This article reviews the recent studies on H2O2 adaptation of Saccharomyces cerevisiae. When the cell exposed in the H2O2 sub-lethal doses, the plasma membrane permeability decreased, meanwhile the plasma membrane fluidity is minished. These changes resulted in a gradient across the plasma membrane, which conferring a higher resistance to oxidative stress. Recent work has also shown that the yeast cells adapted to H2O2 would lead to several changes in the expression of genes coding the key enzymes involved in the biosynthesis of lipid profile and in the organization of lipid microdomains of the plasma membrane, which finally decreased its' permeability and fluidity. The reorganization of the plasma membrane might be the major mechanism of the H2O2 adaptation. Once the yeast cells adapted to the external H2O2, changes in plasma occurred. The H2O2 dependent signaling pathways in the plasma membrane might be activated by high levels of H2O2. But the details of the signaling events should still be further studies.
Cell Membrane ; drug effects ; metabolism ; Cell Membrane Permeability ; drug effects ; Hydrogen Peroxide ; pharmacology ; Membrane Fluidity ; drug effects ; Saccharomyces cerevisiae ; cytology ; drug effects ; Signal Transduction ; drug effects

OBJECTIVETo study the effects of domoic acid (DA) on membrane function of primary cultured rat glial cell.

METHODSAfter the glial cells were treated with 6.4 x 10(-2), 6.4 x 10(-3) and 6.4 x 10(-4) micromol/L DA for 24 h, the activities of Na(+)-K(+)-ATPase and Ca(2+)-Mg(2+)-ATPase, the membrane fluidity and the permeability were measured to reflect the membrane function.

RESULTSAfter treatment of DA for 24 h, the activities of Na(+)-K(+)-ATPase and Ca(2+)-Mg(2+)-ATPase were inhibited significantly, the membrane fluidity decreased and the membrane permeability increased. The fluorescence polarization and microviscosity in the low, middle and high dosage treatment groups were 0.0626 +/- 0.0051, 0.0685 +/- 0.0097, 0.0648 +/- 0.0086 and 0.3154 +/- 0.0298, 0.3510 +/- 0.0571, 0.3286 +/- 0.0504 respectively, compared with the control group (0.0481 +/- 0.0069 and 0.2338 +/- 0.0372) (P < 0.01).

CONCLUSIONDA has obvious effects on membrane function of rat glial cells and may cause further injury on the cells.

Animals ; Cell Membrane ; drug effects ; Cell Membrane Permeability ; drug effects ; Cells, Cultured ; Kainic Acid ; analogs & derivatives ; pharmacology ; Membrane Fluidity ; drug effects ; Neuroglia ; drug effects ; Rats ; Rats, Sprague-Dawley

Anti-Arrhythmia Agents ; blood ; pharmacology ; Blood Pressure ; drug effects ; Cell Membrane ; drug effects ; Disopyramide ; blood ; Humans ; Membrane Potentials ; drug effects

The microstructure of cationic cyclopeptide (TD-34) treated Caco-2 cell membrane was observed, and we discussed the relationship between membrane structure and insulin transmembrane permeability. Atomic force microscope (AFM) was used to observe living cell membrane in air condition and tapping mode. Results showed that the surface of Caco-2 cell membrane treated with TD-34 lost its smoothness and nearly doubled its roughness. Apparent permeability coefficients (P(app)) of insulin in Caco-2 cell monolayers increased 2.5 times. In conclusion, AFM can be used to observe microstructure of cationic cyclopeptide treated cell membrane and cationic cyclopeptide enhanced insulin delivery across Caco-2 cell membrane by increasing membrane fluidity.
Caco-2 Cells ; Cations ; Cell Membrane ; drug effects ; Cell Membrane Permeability ; drug effects ; Humans ; Insulin ; metabolism ; Membrane Fluidity ; drug effects ; Microscopy, Atomic Force ; Peptides, Cyclic ; pharmacology

