scholarly journals Le potentiel thérapeutique d’un lipide de l’avocat (avocatin B) pour le traitement des leucémies aiguës myéloblastiques

2015 ◽  
Vol 8 (2) ◽  
Author(s):  
Tarek Omaiche
Keyword(s):  
Oxidative Stress ◽  
Fatty Acids ◽  
Stem Cells ◽  
Cell Death ◽  
Programmed Cell Death ◽  
Cancer Cells ◽  
Normal Cells ◽  
Mort Cellulaire ◽  
Globules Rouges ◽  
The University

De nos jours, le traitement le plus répandu contre les cancers est la chimiothérapie. C'est une pratique qui se résume à l’utilisation des médicaments qui tuent les cellules qui se divisent rapidement. Cependant, la chimiothérapie est inefficace pour le traitement de certains cancers comme la leucémie aigüe myéloblastique(LMA).Ce type du cancer affecte les cellules souches responsables de la production des plaquettes, des globules rouges et blancs. Cette approche est souvent trop intense puisqu’elle tue  les normales cellulaires qui sont important pour la fonction du corps. Dans ce contexte, le professeur Paul Spagnuolo et son équipe à l’Université de Waterloo ont récemment reporté l’existence d’un lipide de l’avocat nommé l’avocatin B, qui peut efficacement tuer les cellules souches cancéreuses leucémiques sans endommager les cellules souches normales. L’avocatin B affecte l’oxydation des acides gras et réduit la production de l’NADPH, l’NAD et le GSH, des molécules essentielles pour le contrôle du stress oxydatif cellulaire. [1] En absence des défenses anti-oxydantes, les cellules cancéreuses succombent à la mort cellulaire programmée (apoptose).Now a days the most common treatment against cancer is chemotheraphy.This is a practise which uses medications who kills rapidly diving cells.Chemotheraphy is an ineffective treatment against certain cancers like acute myelodi leukemia(AML).This type of cancer affects the stem cells respondisble for the production of platelets,red and white blood cells.This approach is often to much/intense since it kills normal cells which are mportnat for the function of the body.In this context,Dr.Paul Spagnulo and his team at the University of Waterloo have recently reported dthe existence of a lipid in avacodo's called avocatin B,which  can effectively kill the cancer cells without damaging the normal cells.Avocatin B affects the oxidation of fatty acids and reduces(?) the production of NADPH, NAD and GSH; molecules that are essential for the control of oxidative stress. [1] These factors eventually lead to a programmed cell death (apoptosis).        

scholarly journals Control of programmed cell death in normal and leukemic cells: new implications for therapy

Blood ◽  
1993 ◽  
Vol 82 (1) ◽  
pp. 15-21 ◽  
Author(s):  
L Sachs ◽  
J Lotem
Keyword(s):  
Cell Death ◽  
Virus Infection ◽  
Programmed Cell Death ◽  
Cancer Cells ◽  
Adult Life ◽  
Cytotoxic Agents ◽  
Leukemic Cells ◽  
Mutant P53 ◽  
Normal Process ◽  
Normal Cells

Programmed cell death (apoptosis) is a normal process by which cells are eliminated during normal embryonic development and in adult life. Disruption of this normal process resulting in illegitimate cell survival can cause developmental abnormalities and facilitate cancer development. Normal cells require certain viability factors and undergo programmed cell death when these factors are withdrawn. The viability factors are required throughout the differentiation process from immature to mature cells. Although many viability factors are also growth factors, viability and growth are separately regulated. Viability factors can have clinical value in decreasing the loss of normal cells including the loss that occurs after irradiation, exposure to other cytotoxic agents or virus infection including AIDS. There is no evidence that occurs after irradiation, exposure to other cytotoxic agents or virus infection including AIDS. There is no evidence that cancer cells are immortal. Programmed cell death can be induced in leukemic cells by removal of viability factors, by cytotoxic therapeutic agents, or by the tumor-suppressor gene wild-type p53. All these forms of induction of programmed cell death in leukemic cells can be suppressed by the same viability factors that suppress programmed cell death in normal cells. A tumor-promoting phorbol ester can also suppress this death program. The induction of programmed cell death can be enhanced by deregulated expression of the gene c-myc and suppressed by the gene bcl-2. Mutant p53 and bcl-2 suppress the enhancing effect on cell death of deregulated c-myc, and thus allow induction of cell proliferation and inhibition of differentiation which are other functions of deregulated c-myc. The suppression of cell death by mutant p53 and bcl-2 increases the probability of developing cancer. The suppression of programmed cell death in cancer cells by viability factors suggests that decreasing the level of these factors may increase the effectiveness of cytotoxic cancer therapy. Treatments that downregulate the expression or activity of mutant p53 and bcl-2 in cancer cells should also be useful for therapy.

