Commonwealth of Australia 2010
Effects on terrestrial plants
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- 50.Effect of cyanide complexation
Effects on terrestrial plantsEisler (1991) and more recently Larsen et al. (2004) provide a review of cyanide phytotoxicity. No phytotoxicity data were available for plants exposed to cyanide in air, although when HCN is used as a fumigant (concentrated), it may produce adverse effects on fruits due to acidity (refer below). The issue of phytotoxicity is complicated as many plant species contain organocyanide forms, (glucosides) for chemical defence (Larsen et al., 2004). Many species of plants, such as cassava, sorghum, flax, cherries, almonds, and beans, contain cyanogenic glycosides that release HCN when hydrolysed (Towill et al., 1978). Furthermore, all vascular plants and certain fungi and algae produce cyanide as a by-product in the synthesis of the plant hormone and pheromone ethylene (Peiser et al., 1984). Cyanogenesis has an important role in plant defence against predatory herbivores. This herbivore-plant interaction is not simple; the degree of selectivity by herbivores varies among individuals and by differences in hunger and previous diet (Jones, 1988). Cyanide poisoning of livestock by forage sorghums, such as Sudan grass and various hybrid cultivars, is well known (Cade and Rubira, 1982) and has led to the development of several variations of sorghums that have a reduced capability of producing cyanide poisoning (Egekeze and Oehme, 1980). Although mitochondria in plants possess a cyanide-resistant alternative oxidase system (Shugaev, 1999), higher plants contain enzymes that are irreversibly damaged by cyanide (Larsen et al., 2004). Cyanide affects enzymes associated with respiration (through iron complexation in cytochrome oxidase) and ATP production and other processes dependent on ATP, such as ion uptake and phloem translocation, eventually leading to death (Towill et al., 1978). Cyanide produces chromosomal aberrations in some plants, but the mode of action is unknown (Towill et al., 1978). At lower concentrations, effects include inhibition of germination and growth, but cyanide sometimes enhances seed germination by stimulating the pentose phosphate pathway and inhibiting catalase (Towill et al., 1978; Solomonson, 1981). The detoxification mechanism of cyanide is mediated by the rhodanese enzyme, which is widely distributed in plants (Solomonson, 1981; Leduc, 1984). USEPA (2006c) lists brief results for phytotoxicity tests with the grass species alkali sacaton (Sporobolus airoides) and creosote bush (Larrea tridentata) and sodium cyanide in water at a pH of 10.5. Eighty seeds were sown per pot (3 pots per treatment) placed in a growth chamber, with exposure to the cyanide solution by irrigation. In both tests, germination was poor, mortality was >50% after 2-3 months, with chlorosis and necrosis evident. However, the concentration of sodium cyanide tested was not specified and the high pH may also have influenced phytotoxicity. Larsen et al. (2004ab) investigated the phytotoxicity of cyanide (KCN) to basket willows (Salix viminalis). In aqueous solutions, 2 mg CN/L depressed transpiration after 72 h by about 50% and all died after 3 weeks exposure. Trees exposed to 0.4 mg CN/L in aqueous solution initially showed a depression of transpiration, but recovered after 72 hours. As this depression was also evident in the control due to lack of nitrogen in the nutrient solution, the effect was not significant. Doses of 8 and 20 mg CN/L in aqueous solution quickly resulted in mortality (<1 week) to the trees. At the end of the test, almost all cyanide had disappeared from the solutions. Levels of cyanide in plants were related to the toxicity, with no elevated levels of cyanide in plants exposed to 0.4 mg CN/L. Willows grown in sand showed no toxic effects when irrigated with cyanide solutions at 10 mg CN/L, but after 96 h transpiration was reduced to ~50% at 20 mg CN/L and to <20% at 30-50 mg CN/L. Accumulation of CN in plant tissue was observed at 40 and 50 mg CN/L, up to ~4 mg/kg in leaves and ~15 mg/kg in roots. Mathematical modelling predicted that at <10 mg CN/L, the cyanide would be rapidly metabolised, whereas at higher doses uptake would occur more rapidly than metabolism and cyanide would accumulate in the plant tissue. Plants in sand survived irrigation with 20 mg CN/L, but those treated with 30 mg/L died. The roots of the surviving willows were able to consume about 10 mg CN/kg (fresh weight)/hour. Vascular plants possess the enzymes beta-cyanoalanine synthase and beta-cyanoalanine hydrolase, which convert free cyanide to asparagine, an amino acid important for nitrogen storage (Larsen et al., 2004; Miller and Conn, 1980). The synthase combines HCN with L-cysteine to produce beta-cyanoalanine (Blumenthal et al., 1968). Larsen et al. (2004a) investigated the in-vivo phytoremediation capacity of willow and other woody plants (poplar, elder, rose and birch) to remove cyanide from growth media. Tests were performed with detached leaves and roots in KCN solutions of different concentrations. The highest removal capacity was obtained for basket willow hybrids (Salix viminalis x schwerinii). The Michaelis–Menten kinetics was determined. Realistic values of the half-saturation constant, KM, were between 0.6 and 1.7 mg CN/L; the maximum metabolic capacity, vmax, was around 9.3 mg CN/kg (fresh weight)/hour. Larsen et al. (2004a) estimated that with a vmax of 14.5 mg/kg/hour, about 1100 kg of free cyanide could potentially be removed by 1 hectare of willows during a growth period of 200 days.
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