Recovery from amiodarone-induced lipidosis in laboratory animals: a toxicological study.

Numerous amphiphilic cationic drugs cause lipid-lysosomal storage in animal tissues; one of these drugs is amiodarone, a major antiarrhythmic agent. The toxicological effects of amiodarone were studied in three animal species (rats, dogs, and monkeys). It was shown that sublethal dose levels of amiodarone induced lipid storage in a great variety of tissues in rats (Fischer and Sprague-Dawley strains) and dogs.

Oxetorone-induced hyperprogesteronemia and the development of uterine decidual lesions in rats.

Application of the deciduoma formation test showed that 3-benzofurol[3,2-c][1] benzoxepin-6(12H)-ylidene-N,N-dimethyl-l-propanamin-(E )-2-butenedioate (1:1) (oxetorone, L-6257, Nocertone) stimulated secretion of progesterone by the ovaries in rats and that this hyperprogesteronemia resulted from an increased secretion of prolactin. The studies carried out also showed that the apparition of uterine decidual lesions observed in certain animals undergoing chronic oxetorone treatment was linked to this hyperprogesteronemia. In view of the specific physiology of prolactin in rodents, such uterine lesions can only develop in these animals and cannot occur in man.

[Pseudotumoral uterine reaction in the rat treated with a benzofuro-benzoxepin].

When orally administered, 5-(3-diméthylamino propyliden)-benzofuro [2,3-c] benzoxepin-1, which antagonizes several biogenic amines, is slightly sedative and has also endocrinological properties in the Rat, induces the appearance of localized lesions of uterine stroma in 2 to 16% of the animals. The cytological picture could suggest a tumorogenesis. In fact, these lesions represent a non-tumoral reactional hyperplasia with nuclear abnormalities due to a hormonal stimulation.