Other affiliations: Laval University
Bio: Archana Sharma is an academic researcher from University of Calcutta. The author has contributed to research in topic(s): Sister chromatid exchange & Chromosome. The author has an hindex of 35, co-authored 234 publication(s) receiving 5783 citation(s). Previous affiliations of Archana Sharma include Laval University.
TL;DR: 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.
Abstract: 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. All mercury resistance genes are clustered into an operon. The expression of the operon is regulated and is inducible by Hg(II). Lead tolerance in Festuca ovina is an inherited characteristic, evolved by the production of compounds within the plants, specifically for protection against the toxic effects of heavy metals. A small number of genes are probably producing the major effects, and modifiers for dominance are present, which are probably affected by the genome as a whole. Arsenic tolerance appears to be genetically controlled in a fairly simple Mendelian manner but the specific mechanisms may be one or several, acting in cohesion. The ars operon provides resistance to arsenicals and as well antimonials. Arsenic-resistant bacterial and yeast strains may prove an important tool for identifying the genes for arsenic transporters in higher plants.
TL;DR: The possible causal mechanisms of mercury toxicity are changes in the permeability of the cell membrane, reactions of sulphydryl (-SH) groups with cations, affinity for reacting with phosphate groups and active groups of ADP or ATP, and replacement of essential ions, mainly major cations.
Abstract: Mercury poisoning has become a problem of current interest as a result of environmental pollution on a global scale. Natural emissions of mercury form two-thirds of the input; manmade releases form about one-third. Considerable amounts of mercury may be added to agricultural land with sludge, fertilizers, lime, and manures. The most important sources of contaminating agricultural soil have been the use of organic mercurials as a seed-coat dressing to prevent fungal diseases in seeds. In general, the effect of treatment on germination is favorable when recommended dosages are used. Injury to the seed increases in direct proportion to increasing rates of application. The availability of soil mercury to plants is low, and there is a tendency for mercury to accumulate in roots, indicating that the roots serve as a barrier to mercury uptake. Mercury concentration in aboveground parts of plants appears to depend largely on foliar uptake of Hg0 volatilized from the soil. Uptake of mercury has been found to be plant specific in bryophytes, lichens, wetland plants, woody plants, and crop plants. Factors affecting plant uptake include soil or sediment organic content, carbon exchange capacity, oxide and carbonate content, redox potential, formulation used, and total metal content. In general, mercury uptake in plants could be related to pollution level. With lower levels of mercury pollution, the amounts in crops are below the permissible levels. Aquatic plants have shown to be bioaccumulators of mercury. Mercury concentrations in the plants (stems and leaves) are always greater when the metal is introduced in organic form. In freshwater aquatic vascular plants, differences in uptake rate depend on the species of plant, seasonal growthrate changes, and the metal ion being absorbed. Some of the mercury emitted from the source into the atmosphere is absorbed by plant leaves and migrates to humus through fallen leaves. Mercury-vapor uptake by leaves of the C3 speciesoats, barley, and wheat is five times greater than that by leaves of the C4 species corn, sorghum, and crabgrass. Such differential uptake by C3 and C4 species is largely attributable to internal resistance to mercury-vapor binding. Airborne mercury thus seems to contribute significantly to the mercury content of crops and thereby to its intake by humans as food. Accumulation, toxicity response, and mercury distribution differ between plants exposed through shoots or through roots, even when internal mercury concentrations in the treated plants are similar. Throughfall and litterfall play a significant role in the cycling and deposition of mercury. The possible causal mechanisms of mercury toxicity are changes in the permeability of the cell membrane, reactions of sulphydryl (-SH) groups with cations, affinity for reacting with phosphate groups and active groups of ADP or ATP, and replacement of essential ions, mainly major cations. In general, inorganic forms are thought to be more available to plants than are organic ones.
•01 Jan 1965
TL;DR: The cytotoxic and phytotoxic activities of cobalt and its compounds depend on the physico-chemical properties of these complexes, including their electronic structure, ion parameters (charge-size relations) and coordination.
