1992-04-02_REVISION - M1988112 - Laserfiche WebLink

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' CYANIDE 45 ' Table 5. Continued. Species, dose, and other variables Effects References ' Laboratory white rat, (continued) As above, protein deficient Reduction in body weight 37 ' diet gain, reduction in serum thiocyanate concentration Weanling males fed diets No deaths or clinical signs 38 containing 1,500 mg KCN/kg, of toxicity; both groups had or 2.240 mg potassium thiocyanate decreased thyroid gland ' (KSCNI/kg for 50 weeks activity; cyanide, but not thiocyanate, caused reduction ingrowth rate ' Isolated liver segments from Oxygen consumption reduced 39 starved rats exposed to 80%, and evidence of 100 mg KCN/L hepatotoxicity as judged by enyzme release, glutathione ' depletion, and calcium accumulation in liver; hepatotoxicity prevented by feeding rats fructose Domestic pig, Sus spp. Fed diet containing 96 mg No elTect on food consumption 40 CN/kg ration, as cassava or protein metabolism ' peel, for 72 days ~~ 1. EPA 1980; 2. Sterner 1979; 3. Christcl et al. 1977; 4. Savaric and Sterner 1979; 5. Tewe 1984; 6. Tewe 1988:'. Tewc 1982a; 8. Curry 1963; 9. Grandas et al. 1989; 10. Ballantynr 1987a; 11. Towill cl al. 1978; 12. Ukhun and llil,ic 1989; 13. Egekezc and ' Ochme 1980; 14. Wev 1981; 15. Casadci et al. 19R4; 16. Purser et al. 1964; 17. PUfsl'1' 1984; 18. Willhitc and Smith 1981; 19. Yamamoto 1989; 20. EPA 1989: 21. Robinson et ;~1. 1985; 22. Ballantyne et al. 1972; 23. Ballantynr 1988; 24. YamamoW et el. 1979:25. Ballantynr et al. 1974; 26. ltskovitz and Rudolph 1987; 27. Ballantyne 1975: 28. Brattsten et al. ]96$; 29. Lotita et el. 1989; 30. Lrc at al. 1988;31. MacMillan 1989; 32. Keniston et el.1987;33. Yamamoto et al. 1982; 34. Palmer and Olson 1981; 35. ' Beilstein and N'hanger 1984; 36. Aletnr and F etusa 1988; 37. Tewe and Maner 1985; 38. Philbrick et al. 1979; 39. }'Dunes and Strubclt 1988; 40. Tewe and Pessu 1982; 41. N'ey 1989; 42. Marrs and Ballantyne 1967; 43. Buzalch et al. 19(19; 44. Bapat and Abhvankcr 1984. thus preventing cyanide from reaching the target ' tissues and causing death (Buzaleh et al. 1989). Cyanide causes dose- and species-dependent re- sponses on vascular smooth muscle; studies with isolated aortic strips indicate that rabbits are 80 ' ~ times more sensitive than dogs or ferrets (Mustela -putorius; Robinson etal. 1985). Rabbits killed with H CN had higher concentrations of cyanide in blood ' and other tissues and lower tissue cytochrome oxidase activities than did those killed with KCN (Ballantyne et al. 197?). Cyanide promotes dose- ' and calcium-dependent release of dopamine tis- sues in the domestic cat, and reductions in adeno- sine triphosphate (ATPI content ofthe carotid bod}• tObeso et al. 19891. Cyanide-induced hypoxia is be- ' lieved to decrease ATP content of Type I glomus cells. The decrease in the phosphate transfer po- tential is a crucial step in the overall transduction process, that is, the activation of the transmitter reiease from Type I cells, with res4ltant release and activation of sensory nerve endings (Obeso et al. 1989). Studies with isolated heart of the domes- tic ferret demonstrate that cyanide af7ects intra- cellular ionic exchange of H', Na', and calcium (Fry et al. 19871; inhibits cardiac action potential (Elliott et al. 1989); and inhibits oxidative phosphorylation accompanied by an intracellular acidosis, a decrease in phosphocreatinine, and a rise in inorganic phosphate (Eisner et al. 19871. When oxidative phosphorylation is inhibited in cardiac muscle, there is a rapid decrease of devel- oped force or pressure; most of the decrease of de- veloped pressure produced by cyanide in ferret heart is not produced by intracellular acidosis, and may result from increased inorganic phosphate (Eisner et al. 1987). Observed changes in rat cere-