ABSTRACT
Abstract Stress tolerance is a key attribute that must be considered when using yeast cells for industrial applications. High temperature is one factor that can cause stress in yeast. High environmental temperature in particular may exert a natural selection pressure to evolve yeasts into thermotolerant strains. In the present study, three yeasts (Saccharomyces cerevisiae, MC4, and Kluyveromyces marxianus, OFF1 and SLP1) isolated from hot environments were exposed to increased temperatures and were then compared with a laboratory yeast strain. Their resistance to high temperature, oxidative stress, and antioxidant response were evaluated, along with the fatty acid composition of their cell membranes. The SLP1 strain showed a higher specific growth rate, biomass yield, and biomass volumetric productivity while also showing lower duplication time, reactive oxygen species (ROS) production, and lipid peroxidation. In addition, the SLP1 strain demonstrated more catalase activity after temperature was increased, and this strain also showed membranes enriched in saturated fatty acids. It is concluded that the SLP1 yeast strain is a thermotolerant yeast with less oxidative stress and a greater antioxidant response. Therefore, this strain could be used for fermentation at high temperatures.
Subject(s)
Saccharomyces cerevisiae/physiology , Stress, Physiological , Kluyveromyces/physiology , Oxidative Stress , Antioxidants/metabolism , Saccharomyces cerevisiae/growth & development , Saccharomyces cerevisiae/radiation effects , Saccharomyces cerevisiae/chemistry , Kluyveromyces/growth & development , Kluyveromyces/radiation effects , Kluyveromyces/chemistry , Lipid Peroxidation , Catalase/analysis , Cell Membrane/chemistry , Reactive Oxygen Species/metabolism , Biomass , Fatty Acids/analysis , Hot TemperatureABSTRACT
BACKGROUND: Nitrosative and oxidative stress play a key role in obesity and diabetes-related mitochondrial dysfunction. The objective was to investigate the effect of curcumin treatment on state 3 and 4 oxygen consumption, nitric oxide (NO) synthesis, ATPase activity and lipid oxidation in mitochondria isolated from liver and kidneys of diabetic db/db mice. RESULTS: Hyperglycaemia increased oxygen consumption and decreased NO synthesis in liver mitochondria isolated from diabetic mice relative to the control mice. In kidney mitochondria, hyperglycaemia increased state 3 oxygen consumption and thiobarbituric acid-reactive substances (TBARS) levels in diabetic mice relative to control mice. Interestingly, treating db/db mice with curcumin improved or restored these parameters to normal levels; also curcumin increased liver mitochondrial ATPase activity in db/db mice relative to untreated db/db mice. CONCLUSIONS: These findings suggest that hyperglycaemia modifies oxygen consumption rate, NO synthesis and increases TBARS levels in mitochondria from the liver and kidneys of diabetic mice, whereas curcumin may have a protective role against these alterations.
Subject(s)
Animals , Male , Mice , Lipid Peroxidation/drug effects , Curcumin/pharmacology , Diabetes Mellitus, Type 2/diet therapy , Kidney/drug effects , Liver/drug effects , Mitochondria/drug effects , Oxygen Consumption/drug effects , Body Weight/drug effects , Mitochondria, Liver/drug effects , Mitochondria, Liver/enzymology , Adenosine Triphosphatases/drug effects , Oxidative Stress/drug effects , Cell Respiration/drug effects , Dietary Supplements , Diabetes Mellitus, Type 2/complications , Diabetes Mellitus, Type 2/physiopathology , Disease Models, Animal , Selective Breeding , Genotype , Hyperglycemia/diet therapy , Hyperglycemia/etiology , Mitochondria/enzymology , Nitric Oxide/analysis , Nitric Oxide/metabolismABSTRACT
Background. The mechanisms whereby rat hepatocytes undergo irreversible injury due to a lack of oxygen have not been established. Methods. Liver cells were used for reperfusion injury, and four compartmentalized pathways were evaluated durgin hypoxia (N2/CO2, 19:1) for 30 min followed by oxygen (O2/CO2, 19:1) for 30 min. Results. Cell viability decreased during the hypoxic, but not during the reoxygenation, phase. Glycogenolysis, as measured by glucose release, was significantly increased during hypoxia as compared to control in oxygen (205ñ15 vs. 155 ñ 10 mmol glucose/mg protein/h, respectiely), and did not return to normal levels by reoxygenation. Gluconeogenesis was importantly decreased during hypoxia (102 ñ 10 vs. 8 ñ 2 mmol glucose/mg protein/h) with partial recovery during reoxygenation. Ureagenesis diminished in hypoxia, but recovered during reoxygenation. Additionally, 3-hydroxy-butyrate formation was augmented by hypoxia, with some recovery when oxygen was present. Conclusions. These results suggest that compartmentalized pathways are protected from hypoxic injury in isolated hepatocytes, and also suggest it as a model to test the idea that enzymes of those parthways are organized into multienzyme complexes in vivo