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Humicola lutea 103 is a copper-tolerant fungal strain able to grow in the presence of 300 μg·mL–1Cu2+under submerged cultivation. To prevent the consequences of copper overload, microorganisms have evolved molecular mechanisms that regulate its uptake, intracellular traffic, storage, and efflux. In spite of this avoidance strategy, high heavy-metal concentrations caused distinct and widespread ultrastructural alterations in H. lutea. The mitochondria were the first and main target of the toxic action. The effect of copper on activities of the key enzymes (hexokinase, glucose-6-phosphate dehydrogenase, malate dehydrogenase, and isocitrate dehydrogenase) included in the 3 main metabolic pathways, glycolysis, pentose phosphate pathway, and tricarboxylic acid cycle, was investigated. High metal concentrations exhibited a dramatic negative effect on hexokinase, while the other 3 enzymes showed a significant and dose-dependent stimulation. On the basis of the present and previous results we concluded that the copper-induced oxidative stress plays an important role in the fungal tolerance to high Cu2+concentrations.

Pentachlorophenol (PCP) caused a rapid and pronounced increase in the rate of biosynthesis of the superoxide dismutase (SOD) in fungal strain Humicola lutea 110. Mn-containing SOD (Mn-SOD) was mainly responsible for modulating total cell SOD. The kinetics of SOD synthesis in the presence of PCP demonstrated the induction model of enzyme formation. This model was also supported by deinduction experiments, because the removal of the PCP was followed by a marked decrease in SOD activity. PCP also caused a moderate induction of catalase. The concentrations, which were effective in inducing the Mn-SOD, increased the cyanide-resistant respiration. It seems likely that PCP increased the rate of intracellular production of superoxide [Formula: see text]. Addition of inhibitors of transcription and translation to cultures in the presence of inducer (PCP) inhibited further accumulation of SOD activity. These data suggest that PCP, probably by the increase of [Formula: see text] content, accelerates new enzyme synthesis in fungal strain Humicola lutea 110.Key words: superoxide dismutase, superoxide, induction, pentachlorophenol, fungi, Humicola lutea.

The effect of glucose on superoxide dismutase (SOD) activity produced in Humicola lutea 110 was determined. The relatively high glucose concentration in the medium did not repress SOD levels in the cells. Glycerol, a nonfermentable carbon source, caused a slight stimulation of SOD synthesis. Furthermore, the specific rates of enzyme production in the medium with different glucose concentration showed an insignificant difference. Cyclic AMP had no effect on SOD levels. The shift in metabolism as glucose was depleted resulted in an increase in the rate of synthesis of both isocitric dehydrogenase and SOD. Pentachlorophenol and paraquat, which cause the production of superoxide radicals, caused an increase in SOD activity. These results led us to conclude that it is superoxide ion rather than glucose that is controlling SOD levels.Key words: Humicola lutea, fungi, superoxide dismutase, intracellular enzyme, glucose effect.

To extend the knowledge about the relationship between heat shock and oxidative stress in lower eukaryotes, the filamentous fungus Aspergillus niger 26 was chosen as a model system. Here, the response of A. niger cells to heat shock is reported. The temperature treatment significantly increased the levels of reactive oxygen species, superoxide anions (O2•–), and hydrogen peroxide and the rate of cyanide-resistant respiration as a marker of oxidative stress. Enhanced reactive oxygen species generation coincided with an increase in the content of oxidative damaged protein and in the accumulation of the storage carbohydrates trehalose and glycogen. Thermal survival of the A. niger cells corresponded to a significant increase in the levels of the antioxidant enzymes superoxide dismutase and catalase for all variants. These observations suggest that heat and oxidative stress have a common cellular effect.