Chemically Induced Adrenocortical Lesions

Abstract

As a result of increasing toxicological testing, examples of chemically induced adrenocortical degeneration are becoming frequently documented in contrast to rarely reported spontaneous lesions of laboratory animals (Capen et al. 1975; Anderson and Capen 1978). Compounds such as glucocorticoids (Sasano et al. 1966; Purjesz et al. 1964), 7,12-dimethylbenzanthracene (Murad et al. 1973), aminoglutethimide (Camacho et al. 1967; Malendowicz 1972), spironolactone (Fisher and Horvat 1971), o,p′-DDD, the active isomer of technical grade DDD (Nelson and Woodard 1949; Hennigar et al. 1964), α-(1,4-dioxido-3-methyl-quinoxalin-2-yl-)-N-methylnitrone (DMNM) (Yarrington et al. 1981, to be published), amphenone (Hertz et al. 1955) and 1,1′ thiodiethylideneferrocene (Yarrington, 1981 unpublished observations) can inhibit steroidogenesis while causing morphologically degenerative changes of the adrenal cortex. Some of these so-called adrenocorticolytic compounds which cause widespread adrenal cortical degenerations have a species-specific toxicity such as o,p′-DDD in the dog and 7,12-dimethylbenzanthracene in the rat (Nelson and Woodard 1949; Murad et al. 1973). In contrast, chemicals like DMNM and 1,1′ thiodiethylidene-ferrocene cause adrenal cortical lesions in numerous species, including dogs, rats, and monkeys (Yarrington 1981, unpublished observations; Yarringtion et al. 1981).