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Toxicological profiles - Toxaphen

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1986; Lackey 1949), rats (Chu et al. 1988; Kennedy et al. 1973; Koller et al. 1983; Ortega et al. 1957), and mice (Allen et al. 1983) following intermediate-duration exposure to 4, 5–45, and 13 mg/kg toxaphene, respectively. These changes included generalized hydropic degenerative changes, cytoplasmic vacuolization, centrilobular cell hypertrophy, peripheral migration of basophilic cytoplasmic granules, and the presence of lipospheres. 5 mg/kg/day (Garcia and Mourelle 1984) toxaphene. Toxaphene may also induce hypoxia and alter hepatic energy metabolism because it has been shown to decrease lactate dehydrogenase activity (Gertig and Nowacyzk 1975; Kuz'minskaya and Alekhina 1976).

At 24 hours after administration, most radioactivity was found in the white fat. Lesser amounts of the radiolabel were detected in liver and kidney. Mice that received an oral dose of 25 mg/kg 36Cl-toxaphene in corn oil were observed to retain 36Cl activity in fat, brain, kidney, liver, muscle, and testes. 6 ppm) when tissues were analyzed 8 days after administration (Crowder and Whitson 1980). 5 and 19 mg/kg 14C-toxaphene (Ohsawa et al. 1975). After the oral administration of a single dose of 20 mg/kg 36Cl-toxaphene to rats, the greatest levels of radioactivity were seen at 12 hours in almost all tissues.

Results of tissue sample analysis following the oral administration of radiolabeled toxaphene to rats showed that fat is the principal storage tissue (Ohsawa et al. 1975; Pollock and Kilgore 1980b). Other evidence in animals indicates that muscle may also be a storage site for toxaphene as suggested by the observation of a high distribution of toxaphene in muscle following an oral dose in rats, and by evidence that toxaphene residues persist in muscle for up to 20 days post-administration (Crowder and Dindal 1974).

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