile duct in rats were studied in vitro. The rubber slices were incubated with 1 x 10(7) cfu radiolabeled E. coli cells/ml at 37 degrees C for 60 min and then drained and washed thrice in 2 ml PBS, and adherent E. coli cells were quantified by radioactivity counting. The results show that both PC and PI absorbed on the surface of slices reduced the adherence of E. coli cells in at least two ways, i.e. by changing surface properties in vitro and by reducing deposition of host-derived molecules on phospholipid-treated surfaces in vivo. The results may be of use for modification of the biomaterial surface in the clinical situation.