• YAKHAK HOEJI
• /
• v.52 no.5
• /
• pp.361-369
• /
• 2008

In order to evaluate the cytotoxicity of chromium trioxide, and the cell regenerative effect of phenolic acid against chromium trioxide-induced cytotoxicity, cell viability, cell adhesion activity, lactate dehydrogenase (LDH) activity, and morphological changes of cells were performed in these cultures. The toxicity of chromium trioxide (${IC}_{50}$, 44.0 ${\mu}M$) was high according to the toxic criteria. Cell regeneration of benzoic acid derivatives against ${IC}_{50}$ value of chromium trioxide in cell morphology was increased in concentration-dependent manner. These results suggest that benzoic acid derivatives may be used as a cell regenerative agent against chromium-mediated cytotoxicity.

• Toxicological Research
• /
• v.17 no.4
• /
• pp.255-265
• /
• 2001

Epidemiologic studies have demonstrated an association between short-term exposure to particulate air pollutants and increased mortality. However the biological mechanism underlying these associations have not been fully established and also the chemical and physical characteristics of the pollutant particles are not well understood. The metal constituents of air pollutant particles and their bioavailability are considered to Play an important role as possible mediators of Particle-induced airway injury and inflammation. Sprague-Dawley rat alveolar macrophage cells (NR8383) were exposed to airborne and acid-leached particulate matter (PM). Titanium oxide and nickel subsulfide were used as negative and positive controls. Particle-induced reactive oxygen species formation in cells was detected using the fluorescent probe 2',7'-dichlorofluorescin diacetate. Expression of TNF-$\alpha$ and IL-6 were measured by enzyme-linked immunosorbent assay, and PM-induced DNA double-strand breaks were determined with $\lambda$DNA/Hind III marker. Metals associated with air pollutant particles mediated intracellular oxidant production in alveolar macrophages, and the cytotoxicity and proinflammatory cytokine production induced by PM were associated with oxidative stress. The oxidants produced by air pollutant particles also are likely to induce DNA double-strand breaks. Our findings in alveolar macrophage cells exposed to PM and acid-leached PM support the hypothesis that metal components in urban air pollutants and their bioavailabilities might play an Important role in the induction of the adverse health effects.