Metabolism and absorption of toxic glycosides by ruminants

Abstract

The cyanogenic glycoside prunasin is the toxic component in a number of browse species (serviceberry, Amelanchier alnifolia, and chokecherry, Pnmus virginiana); and glycosides of 3-nitropropanol (NPOH), such as miserotoxin, are the poisonous principle in a number of Astragalus species such as timber milkvetch, A. miser var. serotinus. Hydrolysis of the glycosidic bond in rumen contents is the first step in the bioactivation of the glycosides. Diet influences populations of rumen microorganisms and diet may induce the proliferation of bacteria that function in glycoside hydrolysis and detoxification. The absorption of NPOH from the reticulo-rumen was examined in cattle on alfalfa hay and corn silage diets. 3- nitropropionic acid (NPA), the lethal metabolite of NPOH, was detected in both plasma and urine. The plasma levels of NPA were reduced when the diet enhanced the rate of NPOH detoxification in the rumen. The enhancement was achieved with a feed supplement containing nitroethane, a synthetic analogue of NPOH that is much less toxic than the natural toxin. The high levels of NPA in urine (>30 ppm) suggested a procedure for detecting livestock poisoning by nitro-bearing plants. The absorption of hydrogen cyanide (HCN) from the reticulo-rumen was also examined in cattle given sublethal doses of prunasin from serviceberry. Metabolites of HCN in blood and plasma were detected at low levels (<5 ppm) during the initial 6-hour sampling period. High levels of thiocyanate (<20 ppm), a metabolite of HCN, were detected in urine samples collected at 24-48 hours and this also suggested a diagnostic procedure for detecting HCN poisoning in cattle.