Cadmium-induced oxidative cellular damage in human fetal lung fibroblasts (MRC-5 cells).

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

Extreme Type-II Superconductors in a Magnetic Field: A Theory of Critical Fluctuations

A theory of critical fluctuations in extreme type-II superconductors subjected to a finite but weak external magnetic field is presented. It is shown that the standard Ginzburg-Landau representation of this problem can be recast, with help of a novel mapping, as a theory of a new "superconductor", in an effective magnetic field whose overall value is zero, consisting of the original uniform field and a set of neutralizing unit fluxes attached to $N_{\Phi}$ fluctuating vortex lines. The long distance behavior is related to the anisotropic gauge theory in which the original magnetic field plays the role of "charge". The consequences of this "gauge theory" scenario for the critical behavior in high temperature superconductors are explored in detail, with particular emphasis on questions of 3D XY vs. Landau level scaling, physical nature of the vortex "line liquid" and the true normal state, and fluctuation thermodynamics and transport. A "minimal" set of requirements for the theory of vortex-lattice melting in the critical region is also proposed and discussed.Comment: 28 RevTeX pages, 4 .ps figures; appendix A added, additional references, streamlined Secs. IV and V in response to referees' comment