A study of chronic Senecio jacobaea toxicosis in calves and ponies Public Deposited

http://ir.library.oregonstate.edu/concern/graduate_thesis_or_dissertations/6m311s84v

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  • An experiment was designed to simulate field conditions of tansy ragwort poisoning in cattle and horses. Four calves and four ponies were fed pelleted feed containing 5% Senecio jacobaea and two ponies and two calves were used as controls. The feeding continued for two months. Following this, the chronic delayed response of the animals was determined. Liver biopsy was performed every two weeks and serum activity of alkaline phosphatase, gamma-glutamyl transferase and glutamate dehydrogenase was determined at the same time. Serum glutamate dehydrogenase activity rose within two weeks, in many cases followed by the other two enzymes. The glutamate dehydrogenase peaked and dropped to a lower level before death. Both the alkaline phosphatase and the gamma-glutamyl transferase remained elevated many weeks after the consumption of Senecio had ceased. Some previously unreported microscopic lesions in the pony and calf are described. One of the lesions was an intranuclear vacuole. These vacuoles were seen in biopsy specimens only and not in postmortem tissues. These lesions had been previously described in rats poisoned with pyrrolizidine alkaloids. An electron microscope was used to detect the lesions in the previously reported rat studies. They are reported to be invaginations of the cytoplasm into the nucleus. Some cytoplasmic invaginations were seen in a limited electron microscope study in this experiment. These nuclear changes were easily seen with the light microscope in liver biopsy tissue of both calves and ponies. The serum alkaline phosphatase activity rose corresponding to biliary hyperplasia. The gamma-glutamyl transferase activity paralleled the alkaline phosphatase activity in most cases, but the magnitude of change was much greater. The gamma-glutamyl transferase activity was more indicative of active necrosis and returned to normal even with some remaining biliary hyperplasia. Glutamate dehydrogenase activity increased with active necrosis of cells in Rappaport's "zone one" of the liver lobule, the periportal areas.
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