Biomedical subjects

S Krystofová

Publications and source records attributed to S Krystofová.

3 recordsLinked to original sources

PubMed2000

Ca2+ fluxes in developing Trichoderma viride mycelium.

The properties of both Ca2+ influx and efflux in the mycelium during the life cycle of Trichoderma viride were studied by means of 45Ca2+ and by X-ray fluorescence spectroscopy measurements. The properties of the 45Ca2+ influx and effluxes indicate that they are mediated by different transport systems. The Ca2+ influx could be mediated by an electrogenic Ca2+/nH+ antiport, or by an Ca2+ uniport system. Both Ca2+ influx and efflux were stimulated by the uncouplers (and the treatment leading to the suppression of energy metabolism) and by azalomycin F, an antifungal agent. Salicylate stimulated the Ca2+ efflux, but inhibited the Ca2+ influx. In the isolated preparation of crude vacuolar/mitochondrial fraction, salicylate induced the Ca2+ release, as did A23187. Azalomycin F moderately released Ca2+ from the microsomal fraction. On the other hand, uncouplers did not release Ca2+ from the isolated organelles, but inhibited to a different extent the ATP-dependent and -independent Ca2+ influx. The results could be explained in terms of the capacitative Ca2+ influx mechanism. The rate of 45Ca2+ influx, or of the 40Ca2+ content, was maximal after about 30 h of submerged cultivation, and then decreased. The results show that loading of internal Ca2+ stores occurs in the early stages of the development of mycelium only, and the Ca2+ influx mechanism is developmentally down-regulated, being almost nonexistent during its later stages. In older mycelium, growth seems to be autonomous of the extracellular Ca2+ until the onset of conidiation.

Anti-Bacterial Agents↗

PubMed1995

The 45Ca2+ uptake by Trichoderma viride mycelium. Correlation with growth and conidiation.

The properties of Ca2+ uptake by Trichoderma viride were studied using radionuclide 45Ca2+ in conjunction with the study of effects of agents influencing the Ca2+ homeostasis on the 45Ca2+ uptake, vegetative growth and conidiation. Mycelium of T. viride was found to take up 45Ca2+ in time- and temperature-dependent manner. The 45Ca2+ uptake could be distinguished from the 45Ca2+ binding by the insensitivity to washing with EGTA (ethylene glycol-bis(2-amino ethyl ether)-N,N,N',N'-tetraacetic acid)-containing solution. The 45Ca2+ uptake was only slightly suppressed by the treatment used to de-energize cells. Agents known to influence Ca2+ homeostasis in animal and plant cells were also active in perturbing the Ca2+ homeostasis in T. viride. In this respect, the agents tested had dual (stimulatory or inhibitory) effects on the 45Ca2+ uptake. No clear correlation among the perturbation of the 45Ca2+ uptake and the inhibition of growth and conidiation was found for the group of compounds tested. Sr2+ and Mg2+ inhibited 45Ca2+ uptake but did not inhibit growth and conidiation. Co2+, Cd2+ inhibited both 45Ca2+ uptake and growth. Other agents tested (Cu2+, Ni2+, La3+, dihydropyridines), which inhibited growth of T. viride, induced massive 45Ca2+ uptake by its mycelium. Ba2+ and Mn2+ showed a biphasic effect on 45Ca2+ uptake-inhibition at lower, and stimulation at higher concentrations, but they had only a slight inhibitory effect on the growth or conidiation at higher concentrations. The 45Ca2+ uptake was influenced by addition of monovalent cations to a small extent only. Na+ (up to 75 mmol.l-1), less than K+, slightly suppressed the 45Ca2+ uptake leaving both growth and conidiation unaffected. Upon depriving the fungus of Ca2+ by chelation of extracellular Ca2+ (not Mg2+ or divalent trace metals) by EGTA, which interfered with Ca2+ homeostasis, vegetative growth rate, and starvation-induced conidiation were restricted. These results suggest that the sustained Ca2+ influx occurs across the T. viride plasma membrane which may be a target site for the antifungal action of heavy metal ions, and its perturbation may lead to disturbances in physiological processes including growth and conidiation. The properties of the Ca2+ influx in T. viride observed substantially differ from those observed in animal cells.

Biological Transport↗

PubMed1994

Growth and conidiation of Trichoderma viride are affected by non-steroidal antiinflammatory agents.

Nonsteroid antiinflammatory agents (NSAIA's) (inhibitors of cyclooxygenase and lipoxygenase) of several structural series inhibited growth of Trichoderma viride. The most potent growth inhibitors were indomethacin and its derivative repanidal which inhibited in the range of 0.1 mmol/L. The weakest inhibitors were acetylsalicylic acid and lysine salicylate which exerted only a weak effect at concentrations above 1 mmol/L. The inhibition of growth was accompanied by a stimulation of conidiation in the dark. A light pulse increased the efficiency of these drugs to stimulate the conidiation. Saccharomyces cerevisiae was as sensitive to NSAIA's as T. viride while Botrytis cinerea was less sensitive. The results indicate that arachidonate metabolism may play a role in the growth of fungi and may participate also in the process of conidiation.

Anti-Inflammatory Agents, Non-Steroidal↗