Role of superoxide and hydrogen peroxide in cell lysis during irradiation in vitro of Ehrlich ascitic carcinoma cells in the presence of melanin

1985 ◽  
Vol 63 (4) ◽  
pp. 278-283 ◽  
Author(s):  
I. Aravindakshan Menon ◽  
Surujdeen Persad ◽  
Narendranath S. Ranadive ◽  
Herbert F. Haberman
Keyword(s):  
Hydrogen Peroxide ◽  
Cell Lysis ◽  
Carcinoma Cells ◽  
Dark Reaction ◽  
Oxidase System ◽  
Red Hair ◽  
Ehrlich Ascitic Carcinoma ◽  
Per Se

The reactive species involved in the cell lysis during ultraviolet irradiation of Ehrlich ascitic carcinoma cells in the presence of red hair melanin (RHM) were investigated by determining 51Cr release from labeled cells. Cysteine at 1 mM in the presence of RHM increased the cell lysis during the incubation in the dark as well as during irradiation; this lysis was enhanced by superoxide dismutase (SOD). Catalase abolished the dark reaction and inhibited the cysteine-induced increase of cell lysis during irradiation. The cell lysis by the superoxide-generating xanthine oxidase system was not significantly increased by SOD, but was significantly decreased by nitroblue tetrazolium and completely abolished by catalase. The cell lysis induced by the supernatants obtained from the suspensions of RHM either irradiated alone or with cysteine was abolished by catalase. Sediments of irradiated RHM when incubated in the dark with the cells did not release 51Cr. Irradiation of the cells in the presence of the same sediments produced lysis which was not inhibited by catalase. These studies suggest that superoxide per se is not toxic to the cells, but the H2O2 formed by dismutation of superoxide produces cell lysis either directly or by generating ∙OH through Fenton-type reactions. A large part of the cell lysis seen during irradiation of cells in the presence of RHM is not due to H2O2, but may possibly be due to the melanin free radicals formed during irradiation.

scholarly journals Role of hydrogen peroxide in the cytotoxicity of the xanthine/xanthine oxidase system

1988 ◽  
Vol 249 (2) ◽  
pp. 391-399 ◽  
Author(s):  
E M Link ◽  
P A Riley
Keyword(s):  
Hydrogen Peroxide ◽  
Xanthine Oxidase ◽  
Cytotoxic Effect ◽  
Oxidase System ◽  
H2o2 Decomposition ◽  
Enzymic Reaction ◽  
Single Oxygen ◽  
Phosphate Buffered Saline

1. The survival of mammalian epithelial cells exposed in vitro to the xanthine/xanthine oxidase system in phosphate-buffered saline (PBS) or serum-containing medium (SCMEM) was investigated. 2. The cytotoxic effect observed depended on the composition of the medium in which the enzymic reaction was carried out; a surviving fraction of 5 x 10(-5) was found for cells exposed in PBS and 5.2 x 10(-1) for those in SCMEM. 3. The cytotoxic product(s) formed by the xanthine/xanthine oxidase system was relatively stable in PBS; survival of cells incubated after completion of the enzymic reaction was always less than that found for cells exposed during the reaction in the same system. 4. Superoxide dismutase or mannitol present during the enzymic reaction did not inhibit the cytotoxic effect. 5. NaN3 (a single-oxygen quencher and a catalase inhibitor) added to the system in SCMEM caused a reduction in survival to the level observed for cells exposed to the enzymic reaction in PBS. 6. Catalase completely protected cells, but no protection was observed when both catalase and NaN3 were present in the reaction mixture. 7. A similar cytotoxic effect was produced when cells were treated with H2O2 alone. 8. The rate of H2O2 decomposition in medium was accelerated by the presence of serum, but this was completely inhibited by NaN3. 9. It is concluded that H2O2 is the major cytotoxic product formed by the xanthine/xanthine oxidase system.

The role of hydrogen peroxide in the in vitro cytotoxicity of 3-hydroxykynurenine

1990 ◽  
Vol 15 (11) ◽  
pp. 1101-1107 ◽  
Author(s):  
Clifford L. Eastman ◽  
Tomas R. Guilarte
Keyword(s):  
Hydrogen Peroxide ◽  
In Vitro Cytotoxicity

scholarly journals In vitro elucidation of the role of pericellular matrix in metastatic extravasation and invasion of breast carcinoma cells

2018 ◽  
Vol 10 (4) ◽  
pp. 242-252 ◽  
Author(s):  
Marie-Elena Brett ◽  
Heather E. Bomberger ◽  
Geneva R. Doak ◽  
Matthew A. Price ◽  
James B. McCarthy ◽  
...  
Keyword(s):  
Breast Carcinoma ◽  
Carcinoma Cells ◽  
Malignant Progression ◽  
Pericellular Matrix ◽  
Breast Carcinoma Cells

The hyaluronan-rich pericellular matrix is an important feature of malignant progression in breast carcinoma.

