0141753 



remaining 25 percent excreted in 8 to 10 days (NRC 1977). 

 Shar iatpanahi and Anderson (1984a) found that the half life of 

 arsenic in blood of sheep and goats was 3.2 and 2.1 days, respec- 

 tively after monosodium methanearsonate was removed from the diet. 

 Dehydrated animals and those in poor condition are more suscepti- 

 ble to poisoning, probably due to reduced excretion via the 

 kidneys. Some ingested inorganic arsenate and arsenite have been 

 shown to be methylated i_n vivo by both ruminants and nonruminants 

 (Laksc and Peoples 1975, Tsukamoto et al. 1983). The action is 

 apparently endogenous and the result of intestinal microflora 

 (Penrose 1975). This action may reduce the toxicity of these 

 compounds . 



The toxicosis of arsenic is generally attributed to the 

 trivalent form (Buck et al . 1976). Arsenic reacts with sulfhydryl 

 groups in cells inhibiting sulfhydryl enzyme systems such as 

 pyruvate oxidase, which is essential for proper fat and carbohy- 

 drate metabolism in the cell. Arsenic also uncouples oxidative 

 phosphorylation by substituting for phosphorus; labile arsenylated 

 oxidation products are substituted for stable phosphorylated 

 intermediates (Riviere et al . 1981). Tissues most affected are 

 the alimentary tract, kidney, liver, lung and epidermis (Buck et 

 al. 1976). Capillary damage, especially in the splanchnic area, 

 results in transudation of plasma into the intestinal tract and 

 sharply reduced blood volume. Blood pressure falls to shock 

 levels, the heart muscle becomes depressed, and general circula- 

 tory failure occurs. The capillary transudation of plasma in 

 vesicles results in edema of the gastrointestinal mucosa, eventu- 

 ally leading to epithelial sloughing and the discharge of plasma 

 into the gastrointestinal tract .(Radeleff 1970). 



Chronic arsenic poisoning through faulty diets containing 

 phenylarsonic feed additives are well documented (NRC 1977). 

 Toxicosis by phenylarsonic compounds apparently involves periph- 

 eral nerve degeneration and symptoms include incoordination, 

 inability to control body and limb movements, and ataxia. The 

 condition may progress to quadriplegia (Ledet et al . 1973) 



152 



