Abstract
In order to clarify the mechanism of acute toxicity of autoxidized oils, histopathological studies were carried out. 50% and 100% lethal dosages of methyl linoleate hydroperoxides (LMHPOs) and autoxidized methyl linoleate contained secondary oxidation products were administered orally to mouse. The mice were inspected continuously for 48 hours, the died and survived mice were anatomized. Specimens of small intestine, liver, lung, kidney and other tissues were separated immediately from body.
Gross symptoms were observed in small intestine, liver, lung and kidney by histopathological examination. Marked effect of these compounds was necrosis, fatty degeneration and congestion in tissues. The degree of impairments in each tissue was correlated to the toxicity of samples. From a consideration of histopathological observation, it was recognized that similar symptoms were induced by LMHPOs and secondary oxidation products. However, severe injury was observed on the tissues fed secondary oxidation products.
The toxic effect of secondary oxidation products appears to come from their smaller molecular weight than LMHPOs and the presence of their functional groups such as carbonyl compounds. From the results obtained, the authors conclude that one of the reasons for the toxic effect of secondary oxidation products than hydroperoxides is attributable to the facility of absorption of secondary oxidation products.
