scholarly journals Dexmedetomidine is Resistant to Ferroptosis by Activating mTOR-TFR1 Signaling

2021 ◽  
Author(s):  
Hui Ding ◽  
Jing-Yan Wang ◽  
Yuan-Hai Li ◽  
Yan Huang
Keyword(s):  
Lipid Peroxidation ◽  
Fenton Reaction ◽  
Fluorescence Probe ◽  
Nerve Cells ◽  
The Body ◽  
Iron Ions ◽  
Double Staining ◽  
Ferrous Ions ◽  
Ht22 Cells ◽  
Proliferation And Apoptosis

Abstract Background: With the development of society, Neurodegenerative disease (ND), such as alzheimer's disease, is more and more important to the researchers. Metal iron may play a crucial role in this disease, so our research constructed the iron overloading model in nerve cells, induce the ferroptosis, simulate the state of the nerve in the body, and used the anesthesia Dexmedetomidine (Dex), and study whether the Dex can inhibit the ferroptosis and reduce the ND.Methods: Cell proliferation kit CCK8 and PI/Hoechst fluorescence double staining were used to detect the proliferation and apoptosis of HT22 cells. Western blot (WB) was used to detect the expression of PTGS2 and ACSL4, pathway proteins mTOR, TFR1. ROS content in HT22 cells was determined by DHE fluorescence probe. Lipid Peroxidation in nerve cells was detected by MDA Assay. Mito-ferrorange fluorescent probe was used to detect the level of ferrous ions in cells to demonstrate that ferroptosis occurred in nerve cells and Dex could protect nerve cells from ferroptosis.Results: Dex inhibits ferroptosis by regulating the mTOR-TFR1 pathway, reducing lipid peroxidation, intracellular reactive oxygen accumulation (ROS), reducing iron ions, and alleviating mitochondrial damage. mTOR is a well-known autophagy target and has been found to be closely related to ferroptosis. Dex activates the mTOR pathway, inhibits iron entry into the cell, reduces iron influx, and prevents ferroptosis by fenton reaction between excessive iron and lipids in the cell.Conclusion: Dex protects nerve cells from ferroptosis by regulating the mTOR-TFR1 pathway.

scholarly journals The stimulatory effects of asbestos on NADPH-dependent lipid peroxidation in rat liver microsomes

1987 ◽  
Vol 241 (2) ◽  
pp. 561-565 ◽  
Author(s):  
M Fontecave ◽  
D Mansuy ◽  
M Jaouen ◽  
H Pezerat
Keyword(s):  
Lipid Peroxidation ◽  
Rat Liver ◽  
Active Sites ◽  
Oxygen Radicals ◽  
Liver Microsomes ◽  
Rat Liver Microsomes ◽  
Iron Ions ◽  
Ferrous Ions ◽  
Solid Iron ◽  
Ferric Oxides

Lipid peroxidation in rat liver microsomes induced by asbestos fibres, crocidolite and chrysotile, is greatly increased in the presence of NADPH, leading to malondialdehyde levels comparable with those induced by CCl4, a very strong inducer of lipid peroxidation. This synergic effect only occurs during the first minutes and could be explained by an increase or a regeneration of the ferrous active sites of asbestos by NADPH, which in turn could rapidly be prevented by the adsorption of microsomal proteins on the surface of the fibres. It is not inhibited by superoxide dismutase, catalase and mannitol, indicating that oxygen radicals are not involved in the reaction. It is also not inhibited by desferrioxamine, indicating that it is not due to a release of free iron ions in solution from the fibres. Lipid peroxidation in NADPH-supplemented microsomes is also greatly increased upon addition of magnetite. This could be linked to the presence of ferrous ions in this solid iron oxide, since the ferric oxides haematite and goethite are completely inactive.

Apoptosis Inducible Factor P53 Decrease Glutamate-Associated Damage via Inhibiting Ferroptosis

2021 ◽  
Author(s):  
Zeyong Yang ◽  
Wenting Xuan ◽  
Yaru Jin ◽  
Yuanhai Li
Keyword(s):  
Lipid Peroxidation ◽  
Cell Death ◽  
Protein Expression ◽  
P53 Protein ◽  
Staining Technique ◽  
Cell Counting ◽  
Ferrous Ions ◽  
Ht22 Cells ◽  
Expression Levels ◽  
Ht22 Cell