scholarly journals The Versatile Effects of Dihydromyricetin in Health

2017 ◽  
Vol 2017 ◽  
pp. 1-10 ◽  
Author(s):  
Hongliang Li ◽  
Qisheng Li ◽  
Zhaowen Liu ◽  
Kai Yang ◽  
Zhixi Chen ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Cell Death ◽  
Glucose Metabolism ◽  
Adverse Effects ◽  
Cancer Cells ◽  
Ros Generation ◽  
Normal Cells ◽  
Potential Applications ◽  
Anti Inflammatory ◽  
Ampelopsis Grossedentata

Dihydromyricetin is a flavonoid isolated from Ampelopsis grossedentata, which is traditionally used in China. Dihydromyricetin exhibits health-benefiting activities with minimum adverse effects. Dihydromyricetin has been demonstrated to show antioxidative, anti-inflammatory, anticancer, antimicrobial, cell death-mediating, and lipid and glucose metabolism-regulatory activities. Dihydromyricetin may scavenge ROS to protect against oxidative stress or potentiate ROS generation to counteract cancer cells selectively without any effects on normal cells. However, the low bioavailability of dihydromyricetin limits its potential applications. Recent research has gained positive and promising data. This review will discuss the versatile effects and clinical prospective of dihydromyricetin.

scholarly journals Dose-Dependent Effects of Cold Atmospheric Argon Plasma on the Mesenchymal Stem and Osteosarcoma Cells In Vitro

2021 ◽  
Vol 22 (13) ◽  
pp. 6797
Author(s):  
Artem M. Ermakov ◽  
Olga N. Ermakova ◽  
Vera A. Afanasyeva ◽  
Anton L. Popov
Keyword(s):  
Oxidative Stress ◽  
Reactive Oxygen Species ◽  
Cell Cycle ◽  
Stem Cells ◽  
Cancer Cells ◽  
Transcriptional Activity ◽  
Argon Plasma ◽  
Reactive Oxygen ◽  
Oxygen Species ◽  
Normal Cells

The antimicrobial, anti-inflammatory and tissue-stimulating effects of cold argon atmospheric plasma (CAAP) accelerate its use in various fields of medicine. Here, we investigated the effects of CAAP at different radiation doses on mesenchymal stem cells (MSCs) and human osteosarcoma (MNNG/HOS) cells. We observed an increase in the growth rate of MSCs at sufficiently low irradiation doses (10–15 min) of CAAP, while the growth of MNNG/HOS cells was slowed down to 41% at the same irradiation doses. Using flow cytometry, we found that these effects are associated with cell cycle arrest and extended death of cancer cells by necrosis. Reactive oxygen species (ROS) formation was detected in both types of cells after 15 min of CAAP treatment. Evaluation of the genes’ transcriptional activity showed that exposure to low doses of CAAP activates the expression of genes responsible for proliferation, DNA replication, and transition between phases of the cell cycle in MSCs. There was a decrease in the transcriptional activity of most of the studied genes in MNNG/HOS osteosarcoma cancer cells. However, increased transcription of osteogenic differentiation genes was observed in normal and cancer cells. The selective effects of low and high doses of CAAP treatment on cancer and normal cells that we found can be considered in terms of hormesis. The low dose of cold argon plasma irradiation stimulated the vital processes in stem cells due to the slight generation of reactive oxygen species. In cancer cells, the same doses evidently lead to the formation of oxidative stress, which was accompanied by a proliferation inhibition and cell death. The differences in the cancer and normal cells’ responses are probably due to different sensitivity to exogenous oxidative stress. Such a selective effect of CAAP action can be used in the combined therapy of oncological diseases such as skin neoplasms, or for the removal of remaining cancer cells after surgical removal of a tumor.

scholarly journals Bioactive Compounds: Multi-Targeting Silver Bullets for Preventing and Treating Breast Cancer

Cancers ◽  
2019 ◽  
Vol 11 (10) ◽  
pp. 1563 ◽  
Author(s):  
Nethaji Muniraj ◽  
Sumit Siddharth ◽  
Dipali Sharma
Keyword(s):  
Cell Death ◽  
Programmed Cell Death ◽  
Cancer Cells ◽  
Bioactive Compounds ◽  
Cancer Therapeutics ◽  
The Body ◽  
Cancer Drug ◽  
Metastatic Progression ◽  
Normal Cells ◽  
Cancer Drug Discovery

Each cell in our body is designed with a self-destructive trigger, and if damaged, can happily sacrifice itself for the sake of the body. This process of self-destruction to safeguard the adjacent normal cells is known as programmed cell death or apoptosis. Cancer cells outsmart normal cells and evade apoptosis and it is one of the major hallmarks of cancer. The cardinal quest for anti-cancer drug discovery (bioactive or synthetic compounds) is to be able to re-induce the so called “programmed cell death” in cancer cells. The importance of bioactive compounds as the linchpin of cancer therapeutics is well known as many effective chemotherapeutic drugs such as vincristine, vinblastine, doxorubicin, etoposide and paclitaxel have natural product origins. The present review discusses various bioactive compounds with known anticancer potential, underlying mechanisms by which they induce cell death and their preclinical/clinical development. Most bioactive compounds can concurrently target multiple signaling pathways that are important for cancer cell survival while sparing normal cells hence they can potentially be the silver bullets for targeting cancer growth and metastatic progression.

