Protective effect of diosmetin on in vitro cell membrane damage and oxidative stress in cultured rat hepatocytes

This study aimed to evaluate the in vitro cytotoxicity and oxidative stress induced by the copper oxide nanoparticles (CuO NPs) in human embryonic kidney cell line (HEK-293) cells following exposure. CuO NPs size <50 nm were used in this study. HEK-293 cell cultures were exposed to different concentrations of CuO NPs between 3 µg/ml and 300 µg/ml and quartz (known as cytotoxic agent) and assessed for cell viability-mitochondrial function (MTT assay), cell membrane damage (lactate dehydrogenase (LDH) assay), reduced glutathione (GSH), interleukin-8 (IL-8), and lipid peroxidation levels. The IC50 value of NPs was found to be 65.5 µg/ml. Exposure of HEK cells to CuO NPs (10–300 µg/ml) resulted in concentration-dependent cell membrane damage, increased production of IL-8, increased thiobarbituric acid reactive substance (TBARS), and decreased intracellular GSH levels. The significant increases in IL-8, TBARS, and LDH levels along with decreased GSH levels indicated induction of oxidative stress in cells. Our preliminary data suggest that oxidative stress might contribute to CuO NPs-induced cytotoxicity in HEK-293 cells.

Download Full-text

Protective effect of (−)-epigallocatechin-3-gallate on capsaicin-induced DNA damage and oxidative stress in human erythrocyes and leucocytes in vitro

Cytotechnology ◽

10.1007/s10616-014-9695-2 ◽

2014 ◽

Vol 67 (2) ◽

pp. 367-377 ◽

Cited By ~ 11

Author(s):

Dilek Pandır

Keyword(s):

Oxidative Stress ◽

Dna Damage ◽

Protective Effect ◽

And Oxidative Stress

Download Full-text

Decreased life span and membrane damage of carbamylated erythrocytes in vitro

Blood ◽

10.1182/blood.v47.6.909.909 ◽

1976 ◽

Vol 47 (6) ◽

pp. 909-917 ◽

Cited By ~ 8

Author(s):

TA Lane ◽

ER Burka

Keyword(s):

Cell Membrane ◽

Life Span ◽

Membrane Damage ◽

Membrane Lipid ◽

Red Cell ◽

Significant Modification ◽

Red Cell Membrane ◽

Cell Membrane Damage ◽

Sickle Erythrocytes

Abstract Red blood cells exposed to cyanate (CNO) in vitro have a concentration- dependent decreased cell survival time associated with an inhibition of the ability of the cell membrane to synthesize lipids. The t1/2 of rabbit erythrocytes exposed to 30 mM or 50 mM cyanate for 1 hr at 37 degrees C is reduced from the normal 24 days to 15 and 9 days, respectively. The cyanate-induced defect in membrane lipid metabolism is irreversible. Carbamylation of membrane proteins and damage to metabolism are minimized by limiting exposure in vitro to 15 mM cyanate at 4 degrees C for 30 min. Cells carbamylated under these conditions do not have a shortened life span. Levels of globin carbamylation of 0.5 moles CNO/mole hemoglobin, shown to be clinically effective in prolonging the life span of sickle erythrocytes, are obtained under these conditions and reach maximal levels after only 30 min of incubation. Carbamylation of blood in CPD anticoagulant is inferior to either ACD or heparin. The findings indicate that adequate carbamylation of sickle erythrocytes with minimal red cell membrane damage can be achieved without significant modification of the standard plasmapheresis procedure utilized by the working blood bank.

