Abstract
Magnetometric Evaluation for Cytotoxicity of Potassium Octatitanate Whisker on Alveolar Macrophages of Fischer 344 Rats: Mitsuyasu Watanabe, et al. Department of Preventive Medicine and Public Health, Kitasato University School of Medicine—Alveolar macrophages are thought to play a major role in the pathophysiology of lung diseases caused by exposure to various kinds of pathogens and particles. In the present study, the cytotoxic effect of potassium octatitanate whisker (PT) on macrophages was evaluated by means of magnetometry, lactate dehydrogenase (LDH) release measurement, apoptosis measurement and morphological observations. Alveolar macrophages obtained from Fischer rats (F344/N Sic) by bronchoaiveolar lavage were incubated in vitro for 18 h with Fe3O4 as a magnetometric indicator, and PTs as test materials. In the control group and the group exposed to 10 μg/ml of PT, rapid attenuation of the remanent magnetic field (RMF), so called “relaxation,” was observed immediately after cessation of the external magnetic field. In comparison, a delay of relaxation was observed in alveolar macrophages exposed to 20 and 40 μg/ml of PT. The decay constants, which are calculated from decreasing RMF for the first 2 min, in the groups exposed to 20 and 40 μg/ml of PT had significantly lower values than the control. LDH release induced by exposure to 20 and 40 μg/ml of PT increased significantly in a concentration dependent manner in PT‐exposed macrophages, whereas only negligible LDH release was observed in control groups. The level of PT affecting alveolar macrophages was at the same concentration, and in a dose‐dependent manner among relaxation, decay constant and LDH measurement. A DNA ladder detection method and morphological observations detected no apoptosis in PT‐exposed macrophages. Electron microscopic examination revealed vacuolar changes and cell membrane damage in PT‐exposed macrophages, but no significant changes in control macrophages. The results of magnetometry, LDH release, apoptosis measurement and electron microscopic observations suggest concentration dependent cytotoxicity caused by exposure of alveolar macrophages to PT.
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