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.-.__. ....~- .. ;.e. ,- ...~..-e-c-.:_...:..:..-~....~~..m~.. .ems -.a~~»~,^r. ^.. ~bT-.ice' ==' C~ LI I1I I IJ t Lethal and Sublethal Effects Terrestrial Flora and Invertebrates Bacteria exposed to cyanide may exhibit de- creased growth, altered cell morphology, de- creased motility, mutagenicity, and altered respiration (Towill et al. 1978). Mixed microbial populations capable of metabolizing cyanide and not previously exposed to cyanide were adversely afTected at 0.3 mg HCN/kg; however, these popu]e- tions can become acclimatized to cyanide and can then degrade wastes with higher cyanide concen- trations (Towill et al. 1978). Acclimatized popula- tions in activated sewage sludge can often complete!}' convert nitrites to ammonia, some- times at concentrations as high as 60 mg total cya- nides per kilogram (Towill et al. 1978). Cyanide can be degraded by various pathways to yield a va- riety ofproducts, including carbon dioxide, ammo- nia, beta-cyanoalanine, and formamide (Knowles 1988). Several species offungi can accumulate and metabolize cyanide, but the products of cyanide metabolism vary. For example, carbon dioxide and ammonia are formed as end products by Fusarium solani, whereas alpha-amino butyronitrile is a ma- jor cyanide metabolite of Rhizoctonia solani (Towill et al. 1978). Significant amounts of cyanide are formed as secondary metabolites by man}• spe- cies offungi and some bacteria by decarboxylation ofglycine (Knowles 1988). Rhizobacteria may sup- press plant growth in soil through cyanide produc- tion. In one case volatile metabolites-including cyanide-from fluorescent pseudomonad soil bac- teria prevented root growth in seedlings of lettuce, Lactuca satiuo (Alstrom and Burns 1989). Not all cyanogenic isolates inhibited plant growth. Some strains promoted growth in lettuce and beans by 41-64~, in 9 weeks versus 49-53°i growth reduc- tion by inhibitory strains (Alstrom and Burns 1989 i. In higher plants, elevated cyanide concentra- tions inhibited respiration (through iron com- plexation in cvtochrome 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 el al. 1978). At loK•er concentrations, ef- fectsinclude inhibition ofgermination and growth. but cyanide sometimes enhances seed germination by stimulating the pentose phosphate pathway CYANIDE 19 and inhibiting catalase (Towill et al. 1978: Solomonson 1981). The detoxification mechanism of cyanide is mediated by rhodahese. This enzyme is widely distributed in plants (Solomonson 1461; Leduc 19841. The rate of production and release of cyanide by plants to the environment through death and decomposition is unknown (Towill et al. 1978). Free cyanide is not found in intact plant cells. Many species of plants, such as Cassava, sorghum, flax, cherries, almonds, and beans, contain cyanogenic glycosides that release HCN when hy- drolyzed (Towill et al. 1978). 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 t4 the development of several variations of sorghums that have a re- duced capability of producing C}•anide poisoning (Egekeze and Oehme 1980). CyBnogenesis has an important role in plant defense against predatory herbivores. This herbivore-plan! interaction is not simple; the degree of selectivity by herbivores var- iesamongindividuals and by differences in hunger and previous diet (Jones 1988). Cyanide metabolism in higher plants involves amino acids, N-hydroxyamino acids, aldoximes, nitri]es, and cyanohydrins (Haikier et al. 1988). Cyanide is a coproduct of ethylene synthesis in higher plants. The increase in ethylene production that occurs during the senescence of certain flow- ers and the ripening of fruits is accompanied by a rise in beta-cyanoalanine activity; activity of this enzyme correlates closely with that of ACC (1-aminocyclopropane-l-carboxylic acid) oxidase, the last enzyme in the ethylene pathway. Manning (1988) suggested that ACC oxidase reacts with various amino acids to liberate cyanide. C}•anide added to isolated castorbean (fticinus communis) mitochondria significantly enhanced the rate and amount of protein synthesis. Cyanide stimulated mitochondria! protein synthesis in a dose- dependentmanner, with an optimal stimulation of over 2 times at 26 µg2, but at phis concentration mitochondria] respiration was inhibited by 9USo (Kaderbhai et al. 1989). Cyanide is a weak com- petitive inhibitor of green beak (Phaseolus uul- garis)lipoxygenase, an enzyme that catal}•zes the formation of hydroperoxides from polyunsatu- rated fatty acids (Adams 1989). Because degrada- tion of hydroperoxides cau8es unacceptable changes in bean flavor and color, compounds that inhibit lipoxygenase may enjoy wide application in the frozen vegetable industry (Adams 1989. Corn seedlings from cold-resistant cultivars were more