Polychlorierte Biphenyle (PCB) in Lebensmitteln

Zusammenfassung Im Rahmen eines koordinierten Forschungsprogramms des BMFT wurde eine orientierende Studie an möglichst repräsentativen Stichproben durchgeführt. Trotz relativ großer Streubreiten zeichnen sich die Bereiche der wichtigsten Lebensmittelgruppen deutlich voneinander ab mit Mittelwerten um 0,005 /g für fettarme pflanzliche Grundnahrungsmittel, um 0,05 /g für pflanzliche Nahrungsfette, um 0,3 /g für Milch-, Käse und Butterfette, um 0,15 /g für sonstige Nahrungsfette von Landtieren, um 0,03 /g für Hühnereier und um 10 /g für Fischfett. Wichtet man die Gehalte entsprechend der durchschnittlichen Diät in der BRD, so ergibt sich eine tägliche PCB-Aufnahme von rund 29 aus tierischen Fetten und rund 6 aus den übrigen Lebensmitteln. Die Gesamtaufnahme von ca. 35 g pro Tag und capita entspricht etwa dem Wert, der von der WHO als ADI-Wert für HCB (Hexachlorbenzol) in Aussicht genommen wurde.

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Polychlorinated biphenyls (PCB) in foodThe situation in the Federal Republic of Germany

Summary In a coordinated research program of the Federal Ministry of Research and Technology (BMFT), a screening study was carried out with representative samples. In spite of rather large ranges of PCB concentrations, the most important food-stuffs show clearly defined clusters with mean values of approx. 0.005 /g in low fat food components of plant origin such as cereals or potatoes, approx. 0.05 /g in vegetable fats, approx. 0.3 /g in fat from milk, butter and cheese, approx. 0.15 gg/g in animal fat, approx. 0.03 in chicken eggs and approx. 10 /g in fish fat. Considering the mean diet in the FRG, a daily PCB intake of about 29 g from animal fat and of 6 from the other food-stuffs results. The total intake of about 35 g per day and capita is almost the same as the figure conditionally suggested by the WHO as the acceptable daily HCB (hexachlorobenzene) intake.

     

Feature Selection for Recognition of Online Handwritten Bangla Characters

Feature selection through optimization techniques provides an interesting approach to minimize computational time with enhanced prediction capability, and     

Lipid specificity and location of the sterol carrier protein-2 fatty acid-binding site: A fluorescence displacement and energy transfer study

Although it was recently recognized that sterol carrier protein-2 (SCP-2) interacts with fatty acids, little is known regarding the specificity of SCP-2 for long-chain fatty acids or branched-chain fatty-acid-like molecules. Likewise the location of the fatty-acid binding site within SCP-2 is unresolved. A fluorescent cis-parinaric acid displacement assay was used to show that SCP-2 optimally interacted with 14–22 carbon chain lipidic molecules: polyunsaturated fatty acids > monounsaturated, saturated > branched-chain isoprenoids > branched-chain phytol-derived fatty acids. In contrast, the other major fatty-acid binding protein in liver, fatty-acid binding protein (L-FABP), displayed a much narrower carbon chain preference in general: polyunsaturated fatty acids > branched-chain phytol-derived fatty acids > 14- and 16-carbon saturated > branched-chain isoprenoids. However, both SCP-2 and l-FABP displayed a very similar unsaturated fatty-acid specificity profile. The presence and location of the SCP-2 lipid binding site were investigated by fluorescence energy transfer. The distance between the SCP-2 Trp⁵⁰ and bound cis-parinaric acid was determined to be 40 Å. Thus, the SCP-2 fatty-acid binding site appeared to be located on the opposite side of the SCP-2 Trp⁵⁰. These findings not only contribute to our understanding of the SCP-2 ligand binding site but also provide evidence suggesting a potential role for SCP-2 and/or L-FABP in metabolism of branched-chain fatty acids and isoprenoids.     

