Hannover, Universiẗat, Diss., 1998.

Intact strawberry fruit did not produce detectable t-2-H which is derived from -linolenic acid (18:3). However, in response to wounding by gentle bruising, strawberry fruit emitted t-2-H with the largest quantity produced within 10 min following injury. The level of total lipid 18:3 in the fruit increased two-fold in response to wounding whereas free 18:3 declined slightly (about 30%). At 10 min following wounding, fruit exhibited a 25% increase in 13-lipoxygenase (LOX) activity, which leads to the production of 13-hydroperoxyoctadecatrienoic acid (13-HPOT) from 18:3. The activity of hydroperoxide lyase (HPL), which catalyzes formation of cis-3-hexenal (c-3-H), the precursor of t-2-H, from 13-HPOT, increased two-fold at 10 min after wounding. Thus, within 15 min after wounding, free 18:3 substrate availability and the activity of two key enzymes, LOX and HPL, changed in a manner consistent with increased t-2-H biosynthesis. The site and mode of interaction of C6 aldehydes with Botrytis cinerea, a common pathogen of many plant species, was characterized using radiolabeled six carbon (C6) aldehydes, including c-3-H and t-2-H. An approximately 25% molar conversion of 18:3 to C6 aldehydes was obtained by enzymatic manipulation with LOX and HPL extracts. Following exposure of Botrytis cultures to radiolabeled aldehydes, radiolabeled aldehydes were recovered in protein fractions, but not in the lipid fraction. They were incorporated into conidia at a 20-fold higher level than mycelia (per mg fresh weight). About 95% of the radiolabeled aldehyde was recovered in proteins on the surface (wash protein) of the fungal tissue, while 5% was from protein in internal tissue (cell wall and membrane and cytosol). Supplementing radiolabeled aldehydes with nonradiolabled C6 aldehydes to increase the vapor phase concentration affected distribution of radiolabel in each protein fraction. The t-2-H at both 5.4 and 85.6 mol affected protein expression patterns, changing the intensity of expression in over one third of all proteins. Both up- and down-regulation of specific proteins were observed. Though five proteins of interest were analyzed, their identities were not determined. However, the data indicate a clear effect of t-2-H on protein expression in Botrytis cinerea.

In recent years, there have been a number of studies looking at inhibition of microorganisms by spices, herbs or their extracts.  Many of these products have been shown to have antimicrobial activity against foodborne pathogens.  The purpose of this research was to evaluate the antimicrobial activity of three essential oil (EO) compounds (thymol, eugenol, and trans-cinnamaldehyde) alone and in combination with three naturally-occurring apple aroma (AA) compounds (hexanal, trans-2-hexenal and 1-hexanol) to identify the minimum inhibitory concentrations necessary to inhibit E. coli O157:H7.  Three commercial apple juice flavoring mixtures (natural apple cinnamon, natural apple spice and natural red apple) were additionally tested alone for antimicrobial activity against E. coli O157:H7. The standard agar dilution method (SAD) and checkerboard assay were used to evaluate the efficacy of the nine compounds, alone and in combination against E. coli O157:H7.  In general, the EO compounds were significantly more effective against E. coli O157:H7 than the AA compounds (P<0.05).  Cinnamaldehye, with an MIC of 0.2 mg/mL, exhibited the highest degree of activity, followed by thymol, eugenol and trans-2-hexenal, which each had individual MIC values of 1.6 mg/mL.  No synergism was found in the combinations of EO compounds with AA compounds. / Master of Science in Life Sciences

La physiopathologie du diabète de type II se caractérise par de sévères anomaliesmétaboliques telles que l’hyperglycémie et les dyslipidémies contribuant au développementdes maladies cardiovasculaires. Une altération de l’activité de l’AMPK dans les tissus tels quele muscle squelettique et le foie est associée à ces désordres métaboliques alors que sonactivation pharmacologique permet de les rétablir. Toutefois, le complexe hétérotrimériqueαβγ tissu-spécifique de l’AMPK confère une régulation et des rôles distincts qui demeurentinexplorés dans l’intestin, un organe favorisant pourtant l’augmentation de l’absorption desnutriments en situation de diabète de type II. La présente étude démontre une prépondérancedu complexe α1β2γ1 de l’AMPK dans les cellules intestinales Caco-2 dont l’un des rôles de lasous-unité α1 est de réguler l’ACC, l’enzyme de synthèse des acides gras. Contrairement àl’AMPK exprimée dans le foie, elle ne régule pas l’HMG-CoA Réductase impliquée dans lasynthèse du cholestérol. L’activation de l’AMPK mime l’effet de l’insuline en réduisantl’absorption intestinale du glucose et des lipides alors que son altération en situationd’insulino-résistance (e.g : induite par le 4-HHE dans un modèle cellulaire Caco-2 ou induitepar la diète dans le modèle animal Psammomys obesus) favorise l’absorption du glucose etdes lipides, ce qui exacerberait l’hyperglycémie et la dyslipidémie postprandiale associées audiabète de type II. L’AMPK au niveau intestinal constitue donc une cible thérapeutiquepotentielle complémentaire pour la prévention et le traitement du diabète de type II. / Physiopathology of type II Diabetes is characterized by severe metabolic abnormalities suchas hyperglycemia and dyslipidemia also implicated in development of cardiovasculardiseases. Impaired AMPK activity in tissues such as skeletal muscle and liver is associatedwith these metabolic disorders whereas its pharmacologic activation is able to restore suchabnormalities. Nevertheless, tissue-specific heterotrimeric αβγ AMPK likely confers distinctroles and regulation that remain unexplored in intestine, an organ promoting enhancednutrients absorption in type II diabetes situation. This study demonstrates α1β2γ1 AMPKcomplex preponderance in intestinal Caco-2 cells whose α1 subunit role is to regulate ACCenzyme responsible of fatty acid synthesis. Unlike in the liver, AMPK doesn’t regulate HMGCoAreductase enzyme implicated in cholesterol synthesis. AMPK activation mimics insulineffect by reducing intestinal glucose and lipids absorption whereas its alteration in insulinresistancesituation (e.g.: induced by 4-HHE in Caco-2 cell model or in Psammomys obesusanimal model) enhances glucose and lipids absorption which could exacerbate postprandialhyperglycemia and dyslipidemia associated to type II diabetes. Thus, AMPK at the intestinallevel could be a potential therapeutic target in prevention and treatment of type II diabetes