Excess supply of the heavy metals Mn, Cu, Zn, Co, and Ni to barley caused their accumulation in shoots and specially in roots and induced symptoms characteristic of the particular heavy metal involved, the syndrome of which varied with the different treatments. The effectiveness of the heavy metals in inducing visual symptoms was in the order of Ni2+ > Co2+ > Cu2+ > Mn2+ > Zn2+. These treatments caused a decrease in dry matter yield of plants in the order Ni2+ > Co2+ > Zn2+ > Mn2+ > Cu2+.Studies using 59Fe indicated that an excess supply of each of the heavy metals reduced iron absorption by plants and affected its distribution in roots and shoots. Excess of Co2+, Cu2+, Mn2+, and Zn2+ reduced iron translocation to shoots, induced chlorosis, and decreased catalase activity of young leaves. Excess nickel, which was most active in producing toxic effects, did not inhibit translocation of iron to young leaves. Unlike iron deficiency, an excess of Ni2+ did not decrease the activity of catalase and stimulated the activity of peroxidase. Excess supply of each of the heavy metals increased the concentration of non-reducing sugars. Observations suggest that toxicity to heavy metals does not necessarily involve induction of iron deficiency, their redox potentials, or the stability of their organometal complexes.
Zinc deficiency decreased pollen viability in maize (Zea mays L. cv. G2) grown in sand culture. On restoring normal zinc supply to zinc-deficient plants before the pollen mother cell stage of anther development, the vegetative yield of plants and pollen fertility could be recovered to a large extent, but the recovery treatment was not effective when given after the release of microspores from the tetrads. If zinc deficiency was induced prior to microsporogenesis it did not significantly affect vegetative yield and ovule fertility, but decreased the fertility of pollen grains, even of those which visibly appeared normal. If the deficiency was induced after the release of microspores from the tetrads, not only vegetative yield and ovule fertility but pollen fertility also remained unaffected.
A reduction in the size of tassels, male flowers, and anthers resulted from molybdenum deficiency in maize. In molybdenum-deficient plants, anthesis was suppressed or delayed and the anthers had fewer and smaller pollen grains that lacked dense cytoplasmic contents, appeared shrivelled, and had poor viability. Because of molybdenum deficiency, there was a decrease in the activity of starch phosphorylase in mature and freshly shed pollen grains and decreases in the activities of invertase and acid phosphatase at all the five stages at which pollen grains were assayed for the enzymes. The activities of catalase and peroxidase were increased by molybdenum deficiency at all five stages and that of ribonuclease at four out of the five stages of pollen development.
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