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Physiological effects of Astragalus miser var. serotinus, (timber milkvetch) on sheep, rats, and mice.

University of British Columbia

Feeding trials were conducted during 1968 and 1969 to study the physiological effects of Astragalus miser var. serotinus, timber milkvetch, (TMV) in sfieep. In Trial I, TMV was collected from Kamloops and Clinton, pelleted and fed to U groups of Dorset Horn wethers at levels of 0, 35, 70 and 100%. The symptoms exhibited by the sheep fed 100% TMV included backward flexion of the fetlock - joints, hind limb paralysis and inco—ordination of movements. The presence of longitudinal ulcers in the intestines was a characteristic lesion observed in the sheep fed 100% TMV. Fatty infiltration and hemorrhages in the liver and kidney were also observed. After the vetch was cut, dried and pelleted, the miserotoxin content dropped from 2.3 - 3.4% to 0.9%. Trial II was carried out under actual grazing conditions near Kamloops. Yearling ewes fed freshly cut TMV showed symptoms similar to those observed in Trial I. However, the symptoms were less severe and could be observed only when the sheep were exerted. The intestinal ulcers were found to be confined to the jejunum. The activity of the serum glutamic – oxaloacetic transaminase was significantly (p <.05) elevated in the sheep fed TMV indicating extensive tissue destruction. The level of thiamine in blood in both the trials was found to be within the normal range indicating that the beneficial effects of thiamine as a therapeutic agent in TMV poisoning may be indirect. When rats and mice were fed TMV, it was found that they developed a syndrome characterized by the manifestation of convulsive movements terminating in a state of inactivity and a significant decline in body temperature. Extensive hemorrhages were seen in the gastric mucosa. By chromatographic procedures it has been shown that miserotoxin is hydrolyzed to glucose and 3 - nitropropionic acid in the stomach of monogastric animals. In ruminants, miserotoxin is hydrolyzed to glucose and 3 - nitro - 1 - propanol which appears to be responsible for the toxicity.

Text

2011-05-24

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http://hdl.handle.net/2429/34780

Animal Science

University of British Columbia

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