Moniliformin,deoxynivalenol, 3Acetyldeoxynivalenol and zearalenone — Mycotoxins associated with corn cob fusariosis in Poland

An isolated rat liver was perfused with deoxynivalenol (DON) at a dose of 3 mg in a recirculating perfusion system. To identify glucuronide conjugates equal amounts of bile samples, perfusate and liver homogenates were incubated with and without (control) a β-glucuronidase preparation and analyzed by thin layer chromatography and capillary gas liquid chromatography — chemical ionization mass spectrometry. A total of 40.4% of the administered dose of DON was found to be conjugated with glucuronic acid (perfusate 20.4%, bile 19.2%, liver 0.8%), while only 1.3% of the parent DON (perfusate 1.1%, bile 0.2%) was detected. The cleavage of DON-glucuronide was demonstrated by incubating DON-glucuronide containing bile samples with intestine contents under anaerobic conditions.     

Cumulation of mycotoxins in maize cobs infected with<Emphasis Type="Italic">Fusarium gramihearum</Emphasis>

Maize cobs withFusarium ear rot were collected at 1986 season and five infected byFusarium graminearum were analyzed for presence of triohothecenes and zearalenone. Collected material was subsampled forFusarium damaged kernels and corresponding axial stems and healthy looking kernels. All investigated cobs contained deoxynivalenol (DON) (range 18.0–131.5 mg/kg) and zearalenone (ZEA) (range 0.38–2.17 mg/kg), in four cobs 15-acetyl-deoxynivalenol (15-AcDON) (range 5.2–6.2 mg/kg) was present and two cobs besides three all metabolites contained 3-acetyl-deoxynivalenol (3-AcD0N) (range 0.5–0.8 mg/kg).The average of individual toxins amount in axial stems: in mg/kg was equal to: DON — 110.36, ZEA — 4.57, 15-AcD0N — 16.66, and 3-AcD0N — 1.32.Fusarium damaged kernels contained in average the following amount (mg/kg) of: DON 77.00, ZEA 0.98, 15-AcD0N 3.78 and 3-AcD0N 0.06. Healthy looking kernels contained DON 1.96 mg/kg and ZEA 0.07 mg/kg only. Cooccurrence of 3-AcDON and 15-AcDON in two samples was an interesting finding. The amount of DON in total cob was highly correlated (r = 0.94) with percentage ofFusarium damaged kernels in given ear.     

Standardgewichte der Copepoden in der Pommerschen Bucht. Standard Weights of the Pomeranian Bay Copepods

The length weight relationship was determined for Pseudocalanus minutus elongatus, Temora longicornis, Acartia bifilosa, and Acartia longiremis caught in the Pomeranian Bay (Baltic Sea). To determine the weights of the individuals a geometrical method was used and the formula.     

Enantioseparation of phenylglycinol in chiral-modified zeolite HY: a molecular simulation study

A mechanism has been proposed for the separation of valinol enantiomers using a chiral-modified zeolite HY (i.e., zeolite HY containing (+)-(1R;2R)-hydrobenzoin) Molecular modeling of chiral-modified zeolite HY employed in enantioselective separation. Jirapongphan SS, Warzywoda J, Budil DE, Sacco A Jr. Chirality 2007; in press, which accurately predicted the experimentally measured enantioseparation. This methodology has been applied to predict the separation of an enantiomeric pair of phenylglycinol molecules (a precursor in the synthesis of HIV-1 protease inhibitors) using the modified zeolite HY as a CSP. Phenylglycinol and valinol molecules are similar in terms of the presence of polar (i.e., amine and hydroxyl) groups. These functional groups are important in the proposed chiral discrimination. Supercage-based docking simulations yielded an enantioselectivity of 1.3 with (+)-(S)-phenylglycinol molecule better retained in the zeolite. Also, the simulations predicted two binding modes that were the same as those in the valinol system. This suggests that specific structural features (i.e., number and type of polar groups), which generate the hypothesized binding modes, are required in an enantioseparation utilizing the chiral-modified zeolite HY.     

FdhTU-modulated formate dehydrogenase expression and electron donor availability enhance recovery of Campylobacter jejuni following host cell infection

Campylobacter jejuni is a food-borne bacterial pathogen that colonizes the intestinal tract and causes severe gastroenteritis. Interaction with host epithelial cells is thought to enhance severity of disease, and the ability of C. jejuni to modulate its metabolism in different in vivo and environmental niches contributes to its success as a pathogen. A C. jejuni operon comprising two genes that we designated fdhT (CJJ81176_1492) and fdhU (CJJ81176_1493) is conserved in many bacterial species. Deletion of fdhT or fdhU in C. jejuni resulted in apparent defects in adherence and/or invasion of Caco-2 epithelial cells when assessed by CFU enumeration on standard Mueller-Hinton agar. However, fluorescence microscopy indicated that each mutant invaded cells at wild-type levels, instead suggesting roles for FdhTU in either intracellular survival or postinvasion recovery. The loss of fdhU caused reduced mRNA levels of formate dehydrogenase (FDH) genes and a severe defect in FDH activity. Cell infection phenotypes of a mutant deleted for the FdhA subunit of FDH and an ΔfdhU ΔfdhA double mutant were similar to those of a ΔfdhU mutant, which likewise suggested that FdhU and FdhA function in the same pathway. Cell infection assays followed by CFU enumeration on plates supplemented with sodium sulfite abolished the ΔfdhU and ΔfdhA mutant defects and resulted in significantly enhanced recovery of all strains, including wild type, at the invasion and intracellular survival time points. Collectively, our data indicate that FdhTU and FDH are required for optimal recovery following cell infection and suggest that C. jejuni alters its metabolic potential in the intracellular environment.     

