The mechanisms involved in the anti‐carcinogenic activity of selenium remain to be elucidated. In the present study, we examined sodium selenite‐induced oxidative stress and apoptosis in a human hepatoma cell line (HepG2). Sodium selenite (10 μM) exerted clear cytotoxic effect, as shown by the significant increase of lactate dehydrogenase leakage. Selenite‐induced DNA alterations in apoptosis were studied by: 1. comet assay; 2. TdT‐mediated dUTP nick end‐labeling assay. In addition, characteristic apoptotic morphological alterations were also observed in selenite‐treated cells. Our results clearly show that Se‐induced cell death occurs predominantly in the form of apoptosis. Selenite‐induced oxidative stress was evaluated by the measurement of reactive oxygen species production using lucigenin‐dependent chemiluminescence. The involvement of glutathione in selenite‐induced oxidative stress was further demonstrated by the concurrent decline of intracellular reduced glutathione and increase of oxidized glutathione contents in Se‐treated cells. Moreover, the finding that selenite‐induced oxidative stress and apoptosis was significantly attenuated by superoxide dismutase, catalase and deferoxamine provides additional evidence to suggest that Se‐induced oxidative stress mediates the induction of apoptosis, a mechanism related to the anti‐carcinogenic and chemopreventive effect of Se. Int. J. Cancer 81:820–828, 1999. © 1999 Wiley‐Liss, Inc.

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This report demonstrates that the uniportal SVATS approach can be safely and effectively utilized to perform pulmonary segmentectomies. Our series demonstrates that it is possible to access and resect all segments by this novel approach to VATS.

Epidemiological evidence suggests that cadmium (Cd) exposure causes pulmonary damage such as emphysema and lung cancer. However, relatively little is known about the mechanisms involved in Cd pulmonary toxicity. In the present study, the effects of Cd exposure on human fetal lung fibroblasts (MRC-5 cells) were evaluated by determination of lipid peroxidation, intra-cellular production of reactive oxygen species (ROS), and changes of mitochondrial membrane potential. A time- and dose-dependent increase of both lactate dehydrogenase leakage and malondialdehyde formation was observed in Cd-treated cells. A close correlation between these two events suggests that lipid peroxidation may be one of the main pathways causing its cytotoxicity. It was also noted that Cd-induced cell injury and lipid peroxidation were inhibited by catalase and superoxide dismutase, two antioxidant enzymes. By using the fluorescent probe 2',7'-dichlorofluorescin diacetate, a significant increase of ROS production in Cd-treated MRC-5 cells was detected. The inhibition of dichlorofluorescein fluorescence by catalase, not superoxide dismutase, suggests that hydrogen peroxide is the main ROS involved. Moreover, the significant dose-dependent changes of mitochondrial membrane potential in Cd-treated MRC-5 cells, demonstrated by increased fluorescence of rhodamine 123 examined using a laser-scanning confocal microscope, also indicate the involvement of mitochondrial damage in Cd cytotoxicity. These findings provide in vitro evidence that Cd causes oxidative cellular damage in human fetal lung fibroblasts, which may be closely associated with the pulmonary toxicity of Cd.ImagesFigure 1. AFigure 1. BFigure 2. AFigure 2. BFigure 3. AFigure 3. BFigure 4. AFigure 4. BFigure 5.Figure 6.Figure 7. AFigure 7. B