Abstract BACKGROUND: Ferroptosis, a pattern of programmed cell death decided by iron-associated lipid peroxidation, however, its role of p53-mediated xCT pathway in HT22 cell death remains obscure. Herein, this study is to investigate the potential mechanism of the effect of p53-mediated xCT pathway in HT22 cell lines in an iron-relevant mode. METHODS: The viability of HT22 cells were detected by Cell Counting Kit-8(CCK-8) and PI/Hoechst fluorescence double staining. The protein expression levels of p53 and xCT were determined by western boltting. DHE fluorescence staining technique supervised the intracellular reactive oxygen species (ROS), and intracellular lipid oxidant situation was confirmed by BODIPY 581/591 C11 lipid peroxidation sensor. Intracellular ferrous ions were monitored with FeRhoNox™-1 fluoresceent probe. RESULTS: The protein expression levels of p53 was obviously enhanced by tenovin-1 exposure. Accompanied with the upregulation of p53 protein, cell death was decreased significantly because of glutamate and erastin exposure with 8h, and p53-mediated xCT pathway was activated. Intracelluar ROS levels, lipid oxidant situations and ferrous ions were remarkably restricted from Glutamate-p53 groups in comparison with glutamate groups. CONCLUSIONS: Overall, P53-mediated xCT pathway could decrease the glutamate-associated neurotoxicity, which may be relevant to the inhibition of ferroptosis.

Mechanisms of Nickel-Induced Cell Damage in Allergic Contact Dermatitis and Nutritional Intervention Strategies

2020 ◽  
Vol 20 (7) ◽  
pp. 1010-1014 ◽  
Author(s):  
Dana Filatova ◽  
Christine Cherpak
Keyword(s):  
Lipid Peroxidation ◽  
Contact Dermatitis ◽  
Oxidative Damage ◽  
Allergic Contact Dermatitis ◽  
Cell Damage ◽  
Consumer Products ◽  
The Body ◽  
Cellular Damage ◽  
Nutritional Interventions ◽  
Allergic Contact

Background: Hypersensitivity to nickel is a very common cause of allergic contact dermatitis since this metal is largely present in industrial and consumer products as well as in some commonly consumed foods, air, soil, and water. In nickel-sensitized individuals, a cell-mediated delayed hypersensitivity response results in contact to dermatitis due to mucous membranes coming in long-term contact with nickel-containing objects. This process involves the generation of reactive oxidative species and lipid peroxidation-induced oxidative damage. Immunologically, the involvement of T helper (h)-1 and Th-2 cells, as well as the reduced function of T regulatory cells, are of importance. The toxicity, mutagenicity, and carcinogenicity of nickel are attributed to the generation of reactive oxygen species and induction of oxidative damage via lipid peroxidation, which results in DNA damage. Objective: The aim of this research is to identify nutritionally actionable interventions that can intercept nickel-induced cell damage due to their antioxidant capacities. Conclusion: Nutritional interventions may be used to modulate immune dysregulation, thereby intercepting nickel-induced cellular damage. Among these nutritional interventions are a low-nickel diet and an antioxidant-rich diet that is sufficient in iron needed to minimize nickel absorption. These dietary approaches not only reduce the likelihood of nickel toxicity by minimizing nickel exposure but also help prevent oxidative damage by supplying the body with antioxidants that neutralize free radicals.

The musculature and nervous system of the plerocercoid larva of Dibothriorhynchus grossum (Rud.)

Parasitology ◽  
1941 ◽  
Vol 33 (4) ◽  
pp. 373-389 ◽  
Author(s):  
Gwendolen Rees
Keyword(s):  
Nervous System ◽  
Muscle Mass ◽  
Nerve Cells ◽  
The Body ◽  
Lateral Nerve ◽  
Posterior Median ◽  
The Brain ◽  
Ventral Muscle ◽  
Nerve Cords ◽  
Extrinsic Muscles

1. The structure of the proboscides of the larva of Dibothriorhynchus grossum (Rud.) is described. Each proboscis is provided with four sets of extrinsic muscles, and there is an anterior dorso-ventral muscle mass connected to all four proboscides.2. The musculature of the body and scolex is described.3. The nervous system consists of a brain, two lateral nerve cords, two outer and inner anterior nerves on each side, twenty-five pairs of bothridial nerves to each bothridium, four longitudinal bothridial nerves connecting these latter before their entry into the bothridia, four proboscis nerves arising from the brain, and a series of lateral nerves supplying the lateral regions of the body.4. The so-called ganglia contain no nerve cells, these are present only in the posterior median commissure which is therefore the nerve centre.