Download Full-text

Decreased life span and membrane damage of carbamylated erythrocytes in vitro

Blood ◽

10.1182/blood.v47.6.909.bloodjournal476909 ◽

1976 ◽

Vol 47 (6) ◽

pp. 909-917

Author(s):

TA Lane ◽

ER Burka

Keyword(s):

Cell Membrane ◽

Life Span ◽

Membrane Damage ◽

Membrane Lipid ◽

Red Cell ◽

Significant Modification ◽

Red Cell Membrane ◽

Cell Membrane Damage ◽

Sickle Erythrocytes

Red blood cells exposed to cyanate (CNO) in vitro have a concentration- dependent decreased cell survival time associated with an inhibition of the ability of the cell membrane to synthesize lipids. The t1/2 of rabbit erythrocytes exposed to 30 mM or 50 mM cyanate for 1 hr at 37 degrees C is reduced from the normal 24 days to 15 and 9 days, respectively. The cyanate-induced defect in membrane lipid metabolism is irreversible. Carbamylation of membrane proteins and damage to metabolism are minimized by limiting exposure in vitro to 15 mM cyanate at 4 degrees C for 30 min. Cells carbamylated under these conditions do not have a shortened life span. Levels of globin carbamylation of 0.5 moles CNO/mole hemoglobin, shown to be clinically effective in prolonging the life span of sickle erythrocytes, are obtained under these conditions and reach maximal levels after only 30 min of incubation. Carbamylation of blood in CPD anticoagulant is inferior to either ACD or heparin. The findings indicate that adequate carbamylation of sickle erythrocytes with minimal red cell membrane damage can be achieved without significant modification of the standard plasmapheresis procedure utilized by the working blood bank.

Download Full-text

Carvacrol exhibits rapid bactericidal activity against Streptococcus pyogenes through cell membrane damage

Scientific Reports ◽

10.1038/s41598-020-79713-0 ◽

2021 ◽

Vol 11 (1) ◽

Author(s):

Niluni M. Wijesundara ◽

Song F. Lee ◽

Zhenyu Cheng ◽

Ross Davidson ◽

H. P. Vasantha Rupasinghe

Keyword(s):

Cell Membrane ◽

Streptococcus Pyogenes ◽

Bactericidal Activity ◽

Membrane Damage ◽

Membrane Integrity ◽

Streptococcal Pharyngitis ◽

Cell Membrane Integrity ◽

Cell Membrane Damage ◽

Antibiotic Development

AbstractStreptococcus pyogenes is an important human pathogen worldwide. The identification of natural antibacterial phytochemicals has renewed interest due to the current scarcity of antibiotic development. Carvacrol is a monoterpenoid found in herbs. We evaluated carvacrol alone and combined with selected antibiotics against four strains of S. pyogenes in vitro. The minimum inhibitory concentration (MIC) and minimum bactericidal concentration (MBC) of carvacrol against S. pyogenes were 125 µg/mL (0.53 mM) and 250 µg/mL (1.05 mM), respectively. Kill curve results showed that carvacrol exhibits instantaneous bactericidal activity against S. pyogenes. We also demonstrated the potential mechanism of action of carvacrol through compromising the cell membrane integrity. Carvacrol induced membrane integrity changes leading to leakage of cytoplasmic content such as lactate dehydrogenase enzymes and nucleic acids. We further confirmed dose-dependent rupturing of cells and cell deaths using transmission electron microscopy. The chequerboard assay results showed that carvacrol possesses an additive-synergistic effect with clindamycin or penicillin. Carvacrol alone, combined with clindamycin or penicillin, can be used as a safe and efficacious natural health product for managing streptococcal pharyngitis.

Download Full-text

Protective effect of metallothionein on cadmium toxicity in isolated rat hepatocytes

Biochemical Journal ◽

10.1042/bj2300395 ◽

1985 ◽

Vol 230 (2) ◽

pp. 395-402 ◽

Cited By ~ 57

Author(s):

W S Din ◽

J M Frazier

Keyword(s):