The formation of choleglobin and the role of catalase in the erythrocyte

1949 ◽  
Vol 136 (884) ◽  
pp. 435-448 ◽  
Keyword(s):  
Hydrogen Peroxide ◽  
Ascorbic Acid ◽  
Amino Acid ◽  
Catalase Activity ◽  
Acid Oxidase ◽  
Small Decrease ◽  
Amino Acid Oxidase ◽  
Oxidase System ◽  
Inverse Proportion

In haemolysates of non-nucleated erythrocytes there is an inverse proportion between catalase activity and rate of choleglobin formation on addition of ascorbic acid. In the intact erythrocytes catalase protects haemoglobin against oxidation and further destruction by the hydrogen peroxide generated by the D-amino-acid oxidase system or by physiological concentrations of ascorbic acid and glutathione. Acid destromatization of haemolyzed horse erythrocytes causes a small decrease in the catalase activity and an increased rate of inactivation of the remaining catalase by ascorbic acid. The liberation of copper from haemocuprein is quantitatively insufficient to explain the decreased stability of the catalase. Exposing duck oxyhaemoglobin, but not reduced haemoglobin, to a pH of 5⋅5 to 5⋅8, causes an alteration which is apparent from the increase of the rate of choleglobin formation. The mechanism of this alteration is discussed. It partly explains the 'stroma effect', at least in duck erythrocytes. In addition, in the latter, there is a true stroma effect. Choleglobin formation in the presence of ascorbic acid is accelerated by a variety of substances. Some of these perturb haemoglobin, while others increase the formation of hydrogen peroxide from ascorbic acid. The implications of our findings on the mechanism of choleglobin formation and on the role of catalase in the erythrocyte are discussed.

scholarly journals Metformin sensitizes the response of oral squamous cell carcinoma to cisplatin treatment through inhibition of NF-κB/HIF-1α signal axis

2016 ◽  
Vol 6 (1) ◽  
Author(s):  
Xiaofeng Qi ◽  
Wengguang Xu ◽  
Junqi Xie ◽  
Yufeng Wang ◽  
Shengwei Han ◽  
...  
Keyword(s):  
Squamous Cell Carcinoma ◽  
Oral Squamous Cell Carcinoma ◽  
Cell Carcinoma ◽  
Squamous Cell ◽  
Carcinoma Cells ◽  
Oral Cancers ◽  
Underlying Mechanisms

Abstract Resistance towards chemotherapy is a common complication in treatment of oral cancers, which leads to treatment failure and poor outcome. In recent years, a growing body of evidence has shown that tumour hypoxia significantly contributes to chemoresistance. Metformin, a widely used oral hypoglycaemic drug, can reportedly potentiate the efficacy of chemotherapeutic drugs in various cancers; however, the underlying mechanisms are intricate and have not been fully understood. In this study, we explored the role of metformin in chemosensitivity of oral squamous cell carcinoma cells (OSCC) to cisplatin both in vitro and in vivo, and attempted to elucidate its possible underlying mechanisms. Encouragingly, we found that metformin synergistically enhanced cisplatin cytotoxicity and reversed the chemoresistance to certain extent. This mechanism could likely be related with inhibition of the NF-κB/HIF-1α signal axis and lead to the downregulation of hypoxia-regulated genes products. Therefore, metformin could serve as a chemosensitiser for cisplatin-based regimens for OSCC, thereby providing a theoretical basis for future use in the treatment of oral cancers.

Inhibition of hypoxia-inducible factor-1α by PX-478 as a potential targeted therapy in ESCC.

2017 ◽  
Vol 35 (15_suppl) ◽  
pp. e14083-e14083
Author(s):  
Yingming Zhu ◽  
Yuanwei Zang ◽  
Minghuan Li ◽  
Jinming Yu
Keyword(s):  
Targeted Therapy ◽  
Hypoxia Inducible Factor ◽  
Radical Resection ◽  
Carcinoma Cells ◽  
Migration And Invasion ◽  
Hypoxia Inducible Factor 1Α ◽  
Polymerase Chain ◽  
Cox 2

e14083 Background: Hypoxia is a unique microenvironment in solid tumors, including ESCC. We aim to investigate the interaction between hypoxia-inducible factor-1α (HIF-1α), COX-2 and programmed cell death ligand-1 (PD-L1) and uncover the role of HIF-1α inhibitor PX-478 as a potential targeted therapy in ESCC. Methods: Immunohistochemical staining was performed to investigate the levels of HIF-1α, COX-2 and PD-L1 from 133 pT3N0M0 ESCC patients after radical resection. The prognostic value of the expression of HIF-1α, COX-2 and PD-L1 and the correlation with clinicopathologic features was evaluated. Knockdown assay, CCK-8 assay, Western blot, real-time polymerase chain reaction (RT-PCR), flow cytometry and Transwell migration assays were used in cells experiment. Results: HIF-1α and PD-L1 are independent prognostic factors in pT3N0M0 ESCC. Further data showed that HIF-1α plays an important role in regulation of COX-2 and PD-L1 expression. Our in vitro studies demonstrated that HIF-1α inhibitor, PX-478, induced G2 phase arrest, increased apoptosis, and inhibited migration and invasion of esophageal carcinoma cells, and thus significantly inhibit ESCC cells proliferation. Conclusions: Our results provide new insight into the potential role of HIF-1α inhibitors, PX-478 and open up the possibility of PX-478 for targeted therapy of ESCC.

Role of cementoenamel junction on the radicular penetration of 30% hydrogen peroxide during intracoronal bleaching in vitro

1996 ◽  
Vol 12 (3) ◽  
pp. 146-150 ◽  
Author(s):  
E. Koulaouzidou ◽  
T. Lambrianidis ◽  
P. Beltes ◽  
K. Lyroudia ◽  
C. Papadopoulos
Keyword(s):  
Hydrogen Peroxide

In vitro toxicity of hydrogen peroxide against normal vs. tumor rat hepatocytes: Role of catalase and of the glutathione redox cycle

Hepatology ◽  
1988 ◽  
Vol 8 (6) ◽  
pp. 1673-1678 ◽  
Author(s):  
Philippe Mavier ◽  
Bernard Guigui ◽  
Anne-Marie Preaux ◽  
Jean Rosenbaum ◽  
Marie-Claude Lescs ◽  
...  
Keyword(s):  
Hydrogen Peroxide ◽  
Rat Hepatocytes ◽  
In Vitro Toxicity ◽  
Redox Cycle ◽  
Glutathione Redox Cycle ◽  
Glutathione Redox
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