Consequences of vitamin-E deficiency on the phagocytic and oxidative functions of the rat polymorphonuclear leukocyte.

Vitamin E serves an important role in protecting the cellular membrane constituents from peroxidative damage. Biochemical and functional studies were performed on polymorphonuclear leukocytes (PMN) from vitamin-E deficient and control rats to investigate the consequences of uncontrolled peroxidation of the rat PMN membrane. Rats fed a vitamin-E-deficient diet for 2 mo had serum tocopherol levels of only 5.1 % of control and exhibited a twofold increase in membrane polyunsaturated fatty acid (PUFA) peroxidation as measured by malonaldehyde production. As a consequence of vitamin-E deficiency. chemotaxis in response to bacterial culture filtrate was deficient. Ingestion was also impaired when saturating concentrations of IgGand C3b-coated and unopsonized albumin-coated paraffin oil droplets were employed. and ingestion remained deficient when performed in an anaerobic environment. The altered chemotaxis and ingestion in the deficient PMN were restored to normal by 1 8 hr following the parenteral administration of vitamin E. The deficient PMN ingested and killed C3b-coated Staphylococcus aureus 502-A normally when the bacteria-to-cell ratio was no more than 10:1 . Oxygen consumption and hydrogen peroxide release were enhanced in the phagocytosing vitaminE-deficient PMN. Depletion of vitamin E did not lead to impairment of adherence, surface polarization of concanavalin A into caps. or lysosomal enzyme release. These latter functions are subserved by glutathione-responsive microtubules as well as by actomyosin-containing microfilaments. Thus, the consequences of vitamin-E deficiency in PMN were selective to those areas of the membrane involved in triggering chemotactic. ingestive. and oxidative responses.