N2L, a novel lipoic acid-niacin dimer, attenuates ferroptosis and decreases lipid peroxidation in HT22 cells

2021 ◽  
Author(s):  
Weijia Peng ◽  
Zeyu Zhu ◽  
Yang Yang ◽  
Jiawei Hou ◽  
Junfeng Lu ◽  
...  
Keyword(s):  
Lipid Peroxidation ◽  
Lipoic Acid ◽  
Ht22 Cells

scholarly journals The mechanism of Fe2+-initiated lipid peroxidation in liposomes: the dual function of ferrous ions, the roles of the pre-existing lipid peroxides and the lipid peroxyl radical

2000 ◽  
Vol 352 (1) ◽  
pp. 27-36 ◽  
Author(s):  
Lixia TANG ◽  
Yong ZHANG ◽  
Zhongming QIAN ◽  
Xun SHEN
Keyword(s):  
Lipid Peroxidation ◽  
Latent Period ◽  
Time Lag ◽  
Lipid Peroxides ◽  
Peroxyl Radicals ◽  
Dual Function ◽  
Critical Ratio ◽  
Ferrous Ions ◽  
Liposomal System ◽  
Lipid Peroxyl Radicals

The mechanism of Fe2+-initiated lipid peroxidation in a liposomal system was studied. It was found that a second addition of ferrous ions within the latent period lengthened the time lag before lipid peroxidation started. The apparent time lag depended on the total dose of Fe2+ whenever the second dose of Fe2+ was added, which indicates that Fe2+ has a dual function: to initiate lipid peroxidation on one hand and suppress the species responsible for the initiation of the peroxidation on the other. When the pre-existing lipid peroxides (LOOH) were removed by incorporating triphenylphosphine into liposomes, Fe2+ could no longer initiate lipid peroxidation and the acceleration of Fe2+ oxidation by the liposomes disappeared. However, when extra LOOH were introduced into liposomes, both enhancement of the lipid peroxidation and shortening of the latent period were observed. When the scavenger of lipid peroxyl radicals (LOOP), N,N´-diphenyl-p-phenylene-diamine, was incorporated into liposomes, neither initiation of the lipid peroxidation nor acceleration of the Fe2+ oxidation could be detected. The results may suggest that both the pre-existing LOOH and LOOP are necessary for the initiation of lipid peroxidation. The latter comes initially from the decomposition of the pre-existing LOOH by Fe2+ and can be scavenged by its reaction with Fe2+. Only when Fe2+ is oxidized to such a degree that LOOP is no longer effectively suppressed does lipid peroxidation start. It seems that by taking the reactions of Fe2+ with LOOH and LOOP into account, the basic chemistry in lipid peroxidation can explain fairly well the controversial phenomena observed in Fe2+-initiated lipid peroxidation, such as the existence of a latent period, the critical ratio of Fe2+ to lipid and the required oxidation of Fe2+.

scholarly journals Supplement to the article "On the flow of thoughts"

1907 ◽  
Vol XIV (3-4) ◽  
pp. 104-110
Author(s):  
A. Perevoznikov
Keyword(s):  
Body Surface ◽  
Nervous Tissue ◽  
Nerve Cells ◽  
The Body ◽  
Animal Life ◽  
Central Organ

After the publication of the above-mentioned article, I got some facts confirming the principle of the distribution of ideas in the course of thoughts. I will preliminarily give a few general remarks about sensations. In the early periods of animal life, when the nervous tissue with a central organ had already been formed, the sensitivity was uniformly distributed over the surface of the body. Differentiation for sight, hearing, taste, etc., has not yet been. Then the central nervous organ, which was an accumulation of nerve cells in some place of the body, constantly received weak excitation from each part of the body surface.

scholarly journals TRP Channels as Sensors of Aldehyde and Oxidative Stress

Biomolecules ◽  
2021 ◽  
Vol 11 (10) ◽  
pp. 1401
Author(s):  
Katharina E. M. Hellenthal ◽  
Laura Brabenec ◽  
Eric R. Gross ◽  
Nana-Maria Wagner
Keyword(s):  
Lipid Peroxidation ◽  
Transient Receptor Potential ◽  
Trp Channels ◽  
Treatment Options ◽  
Receptor Potential ◽  
The Body ◽  
Trp Channel ◽  
Alcoholic Beverages ◽  
Organ Injury ◽  
Transient Receptor

The transient receptor potential (TRP) cation channel superfamily comprises more than 50 channels that play crucial roles in physiological processes. TRP channels are responsive to several exogenous and endogenous biomolecules, with aldehydes emerging as a TRP channel trigger contributing to a cellular cascade that can lead to disease pathophysiology. The body is not only exposed to exogenous aldehydes via tobacco products or alcoholic beverages, but also to endogenous aldehydes triggered by lipid peroxidation. In response to lipid peroxidation from inflammation or organ injury, polyunsaturated fatty acids undergo lipid peroxidation to aldehydes, such as 4-hydroxynonenal. Reactive aldehydes activate TRP channels via aldehyde-induced protein adducts, leading to the release of pro-inflammatory mediators driving the pathophysiology caused by cellular injury, including inflammatory pain and organ reperfusion injury. Recent studies have outlined how aldehyde dehydrogenase 2 protects against aldehyde toxicity through the clearance of toxic aldehydes, indicating that targeting the endogenous aldehyde metabolism may represent a novel treatment strategy. An addition approach can involve targeting specific TRP channel regions to limit the triggering of a cellular cascade induced by aldehydes. In this review, we provide a comprehensive summary of aldehydes, TRP channels, and their interactions, as well as their role in pathological conditions and the different therapeutical treatment options.

