Pathology of "toxic oils" and selected metals in the MRL/lpr mouse. Toxicol

The Toxic Oil Syndrome epidemic that occurred in Spain in 1981 and affected nearly 20,000 people was caused by ingestion of oil mixtures that contained analine-denatured rapeseed oil. To date, an animal model in which to identify the actual etiologic agents(s) and to investigate the pathogenesis of the disease has not been discovered. In this study, the MRL/lpr was used to assess the histopathologica l response of 3 “toxic oils ” and 3 metals. The oils tested were a denatured rapeseed oil collected from a family who were affected by the Toxic Oil Syndrome epidemic in Spain (CO756) plus two synthesized oils (RSD and RSA). Female mice, 7 weeks of age, received an undiluted (neat) or a 1:10 diluted dose of each oil; mercury (50 ppm), cadmium (100 ppm), or lead (50 ppm). Half of each group was killed after 5 weeks of exposure and the remaining mice after 10 weeks of exposure. Body and organ weights (liver, kidney, thymus, and spleen) were recorded and selected organs were collected for histopathology. Ten weeks after treatment, body weights (BW) of the cadmium and lead groups were signi cantly suppressed, and the body weight of the CO756-neat group was signi cantly increased compared to their respective controls. Kidney/BW were decreased in the RSA-neat and RSA 1:10 groups after 10 weeks of exposure, and the kidney/BW in the mercury and cadmium groups were increased. Spontaneous developmen t (12 weeks of age) and progression (17 weeks of age) of histopathologica l lesions are described for selected organs examined in the naõ ̈ ve mice as are changes that resulted from exposure to the “toxic oils ” and metals. CO756-neat, mercury, and lead suppressed progression of the glomerulonephriti s that normally occurs in the MRL/lpr mouse. Also of interest were lesions that included mononuclea r cuf ng of hepatic bile ducts, progression of the granulomas that forme