Effects of 2,3,7,8-tetrachlorodibenzo-p-dioxin upon hemostasis and hematologic function in the rat.
Author(s) -
Joseph B. Weissberg,
J. G. Zinkl
Publication year - 1973
Publication title -
environmental health perspectives
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.257
H-Index - 282
eISSN - 1552-9924
pISSN - 0091-6765
DOI - 10.1289/ehp.7305119
Subject(s) - aryl hydrocarbon receptor , medicine , hemostasis , receptor , chemistry , endocrinology , biochemistry , gene , transcription factor
2,3,7,8-Tetrachlorodibenzo-p-dioxin (TCDD) has been identified as a toxic contaminant of chlorophenols and related hydrocarbons that are widely used in agriculture and industry. It has been implicated in various diseases, including human cases of chloracne (1) and porphyria cutanea tarda (2) and in chick edema (3). Its teratogenicity has been documented in rats (4) and mice (5). Monkeys fed toxic fat, later found to contain TCDD and other chlorinated derivatives of dibenzo-p-dioxin, were observed to undergo a decrease in the cellular elements of the bone marrow and the peripheral blood (6). in contrast, increases in hematocrit and leukocyte count were observed in rats treated with TCDD (7). Depression of blood platelets in TCDD-treated rats and guinea pigs has been recently observed (8). The present studies were undertaken in order to characterize hematologic changes and in particular platelet function alterations in rats exposed to TCDD.
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