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Long-term Behavioral and Reproductive Consequences of Embryonic Exposure to Low-dose Toxicants
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Genotoxicity of 1,1-dichloroethane

A Colacci, G Arfellini, M Mazzullo

    Research Communications in Chemical Pathology and Pharmacology
    |August 1, 1985
    PubMed

    Insights

    1,1-Dichloroethane covalently binds to macromolecules in rats and mice, indicating weak carcinogenicity. Liver enzymes mediate this binding, with glutathione playing a protective role in its metabolism.

    Area of Science:

    • Toxicology
    • Biochemistry
    • Carcinogenesis

    Background:

    • 1,1-Dichloroethane (1,1-DCE) is a chemical compound with potential toxicological implications.
    • Understanding its interaction with biological molecules is crucial for risk assessment.

    Purpose of the Study:

    • To investigate the in vivo and in vitro covalent binding of 1,1-dichloroethane to macromolecules.
    • To identify the metabolic pathways and enzymes involved in 1,1-DCE binding.
    • To assess the role of glutathione (GSH) in the detoxification of 1,1-DCE.

    Main Methods:

    • In vivo intraperitoneal injection of 1,1-DCE in rats and mice.
    • In vitro incubation of 1,1-DCE with organ microsomes and cytosolic fractions.
    • Analysis of covalent binding to nucleic acids and proteins.
    • Assessment of enzyme induction/inhibition effects.

    Main Results:

    • 1,1-DCE showed covalent binding to macromolecules in vivo, with a Covalent Binding Index typical of weak carcinogens.
    • Liver P-450-dependent microsomal mixed function oxidase system was the primary mediator of in vitro binding to nucleic acids and proteins.
    • Lung microsomes showed weak efficiency, while kidney and stomach microsomes were ineffective.
    • Phenobarbitone pretreatment enhanced binding, whereas 2-diethylaminoethyl-2,2-diphenyl valerate suppressed it.
    • Cytosolic enzymes did not catalyze binding.
    • Glutathione (GSH) addition decreased or suppressed binding, suggesting a detoxificant role.

    Conclusions:

    • 1,1-Dichloroethane exhibits weak carcinogenic potential due to its covalent binding to macromolecules.
    • Hepatic microsomal enzymes are key players in 1,1-DCE activation and binding.
    • Glutathione plays a significant role in detoxifying 1,1-dichloroethane, similar to other chlorinated compounds.

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