The kinase activity of IL-1 receptor-associated kinase 4 is required for interleukin-1 receptor/toll-like receptor-induced TAK1-dependent NFkappaB activation

Two parallel interleukin-1 (IL-1)-mediated signaling pathways have been uncovered for IL-1R-TLR-mediated NFkappaB activation: TAK1-dependent and MEKK3-dependent pathways, respectively. The TAK1-dependent pathway leads to IKKalpha/beta phosphorylation and IKKbeta activation, resulting in classic NFkappaB activation through IkappaBalpha phosphorylation and degradation. The TAK1-independent MEKK3-dependent pathway involves IKKgamma phosphorylation and IKKalpha activation, resulting in NFkappaB activation through dissociation of phosphorylated IkappaBalpha from NFkappaB without IkappaBalpha degradation. IL-1 receptor-associated kinase 4 (IRAK4) belongs to the IRAK family of proteins and plays a critical role in IL-1R/TLR-mediated signaling. IRAK4 kinase-inactive mutant failed to mediate the IL-1R-TLR-induced TAK1-dependent NFkappaB activation pathway, but mediated IL-1-induced TAK1-independent NFkappaB activation and retained the ability to activate substantial gene expression, indicating a structural role of IRAK4 in mediating this alternative NFkappaB activation pathway. Deletion analysis of IRAK4 indicates the essential structural role of the IRAK4 death domain in receptor proximal signaling for mediating IL-1R-TLR-induced NFkappaB activation.     

Carbon Monoxide (CO) Released from Tricarbonyldichlororuthenium (II) Dimer (CORM-2) in Gastroprotection against Experimental Ethanol-Induced Gastric Damage

The physiological gaseous molecule, carbon monoxide (CO) becomes a subject of extensive investigation due to its vasoactive activity throughout the body but its role in gastroprotection has been little investigated. We determined the mechanism of CO released from its donor tricarbonyldichlororuthenium (II) dimer (CORM-2) in protection of gastric mucosa against 75% ethanol-induced injury. Rats were pretreated with CORM-2 30 min prior to 75% ethanol with or without 1) non-selective (indomethacin) or selective cyclooxygenase (COX)-1 (SC-560) and COX-2 (celecoxib) inhibitors, 2) nitric oxide (NO) synthase inhibitor L-NNA, 3) ODQ, a soluble guanylyl cyclase (sGC) inhibitor, hemin, a heme oxygenase (HO)-1 inductor or zinc protoporphyrin IX (ZnPPIX), an inhibitor of HO-1 activity. The CO content in gastric mucosa and carboxyhemoglobin (COHb) level in blood was analyzed by gas chromatography. The gastric mucosal mRNA expression for HO-1, COX-1, COX-2, iNOS, IL-4, IL-1β was analyzed by real-time PCR while HO-1, HO-2 and Nrf2 protein expression was determined by Western Blot. Pretreatment with CORM-2 (0.5–10 mg/kg) dose-dependently attenuated ethanol-induced lesions and raised gastric blood flow (GBF) but large dose of 100 mg/kg was ineffective. CORM-2 (5 mg/kg and 50 mg/kg i.g.) significantly increased gastric mucosal CO content and whole blood COHb level. CORM-2-induced protection was reversed by indomethacin, SC-560 and significantly attenuated by celecoxib, ODQ and L-NNA. Hemin significantly reduced ethanol damage and raised GBF while ZnPPIX which exacerbated ethanol-induced injury inhibited CORM-2- and hemin-induced gastroprotection and the accompanying rise in GBF. CORM-2 significantly increased gastric mucosal HO-1 mRNA expression and decreased mRNA expression for iNOS, IL-1β, COX-1 and COX-2 but failed to affect HO-1 and Nrf2 protein expression decreased by ethanol. We conclude that CORM-2 released CO exerts gastroprotection against ethanol-induced gastric lesions involving an increase in gastric microcirculation mediated by sGC/cGMP, prostaglandins derived from COX-1, NO-NOS system and its anti-inflammatory properties.     

Influence of streptolysin S on lymphocyte functions

Streptolysin S, which was found to be cytotoxic for mouse and human lymphocytes and particularly for their T subpopulation, was also shown to affect some of the functions ascribed to T lymphocytes. In vitro studies demonstrated that streptolysin S-pretreated lymphocytes exhibited reduced responsiveness to phytohemagglutinin and decreased lymphokine production. Streptolysin S could also alter the immune response of mice in vivo. It induced suppression of the immune response to T-dependent antigen (SRBC) but had not influence on response to T-independent antigen (S III). The in vitro and in vivo studies suggest that streptolysin S can impair the function of T lymphocytes or, more precisely, of some subpopulation of T cells.