Lipid peroxidation in neural tissues and fractions from vitamin E-deficient rats

A severe and chronic deficiency of vitamin E results in a characteristic neurological syndrome in both man and experimental animals. This is presumed to result from increased oxidative stress arising from a reduction in antioxidant capacity. In this study we have examined parameters of endogenous lipid peroxidation and susceptibility to in vitro oxidative stress of neural tissues and fractions, and some non-neural tissues from 1-year-old vitamin E-deficient and control rats. We have shown:(1) an increase in endogenous lipid peroxidation (thiobarbituric acid reactive substances and malondialdehyde) in neural tissues from vitamin E-deficient animals compared to controls. (2) The following order of susceptibility of neural tissues to in vitro oxidative stress in both vitamin E-deficient and control animals: brain> > muscle> cord> nerve. (3) The susceptibility of different brain regions to in vitro oxidative stress varied in a consistent manner with the cortex, striatum, and cerebellum showing the greatest and brainstem and hypothalamus the least susceptibility. (4) Fractions isolated from myelinated nerves of brainstem showed the following order of susceptibility to in vitro oxidative stress: axoplasmic membranes and organelles> axolemma enriched fraction> whole homogenate> = myelin. These results would fit with the characteristic neuropathology associated with severe and chronic vitamin E deficiency.