THE RELATIONSHIP BETWEEN NICKEL TOXICITY AND IRON SUPPLY

The influence of varying levels of iron and substrate pH on the uptake of nickel and the intensity of toxicity symptoms in oat plants have been investigated using sand-and water-culture techniques.
Nickel-toxicity symptoms (both necrosis and chlorosis) are less severe when the concentration of iron in the nutrient solution is high. The reduction in degree of necrosis is related to a reduced content of nickel in the leaf blades, whilst that of chlorosis is related to the Ni/Fe ratio in the leaf blades—an internal antagonism being indicated in the latter case.
A reciprocal relationship exists between the nickel and iron contents of the leaf blades; the nickel content is materially reduced by high concentrations of iron in the nutrient solution, and the iron content by nickel, the former being the more pronounced effect.
Uptake of nickel increases with increasing pH for a constant iron level in the substrate, although the degree of necrotic symptoms is similar over pH range 4–7. Iron uptake is reduced by both nickel and increasing pH and results in chlorosis at pH values of 5·5 and above.
For a constant level of iron supply the phosphate content of the stem extracts is higher the greater the degree of nickel toxicity; the phosphorus status of the plant may be a factor in producing nickel toxicity but if so, it has to be considered in relation to other factors.     

TRACE-ELEMENT TOXICITIES IN OAT PLANTS

Excessive amounts of nickel, cobalt, chromium, copper, zinc, manganese, molybdenum and aluminium in nutrient solutions supplied to oat plants in sand culture produce ( a ) chlorosis and ( b ) other symptoms specific to the element involved. The specific symptoms are distinct for each metal, although those of cobalt and nickel might be confused.
The toxic effects of nickel, cobalt, copper, zinc, manganese and molybdenum are associated with high concentrations of the element in the leaf tissue, but this is not always so with chromium and aluminium.
The toxic effects of nickel, chromium, copper and molybdenum are associated with a reduced nitrogen content of the plant. Nickel, cobalt, chromium, zinc and manganese increase the concentration of phosphorus in the tissue whilst aluminium decreases it, probably to a deficiency level.
Aluminium reduces the intensity of toxic symptoms produced by nickel—probably by reducing the uptake of nickel and phosphorus. Copper effectively reduces the leaf necrosis produced by nickel, but not the nickel content of the leaf tissue; it is suggested that one factor in nickel toxicity may be inhibition of one or more functions of copper. The other elements slightly increase chlorosis and some increase necrosis.
The order of activitjl of the elements in producing chlorosis is found to be Ni>Cu>Co>Cr>Zn>Mo>Mn. This order, which is related to that giving yield reduction and is similar to the order of stability of metal complexes, is discussed in relation to induced iron deficiency.     

Melanin Biosynthesis From Dopamine. II. A Mass Spectrometric and Collisional Spectroscopic Investigation

Electron impact (EI) and fast atom bombardment (FAB) mass spectrometry together with collisional activation (CA) experiments were applied to the study of the oxidation pathway of dopamine by tyrosinase. In order to prevent attachment of the protein to the highly reactive intermediates, ultrafiltration was employed to remove the enzyme at different reaction times. FAB, privileging molecular species formation, was successfully used for identification of transient intermediates and their relative concentrations with respect to time, directly in the reaction mixture. The presence of isobaric molecular species made chromatographic separation necessary. Further EI mass spectrometry and collision spectroscopy led to structural identification of pure components. Of these, dopamine-o-quinone, leucoaminochrome, and aminochrome semiquinone were characterized for the first time as real intermediates in dopamine melanogenesis, in agreement with previous hypotheses. This approach elucidated the pathway of dopamine melanogenesis.