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RECORD NUMBER: 173 OF 243

Main Title Oral Toxicity of 1,2-Dichloropropane: Acute, Short-Term, and Long-Term Studies in Rats.
Author Bruckner, J. V. ; MacKenzie, W. F. ; Ramanathan, R. ; Muralidhara, S. ; Kim., H. J. ;
CORP Author Georgia Univ., Athens. Dept. of Pharmacology and Toxicology. ;Experimental Pathology Labs., Inc., Research Triangle Park, NC.;Health Effects Research Lab., Research Triangle Park, NC.
Publisher c1989
Year Published 1989
Report Number EPA/600/J-89/194;
Stock Number PB90-140831
Additional Subjects Toxicity ; Spleen ; Rats ; Pathology ; Tables(Data) ; Photographs ; Anemias ; Blood serums ; Liver ; Survival ; Reproductive system ; Blood chemical analysis ; Enzymes ; Kidney ; Reprints ; Dichloropropane ; Oral administration ; Dose-response relationships ; Liver microsomes ; Organ weight
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NTIS  PB90-140831 Some EPA libraries have a fiche copy filed under the call number shown. 07/26/2022
Collation 20p
Abstract
The investigation characterized the acute and short- and long-term toxic potency of orally administered 1,2-dichloropropane (DCP). In the acute and short-term studies, male rats of 250-300 g were gavaged with 0, 100, 250, 500, or 1000 mg DCP/kg in corn oil once daily for up to 10 consecutive days. Although ingestion of DCP caused body weight loss and CNS depression, few other toxic effects were manifest 24 hr after a single dose of the chemical. Morphological changes were limited to liver centrilobular cells in 500 and 1000 mg/kg rats. Similarly, elevated activity of some serum enzymes occurred only at these two highest dose levels. Hepatic nonprotein sulfhydryl (NPS) levels were decreased and renal NPS levels increased at 24 hr. In the short-term study resistance developed to DCP hepatotoxicity over the 10 consecutive days of exposure, as reflected by progressively lower serum enzyme levels and by decreases in the severity and incidence of toxic hepatitis and periportal vacuolization. Nucleolar enlargement in hepatocytes, however, was observed at all dosage levels at 5 and 10 days. There were a number of manifestations of hemolytic anemia, including erythrophagocytosis in the liver, splenic hemosiderosis and hyperplasia of erythropoietic elements of the red pulp, renal tubular cell hemosiderosis, and hyperbilirubinemia.