Thermal inactivation of non-proteolytic Clostridium botulinum type E spores in model fish media and in vacuum-packaged hot-smoked fish products.

Thermal inactivation of nonproteolytic Clostridium botulinum type E spores was investigated in rainbow trout and whitefish media at 75 to 93°C. Lysozyme was applied in the recovery of spores, yielding biphasic thermal destruction curves. Approximately 0.1% of the spores were permeable to lysozyme, showing an increased measured heat resistance. Decimal reduction times for the heat-resistant spore fraction in rainbow trout medium were 255, 98, and 4.2 min at 75, 85, and 93°C, respectively, and those in whitefish medium were 55 and 7.1 min at 81 and 90°C, respectively. The z values were 10.4°C in trout medium and 10.1°C in whitefish medium. Commercial hot-smoking processes employed in five Finnish fish-smoking companies provided reduction in the numbers of spores of nonproteolytic C. botulinum of less than 103. An inoculated-pack study revealed that a time-temperature combination of 42 min at 85°C (fish surface temperature) with >70% relative humidity (RH) prevented growth from 106 spores in vacuum-packaged hot-smoked rainbow trout fillets and whole whitefish stored for 5 weeks at 8°C. In Finland it is recommended that hot-smoked fish be stored at or below 3°C, further extending product safety. However, heating whitefish for 44 min at 85°C with 10% RH resulted in growth and toxicity in 5 weeks at 8°C. Moist heat thus enhanced spore thermal inactivation and is essential to an effective process. The sensory qualities of safely processed and more lightly processed whitefish were similar, while differences between the sensory qualities of safely processed and lightly processes rainbow trout were observed

Genotoxic effect induced by hydrogen peroxide in human hepatoma cells using comet assay

Background: Hydrogen peroxide is a common reactive oxygen intermediate generated by variousforms of oxidative stress. Aims: The aim of this study was to investigate the DNA damage capacity ofH2O2 in HepG2 cells. Methods: Cells were treated with H2O2 at concentrations of 25 μM or 50 μM for5 min, 30 min, 40 min, 1 h or 24 h in parallel. The extent of DNA damage was assessed by the cometassay. Results: Compared to the control, DNA damage by 25 μM and 50 μM H2O2 increasedsignificantly with increasing incubation time up to 1 h, but it was not increased at 24 h. Conclusions:Our Findings confirm that H2O2 is a typical DNA damage inducing agent and thus is a good modelsystem to study the effects of oxidative stress. DNA damage in HepG2 cells increased significantlywith H2O2 concentration and time of incubation but later decreased likely due to DNA repairmechanisms and antioxidant enzyme

Multi-omics for studying and understanding polar life

Polar ecosystems are experiencing amongst the most rapid rates of regional warming on Earth. Here, we discuss ‘omics’ approaches to investigate polar biodiversity, including the current state of the art, future perspectives and recommendations. We propose a community road map to generate and more fully exploit multi-omics data from polar organisms. These data are needed for the comprehensive evaluation of polar biodiversity and to reveal how life evolved and adapted to permanently cold environments with extreme seasonality. We argue that concerted action is required to mitigate the impact of warming on polar ecosystems via conservation efforts, to sustainably manage these unique habitats and their ecosystem services, and for the sustainable bioprospecting of novel genes and compounds for societal gain

