Premium
Effect of ascorbic acid supplementation during the inhalation exposure of guinea‐pigs to industrial dust on bronchoalveolar lavage and pulmonary enzymes
Author(s) -
Kováčiková Zuzana,
Ginter Emil
Publication year - 1995
Publication title -
journal of applied toxicology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.784
H-Index - 87
eISSN - 1099-1263
pISSN - 0260-437X
DOI - 10.1002/jat.2550150414
Subject(s) - bronchoalveolar lavage , ascorbic acid , inhalation , lactate dehydrogenase , chemistry , alkaline phosphatase , pulmonary toxicity , acid phosphatase , guinea pig , lung , medicine , endocrinology , biochemistry , enzyme , anesthesia , food science
The aim of this study was to investigate the interaction between ascorbic acid (AA) and inhaled particles separated from the dumped waste of a nickel smelter and refinery. Tricoloured male guinea pigs were exposed in an inhalation chamber to 50 mg kg −1 of <5 μm particles that mainly consisted of metal oxides. Exposure lasted for 4 weeks (5 days per week and 5 h per day). The drinking water of half of the exposed and half of the control groups was supplemented with 1 g l −1 AA. Each group received 0.4 mmol kg −1 AA in their food. Ascorbic acid supplementation increased the pulmonary AA concentration in both exposed and control groups to the same extent, but in bronchoalveolar lavage fluid the increase was higher in control than in exposed guniea pigs. The number of alveolar macrophages was increased by exposure and AA increased the number only in the exposed group; the acid phosphatase activity of the alveolar macrophages was increased only by AA, and more in the exposed than in the control group. Alkaline phosphatase activity in bronchoalveolar lavage fluid was the same in both supplemented groups, but it was enhanced in the exposed group with a low intake of AA. Effects on lactate dehydrogenase were not consistent. Neither exposure nor AA influenced significantly this enzyme in bronchoalveolar lavage fluid, but in the lung both AA and exposure caused an increase in the activity. The levels were similar in the AA‐treated control and exposed guinea pigs.