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

Abstract

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-doficient 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 IgG- and 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 18 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 vitamin-E-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.