Ca2+ at 1.64 mmol/L markedly increased ethanol tolerance of a self-flocculating fusant of Schizosaccharomyces pombe and Saccharomyces cerevisiae. After 9 h of exposure to 20% (V/V) ethanol at 30 degrees C , no viability remained for the control whereas 50.0% remained for the cells both grown and incubated with ethanol in Ca2+ -added medium. Furthermore, when subjected to 15% (V/V) ethanol at 30 degrees C, the equilibrium nucleotide concentration and plasma membrane permeability coefficient (P' ) of the cells both grown and incubated with ethanol in Ca2+ -added medium accounted for only 50.0% and 29.3% those of the control respectively, indicating that adding Ca2+ can markedly reduce plasma membrane permeability of yeast cells under ethanol stress as compared with the control. Meanwhile, high viability levels acquired by the addition of Ca2+ exactly corresponded to the striking decreases in extracellular nucleotide concentration and P' achieved with identical approach. Therefore, the enhancing effect of Ca2+ on ethanol tolerance of this strain is closely related to its ability to decrease plasma membrane permeability of yeast cells subjected to ethanol stress.
Calcium ; pharmacology ; Cell Membrane ; drug effects ; metabolism ; Cell Membrane Permeability ; drug effects ; Ethanol ; pharmacology ; Saccharomyces cerevisiae ; drug effects ; growth & development ; metabolism ; Schizosaccharomyces ; drug effects ; growth & development ; metabolism ; Temperature

OBJECTIVETo study the mechanism of myricetin inducing the HepG-2 cell line apoptosis.

METHODThe MTT method was employed to study myricetin pharmacodynamics in HepG-2. The light microscope and transmission was used to identify the tumor cell apoptosis in the morphology. The FCM method and the kit of caspase 3, caspase 9 were hired to detect the apoptosis rates, the content of mitochondrial membrane electric potential and the activity of caspase in cancer cells.

RESULTMyricetin significantly inhibits the proliferation and induces the apoptosis of HepG-2 in a dose-dependent manner, which is accompanied with G2/M and S phase arrest. In addition, myricetin also increases the activation of caspase 3,9 and results in a depolarization and delta psi m collapse in a dose-dependent manner.

CONCLUSIONThe molecular pathway of apoptosis of human hepatocellular carcinoma cell lines induced by myricetin might deal with the mitochondria-mediated pathway.

Apoptosis ; drug effects ; Carcinoma, Hepatocellular ; pathology ; Cell Cycle ; drug effects ; Cell Proliferation ; drug effects ; Flavonoids ; pharmacology ; Flow Cytometry ; Hep G2 Cells ; Humans ; Membrane Potentials ; drug effects

In order to study the anti-viral mechanism of extracted ZG from Gardenia, the effect of extracted ZG on Hep-2 cell membrane potential, Na -K+-ATPase activity and membrane fluidity post infected with parainfluenza virus type 1 (PIV-1) was observed. Acetylcholine which was fluorescent labeled with DiBAC4 (3) was taken as positive control to observe the changes of membrane potential and was measured by flow cytometer. The phosphorus determination method and spectrophotometer were used to measure the Na+-K+-ATPase activity of Hep-2 cell membrane post PIV-1 infection. Hep-2 cell membrane phospholipids was labeled with fluorescent NBD-C6-HPC and membrane fluidity was measured by confocal laser scanning microscope. The results demonstated that after PIV-1 infection the Hep-2 cell membrane potential decreased significantly and the membrane was in the state of hyperpolarization, Na+-K+-ATPase activity increased and membrane fluidity decreased significantly. There was no apparent interferring effect of extracted ZG on the changes of membrane potential and Na+-K+-ATPase activity post PIV-1 infection, while membrane fluidity was improved significantly. Acetylcholine improved the state of hyperpolarization. The changes of membrane potential, Na -K+-ATPase activity and membrane fluidity might be the biomechanism of PIV-1 infectoin. The extracted ZG improved membrane fluidity to prevent from PIV-1 infection by protecting the cell membrane, which was probably the mechanism of anti-PIV-1 activity of the extracted ZG, but ZG probably had nothing to do with membrane potential and Na+-K+-ATPase activity.
Acetylcholine ; pharmacology ; Antiviral Agents ; pharmacology ; Cell Line, Tumor ; Cell Membrane ; drug effects ; Gardenia ; chemistry ; Humans ; Membrane Fluidity ; drug effects ; Membrane Potentials ; drug effects ; Parainfluenza Virus 1, Human ; drug effects ; Plant Extracts ; pharmacology ; Sodium-Potassium-Exchanging ATPase ; metabolism

Anti-Arrhythmia Agents/blood ; Anti-Arrhythmia Agents/*pharmacology ; Blood Pressure/drug effects ; Cell Membrane/drug effects ; Disopyramide/blood ; Membrane Potentials/drug effects

OBJECTIVETo investigate the effect of c-Met inhibitor cabozantinib (XL-184) in inhibiting Listeria monocytogenes (LM) from invading Caco-2 cells to reduce the cell injury.

