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Epithelial binding of 1,2-dichloroethane in mice
E B Brittebo1, B Kowalski, H Ghantous
1Department of Pharmacology and Toxicology, Swedish University of Agricultural Sciences, Uppsala Biomedical Centre.
Toxicology
|May 31, 1989
Summary
1,2-dichloroethane (DCE) selectively binds to nasal olfactory mucosa in mice. This binding, potentially due to oxidative metabolism, suggests the nasal olfactory mucosa is a target for DCE toxicity.
Area of Science:
- Toxicology
- Metabolism
- Biochemistry
Background:
- 1,2-dichloroethane (DCE) is an industrial chemical with known toxicity.
- Understanding the metabolic fate and tissue distribution of DCE is crucial for assessing its health risks.
Purpose of the Study:
- To investigate the metabolism and tissue binding of 14C-labelled 1,2-dichloroethane (DCE) in female C57BL-mice.
- To identify potential target organs for DCE toxicity based on metabolite localization and binding.
Main Methods:
- Whole-body autoradiography of tissue sections from mice injected with 14C-DCE.
- In vivo and in vitro experiments assessing DCE metabolite binding.
- Pretreatment with metyrapone to investigate the role of oxidative metabolism.
Main Results:
- Selective localization of non-volatile DCE metabolites in the nasal olfactory mucosa and tracheo-bronchial epithelium.
- Lower metabolite levels detected in the upper alimentary tract, vagina, eyelid, liver, and kidney.
- Nasal mucosa demonstrated a significant in vitro capacity to activate DCE into bound products.
- Metyrapone pretreatment decreased mucosal and epithelial binding, suggesting oxidative metabolism.
Conclusions:
- The nasal olfactory mucosa is a primary target tissue for 1,2-dichloroethane toxicity.
- Oxidative metabolism likely mediates the binding of DCE metabolites to tissues.
- DCE exhibits selective tissue distribution, with a notable accumulation in the respiratory tract epithelium.