Letter to the editor

In vitro activation by tocopherol of the synthesis of ascorbic acid by liver extracts of tocopherol-deficient rats

The effects of feeding vitamin E-deficient diets to rats for one year were investigated to analyse the relationship of the vitamin with other antioxidants and some antioxidative enzymes. Long-term vitamin E deficiency lowered the levels of antioxidants like vitamin E, ascorbic acid and glutathione (GSH) in all tissues analysed and thus increasing the extent of tissue peroxidisability. Vitamin E deficiency had also influenced the activities of superoxide dismutase (SOD), catalase and glutathione peroxidase, the enzymes that are involved in detoxification mechanisms of products arising from free radical metabolism.

To the extent that phospholipid fatty acids occur in membranes, and to the extent that membranes act as barriers to the free movement of water-soluble materials, the inside of the membrane must represent a relatively isolated hydrophobic region vaguely similar to a beaker of fat, as noted in Fig. 10.

In those cases which have been adequately studied a relationship is apparent between antioxidant requirement and dietary PUFA. Confusion arises, however, from the variable nature of this relationship which depend son the deficiency sign and tissue studied.

Experiments designed to measure lipid peroxidation in vivo directly have been largely unsuccessful, except perhaps in adipose tissue where an actual bulk phase of lipid exist. Future success in this area is doubtful unless some method can be devised to qualitatively and quantitatively relate lipofuscin or ceroid pigment formation to lipid peroxidation. It is also apparent that the concept of “depletion” requires refinement, and additional work is needed on model systems to permit the formulation of a reasonable experimental hypothesis relating lipid peroxidation to antioxidant destruction.