ABSTRACT
Soluble sulfide is well known for its toxicity and corrosion for hundreds of years. However, recent studies have demonstrated that hydrogen sulfide (H2S)-a novel gasotransmitter-supports a critical role during neuromodulation, cell proliferation, and cardioprotection for organisms. In particular, soluble sulfide plays multifaceted signaling functions in mammals during oxidative stress processes. However, the specific molecular regulation of soluble sulfide during oxidative stress remains unclear. In this study, Na2S was implemented as a soluble sulfide donor to expose LO2 cells. The 3-(4,5-dimethylthiazolyl-2),-2,5-diphenyltetrazolium bromide (MTT) assay, hydroxyl radical assay, superoxide dismutase (SOD) assay, and glutathione peroxidase (GSH-PX) assay were applied to analyze cytotoxicity, hydroxyl radical levels, SOD and GSH-Px activities, respectively. Soluble sulfide at a concentration 0.01-1.0 mM/L resulted in a marked and concentration-dependent reduction of LO2 cell viability. At low concentrations, sulfide solutions increased SOD activity and GSH-Px activity of LO2 after 24 h exposure, exhibiting a clear hormesis-effect and indicating the protective ability of soluble sulfide against oxidative stress. The decline in SOD and GSH-Px and the increase in hydroxyl radical (0.08-1.0 mM/L) suggested that oxidative damage could be a possible mechanism for sulfide-induced cytotoxicity.
Subject(s)
Hepatocytes/drug effects , Oxidative Stress/drug effects , Sulfides/pharmacology , Animals , Cell Line , Glutathione Peroxidase/metabolism , Hepatocytes/cytology , Hepatocytes/metabolism , Humans , Hydrogen Sulfide , Hydroxyl Radical/metabolism , Superoxide Dismutase/metabolismABSTRACT
The patented technology of a High Gradient Magnetic Separation (HGMS)-Ultraviolet (UV) composite process was used to treat ballast water. Staphylococcus aureus (S. aureus) was selected as the reference bacteria. After treatment by the HGMS-UV process, the concentration of S. aureus on the log 10 scale was lower than 2 at different flow rates, S. aureus suffered the most serious damage, and K(+) leakage of the bacteria was 1.73mg/L higher than separate 60min UV irradiation (1.17mg/L) and HGMS (0.12mg/L) processes. These results demonstrated that the HGMS-UV composite process was an effective approach to treat ballast water. Further, the HGMS process had synergistic action on the subsequent UV irradiation process and accelerated cell membrane damage. Meanwhile, the results of superoxide dismutase (SOD) activities of bacteria and DNA band analyses indicated that the inactivation mechanisms were different for HGMS and UV irradiation.
Subject(s)
Magnetics , Staphylococcus aureus , Ultraviolet Rays , Wastewater , Water Purification/methods , DNA, Bacterial/radiation effects , Free Radicals/metabolism , Oxidation-Reduction , Staphylococcus aureus/growth & development , Staphylococcus aureus/metabolism , Staphylococcus aureus/radiation effects , Wastewater/chemistry , Wastewater/microbiology , Water MicrobiologyABSTRACT
The aims of this study were to verify the hypoxia-reoxygenation injury of primary cultured Kupffer cells and the effect of propofol against the hypoxia-reoxygenation injury through quantitating lactate dehydrogenase (LDH) release and superoxide dismutase (SOD) activity.The sequential treatments with hypoxia and reoxygenation induced significant increasement of LDH release (P.0.01) and decresement of SOD activity(P.0.05) in primary cultured Kupffer cell. The level of LDH release and SOD activity after sequential treatments with hypoxia and reoxygenation were restored to the control level by the propofol treatment in the concentration of 0.5 and 5 microgram/mL. Propofol in concentration of 50 microgram/mL induced significant increasement of LDH release (P.0.01) on both normal culture and hypoxia-reoxygenation culture of the Kupffer cell. As hypoxia and reoxygenation procedures and propofol treatment were concurrently added to the cultured Kupffer cell, propofol treatment in the concentration of 50 microgram/mL decreased significantly the SOD activity (P.0.01). In conclusion, propofol in this hypoxia-reoxygenation model could provide a valuable clue for the study of liver transplantation and of propofol.