Oral Malodorous Compound Causes Oxidative Stress and p53-Mediated Programmed Cell Death in Keratinocyte Stem Cells

2010 ◽  
Vol 81 (9) ◽  
pp. 1317-1323 ◽  
Author(s):  
Bogdan Calenic ◽  
Ken Yaegaki ◽  
Ana Kozhuharova ◽  
Toshio Imai
Keyword(s):  
Oxidative Stress ◽  
Stem Cells ◽  
Cell Death ◽  
Programmed Cell Death ◽  
Keratinocyte Stem Cells

scholarly journals Differences of Key Proteins between Apoptosis and Necroptosis

2021 ◽  
Vol 2021 ◽  
pp. 1-10
Author(s):  
Min Yeong Park ◽  
Sang Eun Ha ◽  
Preethi Vetrivel ◽  
Hun Hwan Kim ◽  
Pritam Bhangwan Bhosale ◽  
...  
Keyword(s):  
Cell Death ◽  
Protein Kinase ◽  
Programmed Cell Death ◽  
Cancer Cells ◽  
The Body ◽  
Caspase 8 ◽  
Normal Cells ◽  
Different Types

Many different types of programmed cell death (PCD) have been identified, including apoptosis and necroptosis. Apoptosis is a type of cell death that is controlled by various genes. It is in charge of eliminating aberrant cells such as cancer cells, replenishing normal cells, and molding the body as it develops. Necroptosis is a type of programmed cell death that combines necrosis and apoptosis. In other words, it takes on a necrotic appearance, although cells die in a controlled manner. Various investigations of these two pathways have revealed that caspase-8, receptor-interacting serine/threonine-protein kinase 1 (RIPK1), and RIPK3 are crucial proteins in charge of the switching between these two pathways, resulting in the activation or inhibition of necroptosis. In this review, we have summarized the key proteins between apoptosis and necroptosis.

Glial cytotoxicity of low doses of cadmium as a model of heavy metal pollution influence on vertebrates

2020 ◽  
Vol 31 (1) ◽  
pp. 3-10
Author(s):  
V. S. Nedzvetsky ◽  
V. Ya. Gasso ◽  
A. M. Hahut ◽  
I. A. Hasso
Keyword(s):  
Oxidative Stress ◽  
Cell Death ◽  
Programmed Cell Death ◽  
Oxidative Damage ◽  
Cadmium Chloride ◽  
Glioma Cells ◽  
Low Doses ◽  
Genotoxic Effects ◽  
Cadmium Ions

Cadmium is a common transition metal that entails an extremely wide range of toxic effects in humans and animals. The cytotoxicity of cadmium ions and its compounds is due to various genotoxic effects, including both DNA damage and chromosomal aberrations. Some bone diseases, kidney and digestive system diseases are determined as pathologies that are closely associated with cadmium intoxication. In addition, cadmium is included in the list of carcinogens because of its ability to initiate the development of tumors of several forms of cancer under conditions of chronic or acute intoxication. Despite many studies of the effects of cadmium in animal models and cohorts of patients, in which cadmium effects has occurred, its molecular mechanisms of action are not fully understood. The genotoxic effects of cadmium and the induction of programmed cell death have attracted the attention of researchers in the last decade. In recent years, the results obtained for in vivo and in vitro experimental models have shown extremely high cytotoxicity of sublethal concentrations of cadmium and its compounds in various tissues. One of the most studied causes of cadmium cytotoxicity is the development of oxidative stress and associated oxidative damage to macromolecules of lipids, proteins and nucleic acids. Brain cells are most sensitive to oxidative damage and can be a critical target of cadmium cytotoxicity. Thus, oxidative damage caused by cadmium can initiate genotoxicity, programmed cell death and inhibit their viability in the human and animal brains. To test our hypothesis, cadmium cytotoxicity was assessed in vivo in U251 glioma cells through viability determinants and markers of oxidative stress and apoptosis. The result of the cell viability analysis showed the dose-dependent action of cadmium chloride in glioma cells, as well as the generation of oxidative stress (p <0.05). Calculated for 48 hours of exposure, the LD50 was 3.1 μg×ml-1. The rates of apoptotic death of glioma cells also progressively increased depending on the dose of cadmium ions. A high correlation between cadmium concentration and apoptotic response (p <0.01) was found for cells exposed to 3–4 μg×ml-1 cadmium chloride. Moreover, a significant correlation was found between oxidative stress (lipid peroxidation) and induction of apoptosis. The results indicate a strong relationship between the generation of oxidative damage by macromolecules and the initiation of programmed cell death in glial cells under conditions of low doses of cadmium chloride. The presented results show that cadmium ions can induce oxidative damage in brain cells and inhibit their viability through the induction of programmed death. Such effects of cadmium intoxication can be considered as a model of the impact of heavy metal pollution on vertebrates.

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