scholarly journals THE VALUE OF BASAL EXPRESSION LEVEL OF HEMOXYGENASE-1 FOR SENSITIVITY OF HUMAN MELANOMA CELLS TO OXIDATIVE STRESS IN VITRO

2020 ◽  
Vol 19 (3) ◽  
pp. 38-45
Author(s):  
T. A. Sidorova ◽  
E. Sh. Solomko ◽  
Yu. A. Khochenkova ◽  
A. A. Prokofieva ◽  
D. A. Khochenkov
Keyword(s):  
Oxidative Stress ◽  
Reactive Oxygen Species ◽  
Tumor Cells ◽  
Reactive Oxygen ◽  
Melanoma Cells ◽  
Human Melanoma ◽  
Oxygen Species ◽  
Basal Expression ◽  
Reactive Oxygen Species Content ◽  
In Cells

Introduction. The molecular basis of radio- and photodynamic therapy (PDT), the mechanism of action of a number of antitumor chemotherapy drugs is oxidative stress (OS). The enzyme hemoxygenase-I (НO-1), a molecular marker of OS, is a key participant in the system of protection and adaptation of tumor cells under stress.Objective. To find out whether the sensitivity of human melanoma tumor cells to OS depends on the basal and modulator-induced levels of НO-1 expressionMaterial and methods. Human melanoma cell lines were used in the study. The expression of mRNA НO-1 in cells was studied by real-time RT-PCR, the reactive oxygen species content in cells – by flow cytometry and the cytotoxicity of drugs – by MTT assay.Results. According to our data, human melanoma cells have different basal levels of HO-1 transcription: high (3.0–3.5 o. u.) in lines MelIL, MelP, medium (1.5 o. u.) in lines MeWo, MelZ, MelIbr and low (0.5 o. e.) – MelMe, A375).There is no direct correlation between the level of basal cell expression of HO-1 and their sensitivity to the OS inducer – Н2О2. The hemin-induced increase in HO-1 expression in cells is accompanied by doubled resistance to Н2О2. It was found that HO-1 repression in the presence of apigenin was registered in melanoma cells with different basal levels, but sensitization to Н2О2 (2–4 times) was observed only for cells with medium (MeWo) and low (A375) levels of basal HO-1 expression. It was found that the decrease in basal expression of HO-1 induced by apigenin is accompanied by an increase in the reactive oxygen species content in cells.Conclusions. The results of our research allow us to recommend natural flavon apigenin, a modulator of HO-1 expression, for inclusion in the chemotherapy and PDT regimens to increase the effectiveness of human melanoma treatment.

scholarly journals Melatonin Induces Melanogenesis in Human SK-MEL-1 Melanoma Cells Involving Glycogen Synthase Kinase-3 and Reactive Oxygen Species

2020 ◽  
Vol 21 (14) ◽  
pp. 4970
Author(s):  
Juan Perdomo ◽  
Carlos Quintana ◽  
Ignacio González ◽  
Inmaculada Hernández ◽  
Sara Rubio ◽  
...  
Keyword(s):  
Reactive Oxygen Species ◽  
Glycogen Synthase ◽  
Reactive Oxygen Species Generation ◽  
Reactive Oxygen ◽  
Melanoma Cells ◽  
Human Melanoma ◽  
Glycogen Synthase Kinase ◽  
Oxygen Species ◽  
Glycogen Synthase Kinase 3Β ◽  
Human Melanoma Cells

Melatonin is present in all living organisms where it displays a diversity of physiological functions. Attenuation of melanogenesis by melatonin has been reported in some mammals and also in rodent melanoma cells. However, melatonin may also stimulate melanogenesis in human melanoma cells through mechanisms that have not yet been revealed. Using the human melanoma cells SK-MEL-1 as a model, an increase in both tyrosinase activity and melanin was already observed at 24 h after melatonin treatment with maximal levels of both being detected at 72 h. This effect was associated with the induction in the expression of the enzymes involved in the synthesis of melanin. In this scenario, glycogen synthase kinase-3β seems to play a significant function since melatonin decreased its phosphorylation and preincubation with specific inhibitors of this protein kinase (lithium or BIO) reduced the expression and activity of tyrosinase. Blocking of PI3K/AKT pathway stimulated melanogenesis and the effect was suppressed by the inhibitors of glycogen synthase kinase-3β. Although melatonin is a recognized antioxidant, we found that it stimulates reactive oxygen species generation in SK-MEL-1 cells. These chemical species seem to be an important signal in activating the melanogenic process since the antioxidants N-acetyl-l-cysteine and glutathione decreased both the level and activity of tyrosinase stimulated by melatonin. Our results support the view that regulation of melanogenesis involves a cross-talk between several signaling pathways.

scholarly journals Caffeic Acid - Potential Antioxidant in Cultured Human Retinal Pigment Epithelial Cells

