ANTIOXIDANTS IN BRONCHOALVEOLAR LAVAGE FLUID CELLS ISOLATED FROM OZONE-EXPOSED NORMAL AND ASCORBATE-DEFICIENT GUINEA-PIGS

Citation
Up. Kodavanti et al., ANTIOXIDANTS IN BRONCHOALVEOLAR LAVAGE FLUID CELLS ISOLATED FROM OZONE-EXPOSED NORMAL AND ASCORBATE-DEFICIENT GUINEA-PIGS, Experimental lung research, 22(4), 1996, pp. 435-448
Citations number
29
Categorie Soggetti
Respiratory System
Journal title
ISSN journal
01902148
Volume
22
Issue
4
Year of publication
1996
Pages
435 - 448
Database
ISI
SICI code
0190-2148(1996)22:4<435:AIBLFC>2.0.ZU;2-B
Abstract
Preview studies have indicated that systemic deficiency in one of the critical antioxidants, ascorbate, does not significantly exacerbate oz one-induced lung injury and changes in lung antioxidants following lon ger-term exposure. Because alveolar cells encounter the highest ozone dose upon exposure and lack direct blood supply, systemic ascorbate de ficiency may exacerbate ozone response on antioxidants within these ce lls. Female Hartley guinea pigs (30 days old) were fed either a regula r guinea pig chow or chow that lacked ascorbate. The dietary regimen w as started 1 week prior to exposure, continued through ozone exposure (0, 0.2, 0.4, or 0.8 ppm, 23 h/day, 1 week), and during 1 week recover y in clean air following exposure. Immediately after I week of exposur e or recovery, lungs were lavaged and cells were counted in bronchoalv eolar lavage fluid (BALF). Protein, ascorbate, uric acid, total glutat hione (GSH), and cu-tocopherol were analyzed in these cells. Ozone cau sed an increase in total BALF cells and total cellular protein after 0 .4 and 0.8 ppm ozone. The increase was more pronounced in ascorbate-de ficient guinea pigs. Protein per million cells, however, was not chang ed by ozone or diet. In ascorbate-sufficient guinea pigs, ascorbate le vels were increased only after 0.2 ppm ozone. However, uric acid (at 0 .4 and 0.8 ppm ozone) and GSH (at all concentrations of ozone) levels were increased in both dietary groups. Ascorbate deficiency did not af fect basal uric acid or GSH levels in BALF cells. There was a small di et-related depletion in cellular alpha-tocopherol. Ozone exposure also decreased alpha-tocopherol regardless of diet. The above changes exce pt for alpha-tocopherol appeared to be reversed after 1 week of recove ry in both dietary groups. In summary, ozone is capable of inducing a mechanism that increases antioxidants such as ascorbate, GSH, and uric acid. GSH and uric acid are not affected by ascorbate deficiency, but alpha-tocopherol is depleted. GSH and uric acid may be critical in oz one-induced adaptation during ascorbate deficiency.