Exoglucanase‐encoding genes from three Wickerhamomyces anomalus killer strains isolated from olive brine

Wickerhamomyces anomalus killer strains are important for fighting pathogenic yeasts and for controlling harmful yeasts and bacteria in the food industry. Targeted disruption of key genes in β‐glucan synthesis of a sensitive Saccharomyces cerevisiae strain conferred resistance to the toxins of W. anomalus strains BS91, BCA15 and BCU24 isolated from olive brine. Competitive inhibition of the killing activities by laminarin and pustulan refer to β‐1,3‐ and β‐1,6‐glucans as the main primary toxin targets. The extracellular exoglucanase‐encoding genes WaEXG1 and WaEXG2 from the three strains were sequenced and were found to display noticeable similarities to those from known potent W. anomalus killer strains. Accession Nos for WaEXG1 genes for the strains in brackets are JQ734563 (BS91), JQ734564 (BCA15) and JQ734565 (BCU24); for WaEXG2 genes JQ734566 (BS91), JQ734567 (BCA15) and JQ734568 (BCU24), respectively. Copyright © 2012 John Wiley & Sons, Ltd.     

High Dietary Fat Exacerbates Weight Gain and Obesity in Female Liver Fatty Acid Binding Protein Gene-Ablated Mice

Since liver fatty acid binding protein (L-FABP) facilitates uptake/oxidation of long-chain fatty acids in cultured transfected cells and primary hepatocytes, loss of L-FABP was expected to exacerbate weight gain and/or obesity in response to high dietary fat. Male and female wild-type (WT) and L-FABP gene-ablated mice, pair-fed a defined isocaloric control or high fat diet for 12 weeks, consumed equal amounts of food by weight and kcal. Male WT mice gained weight faster than their female WT counterparts regardless of diet. L-FABP gene ablation enhanced weight gain more in female than male mice—an effect exacerbated by high fat diet. Dual emission X-ray absorptiometry revealed high-fat fed male and female WT mice gained mostly fat tissue mass (FTM). L-FABP gene ablation increased FTM in female, but not male, mice—an effect also exacerbated by high fat diet. Concomitantly, L-FABP gene ablation decreased serum β-hydroxybutyrate in male and female mice fed the control diet and, even more so, on the high-fat diet. Thus, L-FABP gene ablation decreased fat oxidation and sensitized all mice to weight gain as whole body FTM and LTM—with the most gain observed in FTM of control vs high-fat fed female L-FABP null mice. Taken together, these results indicate loss of L-FABP exacerbates weight gain and/or obesity in response to high dietary fat.     

Liver and intestinal fatty acid-binding protein expression increases phospholipid content and alters phospholipid fatty acid composition in L-cell fibroblasts

Although fatty acid-binding proteins (FABP) differentially affect fatty acid uptake, nothing is known regarding their role(s) in determining cellular phospholipid levels and phospholipid fatty acid composition. The effects of liver (L)- and intestinal (I)-FABP expression on these parameters were determined using stably transfected L-cells. Expression of L- and I-FABP increased cellular total phospholipid mass (nmol/mg protein) 1.7- and 1.3-fold relative to controls, respectively. L-FABP expression increased the masses of choline glycerophospholipids (ChoGpl) 1.5-fold, phosphatidylserine (PtdSer) 5.6-fold, ethanolamine glycerophospholipids 1.4-fold, sphingomyelin 1.7-fold, and phosphatidylinositol 2.6-fold. In contrast, I-FABP expression only increased the masses of ChoGpl and PtdSer, 1.2- and 3.1-fold, respectively. Surprisingly, both L- and I-FABP expression increased ethanolamine plasmalogen mass 1.6- and 1.1-fold, respectively, while choline plasmalogen mass was increased 2.3- and 1.7-fold, respectively. The increase in phospholipid levels resulted in dramatic 48 and 33% decreases in the cholesterol-to-phospholipid ratio in L- and I-FABP expressing cells, respectively. L-FABP expression generally increased polyunsaturated fatty acids, primarily by increasing 20∶4n−6 and 22∶6n−3, while decreasing 18∶1n−9 and 16∶1n−7. I-FABP expression generally increased only 20∶4n−6 proportions. Hence, expression of both I- and L-FABP differentially affected phospholipid mass, class composition, and acyl chain composition. Although both proteins enhanced phospholipid synthesis, the effect of L-FABP was much greater, consistent with previous work suggesting that these two FABP differentially affect lipid metabolism.