An electrophoretic study of vitamin E status and expression of heat shock proteins in alveolar type II and liver cells

Vitamin E is the most important lipophilic antioxidant. Oxidative injuries are prevented or minimized by vitamin E supplementation. Various physiologi cal and pathological situations are accompanied by vitamin E deficiency. Ho wever, it is not clear whether alimentary vitamin E deficiency in itself co nstitutes oxidant stress that induces appropriate responses, which, in turn , can be avoided by adequate vitamin E supplies, or whether the remaining c ellular antioxidants compensate a temporary vitamin E deficiency. We studie d effects of the dietary vitamin E status on cellular vitamin E levels and on the expression of heat shock proteins (HSPs) in alveolar type II cells a nd liver. The expression of HSPs, representing an early and very sensitive marker of cellular stress, was compared with the activity of antioxidative enzymes. Vitamin E depletion caused a substantial increase in HSP32 in alve olar type II cells, whereas in liver there was a marked increase in HSP70. The activity of the antioxidant enzymes, however, did not change significan tly. A reversal of HSP expression to almost normal levels was seen after vi tamin E resupplementation. These results indicate that, under normal condit ions, a suboptimal supply of vitamin E to rats exposes the alveolar type II cells and the liver to reversible cellular stress.