VITAMIN-A-DEFICIENCY ENHANCES OZONE-INDUCED LUNG INJURY

The present study determined the effects of vitamin A (vA) deficiency on the responses to ozone (O-3) challenges in two inbred strains of mi ce that are differentially susceptible to O-3-induced lung inflammatio n. Susceptible C57BL/6J (B6) and resistant C3H/HeJ (C3) dams at 2 wk g estation were fed test diets containing either 0 or 10 mu g retinol/g diet. In mice that were maintained on vA-sufficient (vA+) diet, lung a nd liver tissue concentrations of vA and retinyl palmitate (RP) were s ignificantly (P < 0.05) lower in the B6 strain compared with C3, as me asured by high-performance Liquid chromatography techniques. vA and RP levels were significantly (P < 0.05) reduced in lung and Liver tissue s of 8-wk-old B6 and C3 mice that were maintained on a vA deficient (v A-) diet. vA+ and vA- mice of both strains were exposed to air or 0.3 ppm O-3/72 h, and lung injury was assessed by differential cell count and total protein concentration in bronchoalveolar lavage (BAL) return s. O-3 exposure caused significantly (P < 0.05) greater increases in i nflammatory cells and total protein in BAL returns of vA+ B6 mice than vA+ C3 mice. vA deficiency significantly (P < 0.05) enhanced O-3-indu ced increases in polymorphonuclear leukocytes in C3 mice and epithelia l cell loss in both strains. Compared with vA+ mice, lung permeability was also significantly (P < 0.05) enhanced in vA- mice of both strain s exposed to O-3. vA replacement partially reversed the O-3-induced lu ng injury that was enhanced by vA- diet. Results indicate that vA may have an important role in the pathogenesis of O-3-induced lung injury in differentially susceptible inbred strains of mice.