Methyl linoleate hydroperoxide toxicity

Pure fatty acid hydroperoxides are very toxic to experimental animals when administered intravenously (i.v.) but not oraUy (Horgan et al., 1957 Olcott and Dolev, 1963 Findlay et al., 1970). Cortesi and Privett (1972) have shown that the 24-h lethal i.v. dose of a high purity preparation of methyl linoleate hydroperoxides in adult male rats was approximately 0.07 mmol/100 g body weight, and that the major effect of injected linoleate hydroperoxides was on the lungs. Also, vitamin E deficiency symptoms such as encephalomalacia in chicks (Nishida et al., 1960), and creatinuria and erythrocyte hemolysis in rabbits (Kokatnur et al., 1966) have been observed in animals infused with methyl linoleate hydroperoxides. 

Many secondary oxidation products of fatty acids have been shown to be more toxic to experimental animals. This is partly due to the fact that the low molecular weight products have shorter carbon chain lengths, and are more easily absorbed into the intestinal wall than lipid hydroperoxides or their polymeric materials. Oarada et al. (1986), for example, have shown that over 73% of radioactivity was found in the urine and CO2 of rats 12 h after receiving " C-labeled low molecular compounds, compared to less than 25% for methyl linoleate hydroperoxides and the polymeric fraction. 

A comparison between the lung toxicity of methyl linoleate 9,10-ozonide and cumene hydroperoxide on rats showed that the former is 3 times more toxic than the latter <1994MI243>. It was also found that the ozonide did not enhance lipid peroxidation. Glutathione and vitamin E protected rats against the effect of the ozonide. 

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