Abstract: Cobalt, a transition element, is an essential component of several enzymes and co-enzymes. It has been shown to affect growth and metabolism of plants, in different degrees, depending on the concentration and status of cobalt in rhizosphere and soil. Cobalt interacts with other elements to form complexes. The cytotoxic and phytotoxic activities of cobalt and its compounds depend on the physico-chemical properties of these complexes, including their electronic structure, ion parameters (charge-size relations) and coordination. Thus, the competitive absorption and mutual activation of associated metals influence the action of cobalt on various phytochemical reactions. The distribution of cobalt in plants is entirely species-dependent. The uptake is controlled by different mechanisms in different species. Biosorption involves ion-exchange mechanism in algae, but in fungi both metabolism-independent and -dependent processes are operative. Physical conditions like salinity, temperature, pH of the medium, and presence of other metals influence the process of uptake and accumulation in algae, fungi, and mosses. Toxic concentrations inhibit active ion transport. In higher plants, absorption of Co2+ by roots involves active transport. Transport through the cortical cells is operated by both passive diffusion and active process. In the xylem, the metal is mainly transported by the transpirational flow. Distribution through the sieve tubes is acropetal by complexing with organic compounds. The lower mobility of Co2+ in plants restricts its transport to leaves from stems. Cobalt is not found at the active site of any respiratory chain enzymes. Two sites of action of Co2+ are found in mitochondrial respiration since it induces different responses toward different substrates like α-keto glutarate and succinate. In lower organisms, Co2+ inhibits tetraphyrrole biosynthesis, but in higher plants it probably participates in chlorophyll b formation. Exogenously added metal causes morphological damage in plastids and changes in the chlorophyll contents. It also inhibits starch grain differentiation and alters the structure and number of chloroplasts per unit area of leaf. The role of cobalt in photosynthesis is controversial. Its toxic effect takes place by inhibition of PS2 activity and hence Hill reaction. It inhibits either the reaction centre or component of PS2 acceptor by modifying secondary quinone electron acceptor Qb site. Co2+ reduces the export of photoassimilates and dark fixation of CO2. In C4 and CAM plants, it hinders fixation of CO2 by inhibiting the activity of enzymes involved. Cobalt acts as a preprophase poison and thus retards the process of karyokinesis and cytokinesis. The action of cobalt on plant cells is mainly turbagenic. Cobalt compounds act on the mitotic spindle, leading to the formation of chromatin bridges, fragmentation, and sticky bridges at anaphase and binucleate cells. High concentrations of cobalt hamper RNA synthesis, and decrease the amounts of the DNA and RNA probably by modifying the activity of a large number of endo- and exonucleases. The mutagenic action of cobalt salts results in mitochondrial respiratory deficiency in yeasts. In cytokinesis-deficient mutant of Chlamydomonas it increases the amount of sulfhydryl compounds. Cobalt has been shown to alter the sex of plants like Cannabis sativa, Lemna acquinoclatis, and melon cultivars. It decreases the photoreversible absorbance of phytochrome in pea epicotyl and interferes with heme biosynthesis in fungi. Low concentration of Co2+ in medium stimulates growth from simple algae to complex higher plants. Relatively higher concentrations are toxic. A similar relationship is seen with crop yield when the metal is used in the form of fertilizer, pre-seeding, and pre-sowing chemicals. Toxic effect of cobalt on morphology include leaf fall, inhibition of greening, discolored veins, premature leaf closure, and reduced shoot weight. Being a component of vitamin B12 and cobamide coenzyme, Co2+ helps in the fixation of molecular nitrogen in root nodules of leguminous plants. But in cyanobacteria, CoCl2 inhibits the formation of heterocyst, ammonia uptake, and nitrate reductase activity. The interaction of cobalt with other metals mainly depends on the concentration of the metals used. For example, high levels of Co2+ induce iron deficiency in plants and suppress uptake of Cd by roots. It also interacts synergistically with Zn, Cr, and Sn. Ni overcomes the inhibitory effect of cobalt on protonemal growth of moss, thus indicating an antagonistic relationship. The beneficial effects of cobalt include retardation of senescence of leaf, increase in drought resistance in seeds, regulation of alkaloid accumulation in medicinal plants, and inhibition of ethylene biosynthesis. In lower plants, cobalt tolerance involves a cotolerance mechanism. The mechanism of resistance to toxic concentration of cobalt may be due to intracellular detoxification rather than defective transport. In higher plants, only a few advanced copper-tolerant families showed cotolerance to Co2+. Tolerance toward Co2+ may sometimes determine the taxonomic shifting of several members of Nyssaceae. Due to the high cobalt content in serpentine soil, essential element uptake by plants is reduced, a phenomenon known as “serpentine problem,” for New Caledonian families like Flacourtiaceae. Large amounts of calcium in soil may compensate for the toxic effects of heavy metals in adaptable genera grown in this type of soil. The biomagnification of potentially toxic elements, such as cobalt from coal ash or water into food webs, needs additional study for effective biological filtering.
TL;DR: Aluminum toxicity is a major factor in limiting growth in plants in most strongly acid soils, and root elongation is hampered through reduced mitotic activity induced by Al, with subsequent increase in susceptibility to drought.
