ABSTRACT

Summary Cyanogenesis, the abiity of organisms to produce hydrocyanic acid (HCN), has been reported in approximately 1,000 species of plants representing 250 genera and 80 families, but the identity of the cyanogenic compound(s) involved has been established for less than 100 of these species. The first cyanogenic compound identified in the grass family was dhurrin, which was isolated from sorghum plants in 1902. Many other grasses were subsequently reported to be cyanophoric, but until recently Sorghum remained the only grass genus in which the presence of dhurrin had been demonstrated unequivocally. A precise, rapid, and highly specific spectrophotometric assay for dhurrin in seedling leaves was developed at Nebraska in 1977, primarily for use in breeding for low dhurrin content in sudangrass and sorghums. This procedure has been used successfully in selecting sudangrasses with reduced levels of hydrocyanic acid potential (HGN-p). Two cycles of divergent selection for high and low HGN-p in Greenleaf sudangrass have resulted in an average realized heritability of 0.26 and an average broad-sense heritability estimate of 0.84. The high- and low-HGN-p populations each differed from Greenleaf by about 20%. Dry-matter yields for the high- and low-HGN-p populations, obtained during one growing season after only one cycle of selection, were 7,440 and 6,680 kg/ha, respectively, compared with 6,910 kg/ha for unselected Greenleaf. The spectrophotometric assay also has been used to screen seedlings of 72 grasses representing 39 species, 14 genera, and 2 tribes for the presence of dhurrin. Among genera other than Sorghum, dhurrin was found only in the genus Sorghastrum. Levels were in the same range as for Sorghum seedlings considered to be high in dhurrin content. The toxicity of a cyanophoric forage grass is influenced by various factors, one of which is the ability of the grazing animal to detoxify the HGN it encounters. In ruminants, HGN is rapidly detoxified in the rumen and liver by reactions with sulfide or cystine, and the resulting thiocyanate is excreted in the urine. The low rates of gain that are sometimes observed when cattle or sheep graze pure stands of sorghum or sudangrass may, in some cases, be explained in terms of an induced sulfur deficiency in the animal due to the priority requirement of sulfur to detoxify HGN. Therefore, sulfur supplements may reduce the potential 153for HCN poisoning, replace sulfur lost in detoxification of HGN, and insure an adequate dietary level of sulfur for animal needs. Recent studies have shown that released cyanide also may protect animals from the toxic effects of selenium by forming a compound with selenium that is apparently readily excreted in the urine. However, this same reaction may cause selenium deficiency in livestock in areas where selenium levels are low.