Vitamin hydroperoxide toxicity

The health impairing and toxic elfects of oxidation of lipids are due to loss of vitamins, polyenoic fatty acids, and other nutritionally essential components formation of radicals, hydroperoxides, aldehydes, epoxides, dimers, and polymers and participation of the secondary products in initiation of oxidation of proteins and in the Maillard reaction. Dilferent oxysterols have been shown in vitro and in vivo to have atherogenic, mutagenic, carcinogenic, angiotoxic, and cytotoxic properties, as well as the ability to inhibit cholesterol synthesis (Tai et ah, 1999 Wpsowicz, 2002). 

Cells may show a low level of autofluorescence at 413 nm when irradiated at 324 nm. This fluorescence dramatically increases when d -parinaric acid (159) is incorporated into the cell membrane, either by intercalation or esteriflcation. Exposure to oxidation stress of cells enriched with the 159 fluorescent probe causes diminution of the fluorescence intensity and is directly correlated with formation of lipid hydroperoxides. Addition of antioxidants, such as Vitamin E (21), abates fluorescence diminution. A blanc run of cells enriched with 159 but not subjected to oxidation stress is necessary to follow the degradation of 159 when exposed to UV irradiation. This method was applied to track lipid oxidation during apoptosis and other phenomena, triggered by toxic compounds such as H2O2, f-BuOOH and cumyl hydroperoxide (27)"° 11,424... 

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. 

As might be expected, lipid hydroperoxides are more toxic in vitamin E-deficient animals (H). In the rabbit, the LD Q for... 

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. 

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