scholarly journals Oxidative stress in ageing

2017 ◽  
Vol 5 (11) ◽  
pp. 4826 ◽  
Author(s):  
Fasna K. A. ◽  
Geetha N. ◽  
Jean Maliekkal
Keyword(s):  
Oxidative Stress ◽  
Lipid Peroxidation ◽  
Free Radicals ◽  
Free Radical ◽  
Age Groups ◽  
The Body ◽  
Antioxidant Systems ◽  
Lipid Peroxidation Product ◽  
Free Radical Theory ◽  
Radical Theory

Background: Ageing is characterized by a gradual decline in body functions and decreased ability to maintain homeostasis. The free radical theory of ageing proposed by Harman D states that ageing is a result of cumulative damage incurred by free radical reactions. Free radicals are highly reactive molecular species with unpaired electrons; generated in the body by several physiological processes. Prime target to free radical attack are the polyunsaturated fatty acids of cell membranes causing lipid peroxidation. The free radicals are neutralized by the exogenous and endogenous antioxidant systems. Oxidative stress occurs when large number of free radicals are produced or the antioxidant activity is impaired. The present study is focused to find out the role of oxidative stress in ageing.Methods: A cross sectional observational study was undertaken to assess the oxidative stress in ageing; by determining the levels of lipid peroxidation product- malondialdehyde (MDA), the antioxidants- superoxide dismutase (SOD) and ceruloplasmin in various age groups. 150 healthy subjects were selected randomly and categorised into three different age groups of 20-30 years, 40-59 years and 60-90 years; with 50 subjects in each group. Results were expressed as mean ± standard deviation.Results: a significant elevation in serum MDA level and a decline in SOD were observed in 40-59 years and 60-90 years age groups. However, an elevated ceruloplasmin level was found in the above age groups.Conclusions: Aforementioned observations are suggestive of an association between oxidative stress and the progression of ageing process.

scholarly journals INFLUENCE OF «METISEVIT» ON THE ACTIVITY OF ENZYME AND NONENZYME LINK OF ANTIOXIDANT PROTECTION UNDER THE BULL’S BODY CADMIUM LOADING

2016 ◽  
Vol 18 (2(66)) ◽  
pp. 52-59
Author(s):  
B.V. Gutyj ◽  
Y. Lavryshyn ◽  
V. Binkevych ◽  
O. Binkevych ◽  
О. Paladischuk ◽  
...  
Keyword(s):  
Lipid Peroxidation ◽  
Superoxide Dismutase ◽  
Vitamin E ◽  
Glutathione Peroxidase ◽  
Antioxidant Defense ◽  
Cadmium Stress ◽  
Antioxidant Defense System ◽  
The Body ◽  
Antioxidant Protection ◽  
Young Cattle

The article contains the research results of the effect of cadmium chloride on the indexes of enzyme and nonenzyme systems of  antioxidant defense system in young cattle, such as the activity of catalase, superoxide dismutase, glutathione peroxidase, glutathione levels of vitamins A and E. It is established that feeding calves at a dose of toxicant 0.04 mg / kg activity of catalase, superoxide dismutase, glutathione peroxidase, glutathione levels of vitamins A and E in the blood of experimental animals decreased throughout the experiment. The lowest indicators of antioxidant in the blood of young cattle is set on the twenty -fourth day of the experiment, which is associated with increased activation of lipid peroxidation and the balance between antioxidant system and lipid peroxidation intensity. Given the cadmium load of young cattle it is used a new integrated drug with antioxidant action «Metisevit», which includes metifen, sodium selenite and vitamin E wich is founded as stimulating effects on the activity of antioxidant protection. In particular,it is established probable increase in activity of catalase, superoxide dismutase, glutathione peroxidase, glutathione levels, vitamin A and vitamin E in the blood of young cattle, which has performed cadmium stress. These changes occur through comprehensive action components of the drug «Metisevit» that leads to the normalization of metabolic processes and free radical in the body of the bull. The results of the research indicate antioxidant drug «Metisevit» in the application of its young cattle and the validity of his administration to improve the body's antioxidant status of chronic cadmium toxicosis.

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