Oxygen Sensitivity Of Heated Cells Of Escherichia Coli O157:h7

Following defined heat treatments (55 °C for 100 min, 59 °C for 5 min, 61 °C for 1 min), a 6 decimal (6-D) reduction was obtained when cells of Escherichia coli O157:H7 were enumerated in aerobic growth medium. Part of this reduction (3-D) was due to thermal inactivation (as determined when cells were enumerated in anaerobic growth medium), and part (3-D) was due to the inability of sub-lethally heat-injured cells of E. coli O157:H7 to grow in the presence of oxygen: When held anaerobically, the injured cells regained their ability to grow in the presence of oxygen. Following heating at 59 °C for 5 min, repair took 4 h at 30 °C, 48 h at 20 °C, 95 h at 10 °C, but did not occur in 816 h at 5 °C. Recovery from sub-lethal heat injury was not influenced by heat shock. These findings are relevant to the safety of minimally-heated foods.852231237Ahmed, N.M., Conner, D.E., Evaluation of various media for recovery of thermally-injured Escherichia coli O157:H7 (1995) Journal of Food Protection, 58, pp. 357-360Outbreak of Escherichia coli O157:H7 infection - Georgia and Tennessee, June 1995 (1996) Morbidity and Mortality Weekly Report, 45, p. 249Outbreak of Escherichia coli O157:H7 infections associated with drinking unpasteurised apple juice - British Columbia, California, Colorado, and Washington, October 1996 (1996) Morbidity and Mortality Weekly Report, 45, p. 975Outbreaks of Escherichia coli O157:H7 infection associated with eating alfalfa sprouts: Michigan and Virginia, June-July 1997 (1997) Morbidity and Mortality Weekly Report, 46, pp. 741-744Escherichia coli O157:H7 infections associated with eating a nationally distributed commercial brand of frozen ground beef patties and burgers : Colorado, 1997 (1997) Morbidity and Mortality Weekly Report, 46, pp. 777-778Czechowicz, S.M., Santos, O., Zottola, E.A., Recovery of thermally-stressed Escherichia coli O157:H7 by media supplemented with pyruvate (1996) International Journal of Food Microbiology, 33, pp. 275-284George, S.M., Richardson, L.C.C., Pol, I.E., Peck, M.W., Effect of oxygen concentration and redox potential on recovery of sub-lethally heat-damaged cells of Escherichia coli O157:H7, Salmonella enteritidis and Listeria monocytogenes (1998) Journal of Applied Microbiology, 84, pp. 903-909Hungate, R.E., A roll tube method for cultivation of strict anaerobes (1969) Methods in Microbiology 3B, pp. 117-132. , ed. Norris, J.R. and Ribbons, D.W. London : Academic PressHurley, M.A., Roscoe, M.E., Automated statistical analysis of microbial enumeration by dilution series (1983) Journal of Applied Bacteriology, 55, pp. 159-164Jackson, T.C., Hardin, M.D., Acuff, G.R., Heat resistance of Escherichia coli O157:H7 in a nutrient medium and in ground beef patties as influenced by storage and holding temperatures (1996) Journal of Food Protection, 59, pp. 230-237Mackey, B.M., Gibson, G.R., Escherichia coli O157: From farm to fork and beyond (1997) SGM Quarterly, 24, pp. 55-57Meyer, D.H., Donnelly, C.W., Effect of incubation temperature on repair of heat-injured Listeria in milk (1992) Journal of Food Protection, 55, pp. 579-582Murano, E.A., Pierson, M.D., Effect of heat shock and growth atmosphere on the heat resistance of Escherichia coli O157:H7 (1992) Journal of Food Protection, 55, pp. 171-175Murano, E.A., Pierson, M.D., Effect of heat shock and incubation atmosphere on injury and recovery of Escherichia coli O157:H7 (1993) Journal of Food Protection, 56, pp. 568-572Smith, H.R., Verocytotoxin-producing Escherichia coli O157: Cause for concern (1997) SGM Quarterly, 24, pp. 54-55Snyder, O.P., Redox potential in deli foods: Botulism risk? (1996) Dairy, Food and Environmental Sanitation, 16, pp. 546-548Tarr, P.I., Review of 1993 Escherichia coli O157:H7 outbreak: Western United States (1994) Dairy, Food and Environmental Sanitation, 14, pp. 372-373Thippareddi, H., Retzlaff, D., Phebus, R.K., Yung, D.Y.C., Acid and heat tolerance of acid habituated Escherichia coli O157:H7 (1996) Journal of Food Protection, 59 (SUPPL.), p. 42Tilden, J., Young, W., McNamara, A.-M., A new route of transmission for Escherichia coli: Infection from dry fermented salami (1996) American Journal of Public Health, 86, pp. 1142-1145Williams, N.C., Ingham, S.C., Changes in heat-resistance of E. coli O157:H7 following heat shock and acid shock (1996) Journal of Food Protection, 59 (SUPPL.), p. 4