InNeurospora 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⁺ inN. 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 inN. crassa is probably a block at some step(s) in the glycolytic sequence.

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.

Among several metal ions tested, Cu²⁺ was unique in slowing down methylene blue sensitized photodynamic breakdown of some nucleic acid bases and nucleosides. The t_1/2 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 t_1/2 values was found with xanthosine—7 min 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.

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.

The parent wild strainNeurospora crassa Em 5297a and three Ni²⁺ resistantNeurospora 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 inNeurospora crassa Ni^R1. 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 inNeurospora crassa is a derangement in carbohydrate metabolism at step(s) beyond pyruvate and that this is possibly due to decreased invivo activity of Mg²⁺ dependent processes