1970 ◽  
Vol 66 (2) ◽  
Author(s):  
Dumitriţa RUGINǍ ◽  
Adela PINTEA ◽  
Raluca PÂRLOG ◽  
Andreea VARGA
Keyword(s):  
Oxidative Stress ◽  
Reactive Oxygen Species ◽  
Hydrogen Peroxide ◽  
Protective Effect ◽  
Caffeic Acid ◽  
Reactive Oxygen ◽  
Oxygen Species ◽  
Antioxidant Defence ◽  
Rpe Cells ◽  
In Cells

Oxidative stress causes biological changes responsible for carcinogenesis and aging in human cells. The retinal pigmented epithelium is continuously exposed to oxidative stress. Therefore reactive oxygen species (ROS) and products of lipid peroxidation accumulate in RPE. Neutralization of ROS occurs in retina by the action of antioxidant defence systems. In the present study, the protective effect of caffeic acid (3,4-dihydroxy cinnamic acid), a dietary phenolic compound, has been examined in normal and in oxidative stress conditions (500 µM peroxide oxygen) in cultures human epithelial pigment retinal cells (Nowak, M. et al.). The cell viability, the antioxidant enzymes activity (CAT, GPx, SOD) and the level of intracellular reactive oxygen species (ROS) were determined. Exposure to l00 µM caffeic acid for 24 h induced cellular changes indicating the protective effect of caffeic acid in RPE cells. Caffeic acid did not show any cytotoxic effect at concentrations lower than 200 μM in culture medium. Treatment of RPE cells with caffeic acid causes an increase of catalase, glutathione peroxidase and superoxide dismutase activity, especially in cells treated with hydrogen peroxide. Caffeic acid causes a decrease of ROS level in cells treated with hydrogen peroxide. This study proved that caffeic acid or food that contain high levels of this phenolic acid may have beneficial effects in prevention of retinal diseases associated with oxidative stress by improving antioxidant defence systems.

Simvastatin rises reactive oxygen species levels and induces senescence in human melanoma cells by activation of p53/p21 pathway

2013 ◽  
Vol 319 (19) ◽  
pp. 2977-2988 ◽  
Author(s):  
Fernanda Augusta de Lima Barbosa Guterres ◽  
Glaucia Regina Martinez ◽  
Maria Eliane Merlin Rocha ◽  
Sheila Maria Brochado Winnischofer
Keyword(s):  
Reactive Oxygen Species ◽  
Reactive Oxygen ◽  
Melanoma Cells ◽  
Human Melanoma ◽  
Oxygen Species ◽  
Human Melanoma Cells

Piperlongumine Induces Apoptosis in Human Melanoma Cells Via Reactive Oxygen Species Mediated Mitochondria Disruption

2018 ◽  
Vol 70 (3) ◽  
pp. 502-511 ◽  
Author(s):  
Xuejiao Song ◽  
Tiantao Gao ◽  
Qian Lei ◽  
Lidan Zhang ◽  
Yuqin Yao ◽  
...  
Keyword(s):  
Reactive Oxygen Species ◽  
Reactive Oxygen ◽  
Melanoma Cells ◽  
Human Melanoma ◽  
Oxygen Species ◽  
Human Melanoma Cells

Cellular responses to reactive oxygen species-induced DNA damage and aging

2008 ◽  
Vol 389 (3) ◽  
pp. 211-220 ◽  
Author(s):  
Catharina Bertram ◽  
Ralf Hass
Keyword(s):  
Oxidative Stress ◽  
Reactive Oxygen Species ◽  
Dna Damage ◽  
Replicative Senescence ◽  
Reactive Oxygen ◽  
Premature Aging ◽  
Oxygen Species ◽  
X Rays ◽  
Cellular Mechanisms ◽  
In Cells

Abstract Oxidative stress in cells and tissues can occur during pathophysiological developments, e.g., during inflammatory and allergic diseases or during ischemic or toxic and hyperglycemic conditions via the generation of reactive oxygen species (ROS). Moreover, ROS can be generated by radiation (UV, X-rays) and pharmacologically, e.g., by anthracyclins as chemotherapeutic compounds for treatment of a variety of tumors to induce ‘stress or aberrant signaling-inducing senescence’ (STASIS). Although STASIS is distinguished from intracellular replicative senescence, a variety of cellular mechanisms appear similar in both aging pathways. It is generally accepted that oxidative stress and ROS eventually cause DNA damage, whereby insufficient cellular repair mechanisms may contribute to premature aging and apoptosis. Conversely, ROS-induced imbalances of the signaling pathways for metabolic protein turnover may also result in opposite effects to recruit malfunctioning aberrant proteins and compounds that trigger tumorigenic processes. Consequently, DNA damage plays a role in the development of carcinogenesis, but is also associated with an aging process in cells and organisms.

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