METHODSThe cell invasion capacity of LM was assayed in Caco-2 cells incubated with different doses of XL-184 for different durations. Caco-2 cells incubated with XL-184 were seeded on the upper room of the transwell chamber, and the cell monolayer was exposed to LM infection followed by addition of horseradish peroxidase (HRP). The trans-epithelial electric resistance (TEER), HRP concentration and LM colony-forming unit (CFU) were measured in the cell monolayer. Fluorescent staining was used to evaluate the cell viability, and LDH release from the cells was examined to assess the changes in cell membrane permeability.

RESULTSXL-184 significantly decreased LM invasion rate in Caco-2 cells in a dose- and time-dependent manner (P=0.000), and this effect was enhanced by co-incubation of the cells with ampicillin (P<0.05). In the cell membrane permeability assay in the monolayer cells, XL-184 markedly inhibited LM-induced reduction of TEER (P<0.05) and significantly suppressed LM-induced enhancement of cell membrane permeability shown by reduced HRP concentration and LM count in the lower chamber (P=0.000). The cells infected with LM showed significantly lowered cell viability, which was rescued by XL-184 (P<0.01); XL-184 also dose-dependently reduced LDH release from the cells (P<0.05).

CONCLUSIONSXL-184 can suppress LM invasion in Caco-2 cells to reduce the cell injury, suggesting its value as a promising candidate agent for prevention and treatment of LM infections.

Anilides ; pharmacology ; Caco-2 Cells ; Cell Membrane Permeability ; drug effects ; Cell Survival ; Humans ; Listeria monocytogenes ; drug effects ; Pyridines ; pharmacology

OBJECTIVETo compare the toxicity of Euphorbia pekinensis before and after being processed by vinegar on normal liver cells LO2, and discuss its possible mechanism.

METHODLO2 cells were cultured in vitro, and processed with different concentrations of crude and vinegar-processed E. pekinensis. MTT assay was used to measure the inhibitory effect of LO2 cell; Hoechst 33258 staining was used to observe the morphological changes in apoptosis cell; Annexin V-FITC flow cytometry was used to analyze the apoptotic rate of LO2 cell; PI staining flow cytometry was used to analyze its impact on cell cycle. The level or content of ALT, AST, LDH, SOD, MDA and GSH were observed as well.

RESULTCompared with the negative control group, crude E. pekinensis at all concentrations could obviously inhibit LO2 cell proliferation, induce LO2 cell apoptosis and cause cell arrest in S phase, with significant differences (P <0.05). E. pekinensis could significantly increase the levels of ALT, AST and LDH (P <0.05) in the supernatant of cell culture fluid, significantly decrease the level of SOD and the content of GSH (P <0.05) , and significantly increase the content of MDA (P <0.05). Compared with the crude E. pekinensis group, E. pekinensis after being vinegar-processed can significantly reduce cell apoptotic rate, cell cycle arrest, activities of ALT, AST, LDH in the supernatant of cell culture fluid (P <0.05) , and remarkably increase the level of SOD and the content of GSH, but reduce the content of MDA in the supernatant of cell culture fluid.

CONCLUSIONVinegar-processed E. pekinensis can release the cytotoxicity of LO2 cell. Its mechanism may be related to the decrease in the oxidative damage of LO2 cells, thereby reducing the cell cycle arrest and apoptosis.

Acetic Acid ; chemistry ; Apoptosis ; drug effects ; Cell Cycle Checkpoints ; drug effects ; Cell Line ; Cell Membrane ; drug effects ; metabolism ; Cell Proliferation ; drug effects ; Chemistry, Pharmaceutical ; Drugs, Chinese Herbal ; chemistry ; toxicity ; Euphorbia ; chemistry ; Humans ; Liver ; cytology ; Oxidative Stress ; drug effects