Abstract: Aluminum toxicity is a major factor in limiting growth in plants in most strongly acid soils. Toxic effects on plant growth have been attributed to several physiological and biochemical pathways, although the precise mechanism is still not fully understood. In general, root elongation is hampered through reduced mitotic activity induced by Al, with subsequent increase in susceptibility to drought. The initial site of uptake is usually the root cap and the mucilaginous secretion covering the epidermal cells. Al ions bind very specifically to the mucilage by exchange adsorption on the polyuronic acid, complexing with the pectic substances and by the formation of polyhydroxy forms, increasing the number of Al atoms per positive charge. Toxicity has been suggested to be initiated at the sites of mucopolysaccharide synthesis. Al is absorbed on all Ca-binding sites on the cell surface. In the intact tissues, most of the Al is bound to the pectic substances of the cell wall and a part to the nucleic acids and cell membrane. Al is also reported to enter the plant by moving into meristematic cells via the cortex, bypassing the endodermal barrier. Being a polyvalent cation, it follows principally the apoplasmic pathway of transport through cortical cells, but may also enter the stele through the plasmalemma. Ultrastructural studies have shown the maximum accumulation to be in the epidermal and cortical cells. The interaction of Al with different systems follows different pathways. The plasma membrane at the outer boundary of the root cell is a potential target and its physical properties can be altered by Al through interaction with membrane-bound ATPase, lipids, carbohydrates and proteins. The Golgi apparatus has been suggested as the primary site of action, followed by damage to the plasmalemma. Aluminum interferes with the uptake, transport and use of several essential elements, including Cu, Zn, Ca, Mg, Mn, K, P and Fe. Excess of Al reduces the uptake of certain elements and increases that of others, the patterns being dependent on the element, the plant part and species involved. A major factor is the pH concentration. At an acid pH, below 5.5, the antagonism between Ca and Al is probably the most important factor affecting Ca uptake by plants. The molecular mechanism of tolerance of Al is as yet not clear. Tolerant plants reduce the absorption by the root or detoxify Al after absorption. Al tolerant plants may be grouped into those with higher Al concentrations in tops and those with less. In the latter, more Al is entrapped in roots. Uptake of Al may be reduced by binding to cell wall or to membrane lipid. Tolerance may be different in different species and seems to be controlled by one or more genes. Absorption of Al in non-metabolic conditions is affected only slightly by temperature. Anaerobic conditions, like the presence of nitrogen and metabolic inhibitors, damage the endodermal membrane barrier, increasing the uptake and enhancing injurious effects. Aluminum also causes morphological damage to plant parts. It affects photosynthesis by lowering chlorophyll content and reducing electron flow. Reduced respiratory activity might be due to reduced metabolic energy requirement. Protein synthesis is decreased probably due to effect on ribosome distribution at endoplasmic reticulum. Aluminum is known to bind to DNA and nuclei. However, its penetrance to DNA of mitotically active centers is slow. On accumulating in roots, it initially inhibits mitotic activity, possibly through affecting the integrated control function of the root meristem. Aluminum toxicity in acid soil is of special importance due to the destruction of components of forest ecosystems under specific conditions. It reduces biomass yield and tree growth and represses litter-degrading microflora. Further information is required on the factors affecting membrane permeability, distribution and accumulation of Al in different plant parts and different species. Al tolerance may be studied with relation to the presence of different ligands, nitrogen metabolism (nitrate reductase and protein accumulation), nitrogen tolerance in relation to pH change and metal ion activities, the role of Ca and P and interference with water relations and litter degradation.
TL;DR: Western medicine has not yet used flavonoids therapeutically, even though their safety record is exceptional, and suggestions are made where such possibilities may be worth pursuing.
Abstract: Flavonoids are nearly ubiquitous in plants and are recognized as the pigments responsible for the colors of leaves, especially in autumn. They are rich in seeds, citrus fruits, olive oil, tea, and red wine. They are low molecular weight compounds composed of a three-ring structure with various substitutions. This basic structure is shared by tocopherols (vitamin E). Flavonoids can be subdivided according to the presence of an oxy group at position 4, a double bond between carbon atoms 2 and 3, or a hydroxyl group in position 3 of the C (middle) ring. These characteristics appear to also be required for best activity, especially antioxidant and antiproliferative, in the systems studied. The particular hydroxylation pattern of the B ring of the flavonoles increases their activities, especially in inhibition of mast cell secretion. Certain plants and spices containing flavonoids have been used for thousands of years in traditional Eastern medicine. In spite of the voluminous literature available, however, Western medicine has not yet used flavonoids therapeutically, even though their safety record is exceptional. Suggestions are made where such possibilities may be worth pursuing.
