ABSTRACT
The parent wild strain Neurospora crassa Em 5297a and three Ni2+ resistant Neurospora crassa mutants have been shown to excrete pyruvate into the culture medium in Ni2+ and Co2 + toxicities. Ni2+ has a more pronounced effect in this regard. The excretion is progressive with growth inhibition and is abolished by Mg2+ in all strains and by Fe3+ partially in the Em strain but not in Neurospora crassa NiR1. Pyruvate, citrate and malate supplementation reverse growth inhibition caused by excess Ni2+, but with concomitant suppression of Ni2+ accumulation. It is suggested that one of the features of Ni2+ toxicity in Neurospora crassa is a derangement in carbohydrate metabolism at step(s) beyond pyruvate and that this is possibly due to decreased in vivo activity of Mg2+ dependent processes.
ABSTRACT
Neurospora crassa Em 5297a can utilize sodium β-glycerophosphate as a sole phosphorous source (in the place of KH2PO4). Under these conditions a repressible alkaline phosphatase is elaborated which has different pH optimum towards β-glycerophosphate (10.2) and pyrophosphate (9.0) as substrates. This enzyme does not require any metal ion for its activity and could be assayed in the presence of EDTA. However, under conditions of cobalt toxicity, the activity of this enzyme is high and is decreased in copper and nickel toxicities.
ABSTRACT
Among several metal ions tested, Cu2+ was unique in slowing down methylene blue sensitized photodynamic breakdown of some nucleic acid bases and nucleosides. The t½ values were increased in the case of xanthine and uric acid by Cu2+, but without any alteration in the nature or amounts of photoproducts formed. Xanthine was degraded quantitatively to allantoin and urea. The breakdown of the sugar moiety of nucleosides was more drastically retarded than that of the purine ring. The decomposition rate and its magnitude was dependent on the concentration of Cu2+ as well as the nucleoside. The most profound increase in t½ values was found with xanthosine–7min for the purine ring and 65 min for the ribose moiety, at 0.6 mM Cu2+ Hg2+ in the case of xanthine, and some paramagnetic metal ions in the case of the nucleosides, slowed down the photobreakdown to a small extent; however, differential effects were not observed unlike with Cu2+. None of the other metal ions tested significantly influenced the process.
ABSTRACT
Uptake of Co2+ by cobalt-resistant strain is dependent on Co2+ concentration in the medium and is linear with time. The uptake is unaffected by metabolic inhibitors and decreased at low pH values. The uptake is independent of temperature in the range 0–40° C. The transport system is a passive diffusion process, unlike in the parent wild type strain where it is energy-dependent. It is possible that Mg2+ transport system is not involved in Co2+ transport in this strain, since the Co2+ uptake is not suppressed by Mg2+ as in the parent strain.
ABSTRACT
In Neurospora crassa, 0·44 mM Be2+ caused half-maximal inhibition of growth and this inhibition could be fully counteracted by the addition of 2·5 mM Ca2+ to the medium. Mn2+ and Mg2+ were less effective in reversing the growth inhibition caused by Be2+ and the order of effectiveness was Ca2+ > Mn2+ > Mg2+. Fe3+ and Zn2+ were ineffective in reversing Be2+ toxicity. Pyruvate, malate and succinate also reversed the growth inhibition caused by Be2+ in N. crassa. Pyruvate restored growth by a mechanism not involving control of Be2+ accumulation in the mould. The rate of utilisation of glucose by the mycelia grown in the presence of Be2+ was reduced, while that of pyruvate was not affected. The results indicate that the primary metabolic lesion in Be2+ toxicity in N. crassa is probably a block at some step(s) in the glycolytic sequence.