The effects of toxic concentrations of neutral lead acetate (CH3COO)2 Pb, 3 H2O on the germination and growth of rice (Oryza sativa L.) seeds are reported. Elongation inhibition was first detected at lead acetate concentration of 10-3M and became more pronounced with increasing concentrations. Root growth was more strongly inhibited than shoot growth and no germination occurred at 10-1 M. Various hormones, viz. indole 3 acetic acid (IAA), gibberellic acid (GA3) 6 furfurylaminopurine (kinetin), adenosine 3,5 cyclic monophosphate (cAMP), various organic acids and ethylene diamine tetraacetic acid (EDTA) were partially capable of relieving lead inhibition, whereas cations were ineffective. The activity of catalase, peroxidase, IAA oxidase, IAA synthase and ascorbic acid oxidase increased in response to lead addition. It was apparent that reduced growth was associated with increased enzyme activity. The stimulated activity of these enzymes was probably due to an enhanced protein synthesis.

S MUKHERJI

P MAITRA

University of Calcutta (informally known as Calcutta University or CU) is a collegiate public state university located in Kolkata, West Bengal, India.&nbsp;Within India it is recognized as a &quot;Five-Star University&quot; and accredited &quot;A&quot; Grade by National Assessment and Accreditation Council.

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It was established on 24 January 1857, and was one of the first institutions in Asia to be established as a multidisciplinary and Western-style university. Its alumni and faculty include several heads of state, heads of government, social reformers, prominent artists, only academy award winner and Dirac medal winner in India, many Fellows of the Royal Society and five Nobel laureates as of 2019 which is highest in South Asia.

University Of Calcutta

Growth and metabolism of germinating rice (Oryza sativa L.) seeds as influenced by toxic concentrations of lead

Z.PFLANZENPHYSIOL.

Metals can, when present in excess, or under wrong conditions, and in the wrong places, produce errors in the genetic information system. The present review is limited to three examples of heavy metal genotoxicants, namely arsenic (As), lead (Pb) and mercury (Hg) on plant systems. Exposure to lead is mainly through atmospheric pollutants, to mercury through soil and to arsenic through drinking water. Toxic metal ions enter cells by means of the same uptake processes as essential micronutrient metal ions. The amounts of metal absorbed by a plant depend on the concentrations and speciation of the metal in the soil solution, its movement successively from the bulk soils to the root surface, then into the root and finally into the shoot. Excessive concentrations of metals result in phytotoxicity through: (i) changes in the permeability of the cell membrane; (ii) reactions of sulphydryl (-SH) groups with cations; (iii) affinity for reacting with phosphate groups and active groups of ADP or ATP; and (iv) replacement of essential ions. Mercuric cations have a high affinity for sulphydryl groups and consequently can disturb almost any function where critical or non-protected proteins are involved. A mercury ion may bind to two sites of a protein molecule without deforming the chain, or it may bind two neighbouring chains together or a sufficiently high concentration of mercury may lead to protein precipitation. With organomercurials, the mercury atom still retains a free valency electron so that salts of such compounds form a monovalent ion. The effect of lead depends on the concentration, type of salts and plant species involved. Though effects are more pronounced at higher concentrations and durations, in some cases, lower concentrations might stimulate metabolic processes. The major processes affected are seed germination, seedling growth, photosynthesis, plant water status, mineral nutrition, and enzymatic activities. The phytotoxicity of arsenic is affected considerably by the chemical form in which it occurs in the soil and concentration of the metalloid. Due to its chemical similarity to phosphorus, arsenic participates in many cell reactions. Specific organo-arsenical compounds have been found in some organisms and arsenic has been reported to replace phosphorus in the phosphate groups of DNA. In view of the variety of reactions in plants that involve sulphydryl groups and phosphorus, arsenites and arsenates may interfere with physiological and biochemical processes which constitute growth in a number of ways. Mercury, lead and arsenic are effective mitotic poisons (turbagens) at particular concentrations, due to their known affinity for thiol groups and induce various types of spindle disturbances. The clastogenic effects are S-dependent. The availability of cations affect the number of aberrations produced quantitatively. Effects of metallic salts are related directly to the dosage and duration of exposure. Plants, following lower exposure, regain normalcy on being allowed to recover. Studies on genotoxicity of metals discussed in this review showed that genotoxic effects could be in part responsible for metal phytotoxicity, deserving further examination to elucidate the underlying mechanisms. The most noticeable and consistent effect of mercurials was the induction of c-mitosis resulting in the formation polyploid and aneuploid cells, and c-tumours. Inorganic salts of lead induced numerous c-mitoses together with strong inhibition of root growth and lowering of mitotic activity. As(III) is a weak mutagen but potent comutagen. Genotoxic evaluation of chemical mixtures from soil containing arsenic as component by Tradescantia micronucleus assay showed clastogenic effects, but not related specifically to arsenic. Plants growing on metal-contaminated sites need to develop some degree of tolerance to metal toxicity in order to survive. Since all plants contain at least some metal in their tissues, they clearly are incapable of completely excluding potentially toxic elements, but simply of restricting their uptake and/or translocation. The mechanisms for metal tolerance proposed are: (a) metal sequestration by specially produced organic compounds; (b) compartmentalization in certain cell compartments; (c) metal ion efflux; (d) organic ligand exudation. Inside cells, proteins such as ferritins and metallothioneins, and phytochelatins, participate in excess metal storage and detoxification. When these systems are overloaded, oxidative stress defence mechanisms are activated. Bacterial plasmids encode resistance systems for toxic metal ions including mercury, lead and arsenic. Chromosomal determinants of toxic metal resistance are also known. For mercury and arsenic, the plasmid and chromosomal determinants are basically the same. The largest group of metal resistance systems functions by energy-dependent efflux of toxic ions. Mercury-resistant bacteria have genes for the enzymes mercuric ion reductase and organomercurial lyase, which are often plasmid-encoded, and more rarely by transposons and bacterial chromosome. © 2004 Elsevier B.V. All rights reserved.