Bent H. Havsteen1•Institutions (1)
TL;DR: Flavonoids are plant pigments that are synthesised from phenylalanine, generally display marvelous colors known from flower petals, mostly emit brilliant fluorescence when they are excited by UV light, and are ubiquitous to green plant cells.
Abstract: Flavonoids are plant pigments that are synthesised from phenylalanine, generally display marvelous colors known from flower petals, mostly emit brilliant fluorescence when they are excited by UV light, and are ubiquitous to green plant cells. The flavonoids are used by botanists for taxonomical classification. They regulate plant growth by inhibition of the exocytosis of the auxin indolyl acetic acid, as well as by induction of gene expression, and they influence other biological cells in numerous ways. Flavonoids inhibit or kill many bacterial strains, inhibit important viral enzymes, such as reverse transcriptase and protease, and destroy some pathogenic protozoans. Yet, their toxicity to animal cells is low. Flavonoids are major functional components of many herbal and insect preparations for medical use, e.g., propolis (bee's glue) and honey, which have been used since ancient times. The daily intake of flavonoids with normal food, especially fruit and vegetables, is 1-2 g. Modern authorised physicians are increasing their use of pure flavonoids to treat many important common diseases, due to their proven ability to inhibit specific enzymes, to simulate some hormones and neurotransmitters, and to scavenge free radicals.
TL;DR: Genome analysis provides a greatly improved fish gene catalogue, including identifying key genes previously thought to be absent in fish, and reconstructs much of the evolutionary history of ancient and recent chromosome rearrangements leading to the modern human karyotype.
Abstract: Tetraodon nigroviridis is a freshwater puffer fish with the smallest known vertebrate genome. Here, we report a draft genome sequence with long-range linkage and substantial anchoring to the 21 Tetraodon chromosomes. Genome analysis provides a greatly improved fish gene catalogue, including identifying key genes previously thought to be absent in fish. Comparison with other vertebrates and a urochordate indicates that fish proteins have diverged markedly faster than their mammalian homologues. Comparison with the human genome suggests ∼900 previously unannotated human genes. Analysis of the Tetraodon and human genomes shows that whole-genome duplication occurred in the teleost fish lineage, subsequent to its divergence from mammals. The analysis also makes it possible to infer the basic structure of the ancestral bony vertebrate genome, which was composed of 12 chromosomes, and to reconstruct much of the evolutionary history of ancient and recent chromosome rearrangements leading to the modern human karyotype.
TL;DR: A high-quality draft sequence of the N. crassa genome is reported, suggesting that RIP has had a profound impact on genome evolution, greatly slowing the creation of new genes through genomic duplication and resulting in a genome with an unusually low proportion of closely related genes.
Abstract: Neurospora crassa is a central organism in the history of twentieth-century genetics, biochemistry and molecular biology. Here, we report a high-quality draft sequence of the N. crassa genome. The approximately 40-megabase genome encodes about 10,000 protein-coding genes—more than twice as many as in the fission yeast Schizosaccharomyces pombe and only about 25% fewer than in the fruitfly Drosophila melanogaster. Analysis of the gene set yields insights into unexpected aspects of Neurospora biology including the identification of genes potentially associated with red light photobiology, genes implicated in secondary metabolism, and important differences in Ca21 signalling as compared with plants and animals. Neurospora possesses the widest array of genome defence mechanisms known for any eukaryotic organism, including a process unique to fungi called repeat-induced point mutation (RIP). Genome analysis suggests that RIP has had a profound impact on genome evolution, greatly slowing the creation of new genes through genomic duplication and resulting in a genome with an unusually low proportion of closely related genes.
B. Havsteen1•Institutions (1)
TL;DR: The few existing reports on the careful pharmacodynamic, pharmacokinetic and clinical studies which have been made have been summarized to provide a basis for a full-scale investigation of the therapeutic potential of flavonoids.
Abstract: A review has been presented of the biochemistry and pharmacology of a class of natural products, the flavonoids. These substances which are widely distributed in the plant kingdom and present in considerable quantities in common food products, spices and beverages have in a concentrated form (Propolis) been used since ancient times by physicians and laymen to treat a great variety of human diseases but they have yet to pass the tests of modern, controlled, clinical experimentation. An attempt has been made to present the fundamental evidence from the basic biological sciences which is required to stimulate the interest of the clinicians in this new field. The few existing reports on the careful pharmacodynamic, pharmacokinetic and clinical studies which have been made have been summarized to provide a basis for a full-scale investigation of the therapeutic potential of flavonoids.
Author's H-index: 35