Evaluation of the developmental toxicity of 4-bromobenzene using frog embryo teratogenesis assay--Xenopus: possible mechanisms of action

Teratogenesis, Carcinogenesis, and Mutagenesis
D J FortE L Stover

Abstract

Potential mechanisms of 4-bromobenzene-induced developmental toxicity were evaluated using frog embryo teratogenesis assay-Xenopus (FETAX). Early X, laevis embryos were exposed to 4-bromobenzene in two separate definitive concentration-response tests with and without an exogenous metabolic activation system (MAS) or selectively inhibited MAS. The MAS was treated with carbon monoxide (CO) to modulate P-450 activity, cyclohexene oxide (CHO) to modulate epoxide hydrolase activity, and diethyl maleate (DM) to modulate glutathione conjugation. Addition of the intact MAS, and particularly the CHO- and DM-inhibited MASs, dramatically increased the embryo lethal potential of 4-bromobenzene. Addition of the CO-inhibited MAS decreased the developmental toxicity of activated 4-bromobenzene to levels approximating that of the parent compound. Results from these studies suggested that a highly toxic arene oxide intermediate of 4-bromobenzene formed as the result of mixed function oxidase (MFO)-mediated metabolism may play an important role in the development toxicity of 4-bromobenzene in vitro. Furthermore, both epoxide hydrolase and glutathione conjugation appeared to be responsible for activated 4-bromobenzene detoxification.

Citations

Mar 21, 2001·Experimental and Toxicologic Pathology : Official Journal of the Gesellschaft Für Toxikologische Pathologie·A LuppW Klinger
May 17, 2002·Journal of Applied Toxicology : JAT·Douglas J Fort, Robbin R Paul
Nov 20, 2004·Journal of Applied Toxicology : JAT·Douglas J FortClinton D Spaulding

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