Environmental and Experimental Botany

Comparison of mercury, lead and arsenic with respect to genotoxic effects on plant systems and the development of genetic tolerance

An analysis of the available data on the clastogenic effects of metals and their compounds on higher organisms indicates some general trends. Following chronic exposure to subtoxic doses, a decrease in mitotic frequency and an increase in the number of chromosomal abnormalities are observed. These effects are usually directly proportional to the dose applied and the duration of treatment within the threshold limits. Recovery after acute treatment is inversely related to the dosage. The ultimate expression of the effects depends on certain factors, including the mode and vehicle of administration; the form administered; the test system used; the rate of detoxification, distribution, and retention in the different tissues; and interaction with foreign and endogenous substances as well as the mode of action with the biological macromolecules. In mammals, the clastogenic activity of the metals within each vertical group of the periodic table is directly proportional to the increase in atomic weight, electropositivity, and solubility of the metallic cations in water and lipids, except for Li and Ba. This pattern of inherent cytotoxicity increases with successive periods in the horizontal level. It is enhanced by the formation of covalent and coordinate covalent complexes by heavy metals with the biological macromolecules. In plants, the solubility of the metals in water is of much greater importance. The degree of dissociation of metallic salts and the rate of absorption affect significantly the frequency of chromosomal aberrations. In assessing the effects of environmental metal pollution, the presence of other metals and toxic chemicals and the level of nutrition should be taken into account, since in nature, metals occur in combination and these factors modify the cytotoxic effects to a significant extent. Copyright © 1987 Wiley‐Liss, Inc., A Wiley Company

Environmental Mutagenesis

Effects of metals on chromosomes of higher organisms

This paper provides information on the effects of toxic concentrations of zinc sulphate (ZnSO4. 7H2O) on the growth and metabolism of rice Oryza sativa L. seedlings. Root growth inhibition was always more pronounced than was shoot growth inhibition. Root growth was completely inhibited at 40 m m concentration, whereas the magnitude of reduction of shoot length was only 56% at this concentration. Gibberellic acid (GA3) was partially capable of relieving zinc inhibition. The activities of peroxidase, IAA oxidase and ascorbic oxidase of seedlings increased in response to zinc addition, whereas catalase and IAA synthetase decreased. All the hydrolysing enzymes, viz., α-amylase and phytase of endosperm together with RNase and ATPase of the embryo, showed distinct inhibition from the control, the exception being endosperm RNase which was stimulated under zinc treatment. © 1984.

Journal	Z.PFLANZENPHYSIOL.
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