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by sodium thiosulfate (NAS 1977), and by mono- and dithiol- containing <br />compounds and 2,3-dimercaptopropanol (Pershagen and Vahter 1979). Arsenic <br />uptake in rabbit intestine is inhibited by phosphate, casein, and various <br />metal chelating agents (EPA 1980). Mice and rabbits are significantly <br />protected against sodium arsenite intoxication by N-(2,3-dimer- <br />captopropyl)phthalamidic acid (Stine et al. 1984). Conversely, the toxic <br />effects of arsenite are potentiated by excess dithiols, cadmium, and lead, as <br />evidenced by reduced food efficiency and disrupted blood chemistry in rodents <br />(Pershagen and Vahter 1979). <br />Arsenic effectively controls filariasis in cattle; new protective uses <br />are under investigation. The control of parasitic nematodes (Parafilaria <br />bovicola) in cattle was successful after 30 weekly treatments in plungement <br />dips containing 1,600 mg As 0 /1; however, the muscle of treated cattle <br />contained up to 1.3 mg ARg, or 12X the amount in controls (Nevill 1985). <br />Existing anionic organic arsenicals used to control tropical nematode <br />infections in humans have sporadic and unacceptable lethal side effects. <br />Cationic derivatives have been synthesized in an attempt to avoid the side <br />effects and have been examined for effects on adult nematodes (Brugia ap hangi) <br />in gerbils (Meriones unguiculatus). All arsenicals were potent filaricides; <br />the most effective compounds tested killed 95% of adult B. ap hangi after five <br />daily subcutaneous injections of 3.1 mg As/kg body weight (Denham et al. <br />1986). <br />Animals previously exposed to sublethal levels of arsenic may develop <br />tolerance to arsenic on reexposure. Although the mechanism of this process is <br />not fully understood, it probably includes the efficiency of in vivo <br />me??ylation gocesses (EPA 1980). For example, resistance to toxic doses <br />As or As increases in mouse fibroblast cells pretreated with a low As <br />concentration (Fischer et al. 1985). Also, growth is better in <br />arsenic-conditioned mouse cells in the presence of arsenic than in previously <br />unexposed cells, and inorganic arsenic is more efficiently methylated. In <br />vivo biotransformation and excretion of inorganic arsenic as monomethylarsonic <br />acid (MMA) and dimethylarsinic acid (DMA) has been demonstrated in a number of <br />mammalian species, including man. It seems that cells may adapt to arsenic by <br />increasing the biotransformation rate of the element to methylated forms, such <br />as MMA and DMA (Fischer et al. 1985). Pretreatment of ovary cells of Chinese <br />hamster (Cricetus spp.) ovary cells with sodium arsenite provided partial <br />protection against adverse effects of methyl methanesulfonate (MMS), and may <br />even benefit the MMS-treated cells; however, posttreatment dramatically <br />increases the cytotoxic, clastogenic, and mitotic effects induced by MMS (Lee <br />et al. 1986b). <br />Although arsenic is not an essential plant nutrient, small yield <br />increases have sometimes been observed at low soil arsenic levels, especially <br />for tolerant crops such as potatoes, corn, rye, and wheat (Woolson 1975). <br />Arsenic phytotoxicity of soils is reduced with increasing lime, organic <br />matter, iron, zinc, and phosphates (NRCC 1978). In most soil systems, the <br />12