scholarly journals Furan fatty acids efficiently rescue brain cells from cell death induced by oxidative stress

2013 ◽  
Vol 4 (8) ◽  
pp. 1209 ◽  
Author(s):  
Antoinette Teixeira ◽  
Ruud C. Cox ◽  
Maarten R. Egmond
Keyword(s):  
Oxidative Stress ◽  
Fatty Acids ◽  
Cell Death ◽  
Brain Cells ◽  
Furan Fatty Acids

scholarly journals Lipids Nutrients in Parkinson and Alzheimer’s Diseases: Cell Death and Cytoprotection

2020 ◽  
Vol 21 (7) ◽  
pp. 2501 ◽  
Author(s):  
Thomas Nury ◽  
Gérard Lizard ◽  
Anne Vejux
Keyword(s):  
Oxidative Stress ◽  
Fatty Acids ◽  
Cell Death ◽  
Neurodegenerative Diseases ◽  
The Body ◽  
Protein Accumulation ◽  
Common Features ◽  
Apoptosis And Inflammation ◽  
The Brain ◽  
And Oxidative Stress

Neurodegenerative diseases, particularly Parkinson’s and Alzheimer’s, have common features: protein accumulation, cell death with mitochondrial involvement and oxidative stress. Patients are treated to cure the symptoms, but the treatments do not target the causes; so, the disease is not stopped. It is interesting to look at the side of nutrition which could help prevent the first signs of the disease or slow its progression in addition to existing therapeutic strategies. Lipids, whether in the form of vegetable or animal oils or in the form of fatty acids, could be incorporated into diets with the aim of preventing neurodegenerative diseases. These different lipids can inhibit the cytotoxicity induced during the pathology, whether at the level of mitochondria, oxidative stress or apoptosis and inflammation. The conclusions of the various studies cited are oriented towards the preventive use of oils or fatty acids. The future of these lipids that can be used in therapy/prevention will undoubtedly involve a better delivery to the body and to the brain by utilizing lipid encapsulation.

Polyunsaturated fatty acids induce oxidative stress and cell death in dopaminergic SH-SY5Y cells

2010 ◽  
Vol 68 ◽  
pp. e306
Author(s):  
Masayo Shamoto-Nagai ◽  
Yumi Kurokawa-Nose ◽  
Makoto Naoi ◽  
Wakako Maruyama
Keyword(s):  
Oxidative Stress ◽  
Fatty Acids ◽  
Cell Death ◽  
Polyunsaturated Fatty Acids

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 N-Acetylcysteine Reverses the Mitochondrial Dysfunction Induced by Very Long-Chain Fatty Acids in Murine Oligodendrocyte Model of Adrenoleukodystrophy

Biomedicines ◽  
2021 ◽  
Vol 9 (12) ◽  
pp. 1826
Author(s):  
Jie Zhou ◽  
Marcia R. Terluk ◽  
Paul J. Orchard ◽  
James C. Cloyd ◽  
Reena V. Kartha
Keyword(s):  
Oxidative Stress ◽  
Fatty Acids ◽  
Cell Death ◽  
Membrane Potential ◽  
Mitochondrial Dysfunction ◽  
Long Chain Fatty Acids ◽  
Specific Effects ◽  
Low Concentrations ◽  
Long Chain ◽  
Chain Fatty Acids

The accumulation of saturated very long-chain fatty acids (VLCFA, ≥C22:0) due to peroxisomal impairment leads to oxidative stress and neurodegeneration in X-linked adrenoleukodystrophy (ALD). Among the neural supporting cells, myelin-producing oligodendrocytes are the most sensitive to the detrimental effect of VLCFA. Here, we characterized the mitochondrial dysfunction and cell death induced by VLFCA, and examined whether N-acetylcysteine (NAC), an antioxidant, prevents the cytotoxicity. We exposed murine oligodendrocytes (158 N) to hexacosanoic acid (C26:0, 1–100 µM) for 24 h and measured reactive oxygen species (ROS) and cell death. Low concentrations of C26:0 (≤25 µM) induced a mild effect on cell survival with no alterations in ROS or total glutathione (GSH) concentrations. However, analysis of the mitochondrial status of cells treated with C26:0 (25 µM) revealed depletion in mitochondrial GSH (mtGSH) and a decrease in the inner membrane potential. These results indicate that VLCFA disturbs the mitochondrial membrane potential causing ROS accumulation, oxidative stress, and cell death. We further tested whether NAC (500 µM) can prevent the mitochondria-specific effects of VLCFA in C26:0-treated oligodendrocytes. Our results demonstrate that NAC improves mtGSH levels and mitochondrial function in oligodendrocytes, indicating that it has potential use in the treatment of ALD and related disorders.

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.

A General Convergent Strategy for the Synthesis of Tetrasubstituted Furan Fatty Acids (FuFAs)

2019 ◽  
Author(s):  
Yamin Wang ◽  
Gareth Pritchard ◽  
Marc Kimber
Keyword(s):  
Fatty Acids ◽  
Spectral Data ◽  
Synthetic Route ◽  
Furan Fatty Acids

Synthetic route for the synthesis of tetrasubstituted furan fatty acids; including experimental details, characterisation, and spectral data of all intermediates.

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