Protective Effect ◽

Cadmium Toxicity ◽

Membrane Damage ◽

Rat Hepatocytes ◽

Protective Effects ◽

Isolated Rat Hepatocytes ◽

Detoxification Mechanism ◽

Isolated Rat

An isolated rat hepatocyte preparation was used to study the cellular toxicity of cadmium and the protective effects of metallothionein on cadmium-induced toxicity. Exposure of primary suspension cultures of isolated rat hepatocytes to Cd2+ (0-35.7 microM) for 15 min resulted in a dose-dependent reduction in the synthesis of cellular proteins during a subsequent 6 h incubation. Such inhibition could not be correlated with cellular lethality or gross membrane damage. Pre-induction of metallothionein in hepatocytes by zinc treatment in vivo of donor rats protected hepatocytes in vitro from cadmium-induced inhibition of protein synthesis. The protective effects in zinc-pre-induced hepatocytes are not due to alterations in the level of total cellular cadmium, but could be accounted for by the redistribution of intracellular cadmium in the presence of high levels of zinc-metallothionein. The data suggest that metallothionein exerts its protective effect by a kinetic detoxification mechanism, i.e. a decrease in reactive intracellular cadmium.

Download Full-text

Role of Oxidative Metabolism in the Effect of Valproic Acid on Markers of Cell Viability, Necrosis, and Oxidative Stress in Sandwich-Cultured Rat Hepatocytes

Toxicological Sciences ◽

10.1093/toxsci/kfq294 ◽

2010 ◽

Vol 118 (2) ◽

pp. 501-509 ◽

Cited By ~ 35

Author(s):

Tony K. L. Kiang ◽

Xiao Wei Teng ◽

Stoyan Karagiozov ◽

Jayakumar Surendradoss ◽

Thomas K. H. Chang ◽

...

Keyword(s):

Oxidative Stress ◽

Valproic Acid ◽

Cell Viability ◽

Oxidative Metabolism ◽

Rat Hepatocytes ◽

Cultured Rat Hepatocytes ◽

And Oxidative Stress

Download Full-text

Oxidative stress on mitochondria and cell membrane of cultured rat hepatocytes and perfused liver exposed to ethanol

Gastroenterology ◽

10.1016/s0016-5085(97)70147-1 ◽

1997 ◽

Vol 112 (4) ◽

pp. 1331-1343 ◽

Cited By ~ 99

Author(s):

I Kurose ◽

H Higuchi ◽

S Kato ◽

S Miura ◽

N Watanabe ◽

...

Keyword(s):

Oxidative Stress ◽

Cell Membrane ◽

Rat Hepatocytes ◽

Perfused Liver ◽

Cultured Rat Hepatocytes

Download Full-text

L-Ascorbate protects rat hepatocytes against sodium arsenite—induced cytotoxicity and oxidative damage

Human & Experimental Toxicology ◽

10.1177/0960327109357215 ◽

2009 ◽

Vol 29 (2) ◽

pp. 103-111 ◽

Cited By ~ 23

Author(s):

Asit Kumar Bera ◽

Tanmoy Rana ◽

Subhashree Das ◽

Subhasish Bandyopadhyay ◽

Debasis Bhattacharya ◽

...

Keyword(s):

Oxidative Stress ◽

Cell Proliferation ◽

Sodium Arsenite ◽

In Vitro Study ◽

Rat Hepatocytes ◽

Proliferation Index ◽

No Production ◽

Cell Proliferation Index ◽

And Oxidative Stress

Sodium arsenite—exposed hepatocytes of rat showed higher production of nitric oxide (NO) and increased lipid peroxidation (LPO) level vis-a-vis activity of superoxide dismutase (SOD) and catalase (CAT) were significantly lowered. Subsequently, the cell proliferation index (CPI) and cell viability were also reduced. Treatment with L-ascorbate was found effective in normalizing the arsenic-induced alteration of SOD and CAT activity and LPO level in rat hepatocytes. These observations indicated that L-ascorbate also has potent cytoprotective role as it could reduce the NO production and normalize the cell proliferation and viability of hepatocytes. Therefore, the in vitro study suggested that ascorbic acid is helpful to ameliorate the arsenic-induced cytotoxicity and oxidative stress of rat hepatocytes.

Download Full-text