Brief Report: Lipid Peroxidation in Aging Platelets

Abstract Blood platelets showed an age dependent accumulation of lipid peroxides. Lipid peroxidation stimulated by heavy metal also increased with platelet age and rose at a much faster rate than the spontaneous peroxide formation. This suggests the loss of a cellular defense mechanism against lipid peroxidation in aging blood platelets.

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Reactive Oxygen Species, Lipid Peroxidation and Antioxidative Defense Mechanism

Notulae Botanicae Horti Agrobotanici Cluj-Napoca ◽

10.15835/nbha4118929 ◽

2013 ◽

Vol 41 (1) ◽

pp. 44 ◽

Cited By ~ 46

Author(s):

Hossam S. EL-BELTAGI ◽

Heba I. MOHAMED

Keyword(s):

Oxidative Stress ◽

Lipid Peroxidation ◽

Carbonyl Compounds ◽

Defense Mechanism ◽

Lipid Peroxides ◽

Cellular Injury ◽

Oxygen Species ◽

Antioxidative Defense ◽

Inhibit Lipid Peroxidation ◽

Reactive Carbonyl Compounds

Lipid peroxidation can be defined as the oxidative deterioration of lipids containing any number of carbon-carbon double bonds. Lipid peroxidation is a well-established mechanism of cellular injury in both plants and animals, and is used as an indicator of oxidative stress in cells and tissues. Lipid peroxides are unstable and decompose to form a complex series of compounds including reactive carbonyl compounds. The oxidation of linoleates and cholesterol is discussed in some detail. Analytical methods for studying lipid peroxidation were mentioned. Various kinds of antioxidants with different functions inhibit lipid peroxidation and the deleterious effects caused by the lipid peroxidation products.

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Role of Histamine and Leucotaxin in Function of Cellular Defense Mechanism

American Journal of Physiology-Legacy Content ◽

10.1152/ajplegacy.1956.184.2.296 ◽

1956 ◽

Vol 184 (2) ◽

pp. 296-300 ◽

Cited By ~ 3

Author(s):

László Kátó ◽

Béla Gözsy

Keyword(s):

Fluid Flow ◽

Tissue Damage ◽

Inflammatory Process ◽

Defense Mechanism ◽

Volatile Oils ◽

Time Intervals ◽

Cellular Defense ◽

Intradermal Administration ◽

Flow Through

Experiments are presented to the effect that in an inflammatory process histamine and leucotaxin appear successively at different and orderly time intervals, thus assuring an increased fluid flow through the capillary wall. Histamine is released not only in the inflammatory process but also by intradermal administration of such substances (volatile oils or their components) which induce neither the triple response of Th. Lewis nor any tissue damage. This could be explained by the fact that in the tissues histamine is ‘present’ but leucotaxin is ‘formed.’

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Effect of Lead and Copper on Photosynthetic Apparatus in Citrus (Citrus aurantium L.) Plants. The Role of Antioxidants in Oxidative Damage as a Response to Heavy Metal Stress

Plants ◽

10.3390/plants10010155 ◽

2021 ◽

Vol 10 (1) ◽

pp. 155

Author(s):

Anastasia Giannakoula ◽

Ioannis Therios ◽

Christos Chatzissavvidis

Keyword(s):

Oxidative Stress ◽

Lipid Peroxidation ◽

Heavy Metal ◽

Metal Tolerance ◽

Heavy Metal Tolerance ◽

Membrane Integrity ◽

Photosynthetic Apparatus ◽

Heavy Metal Stress ◽

Photosynthetic Parameters ◽

Citrus Aurantium

Photosynthetic changes and antioxidant activity to oxidative stress were evaluated in sour orange (Citrus aurantium L.) leaves subjected to lead (Pb), copper (Cu) and also Pb + Cu toxicity treatments, in order to elucidate the mechanisms involved in heavy metal tolerance. The simultaneous effect of Pb− and Cu on growth, concentration of malondialdehyde (MDA), hydrogen peroxide (H2O2), chlorophylls, flavonoids, carotenoids, phenolics, chlorophyll fluorescence and photosynthetic parameters were examined in leaves of Citrus aurantium L. plants. Exogenous application of Pb and Cu resulted in an increase in leaf H2O2 and lipid peroxidation (MDA). Toxicity symptoms of both Pb and Cu treated plants were stunted growth and decreased pigments concentration. Furthermore, photosynthetic activity of treated plants exhibited a significant decline. The inhibition of growth in Pb and Cu-treated plants was accompanied by oxidative stress, as indicated by the enhanced lipid peroxidation and the high H2O2 concentration. Furthermore, antioxidants in citrus plants after exposure to high Pb and Cu concentrations were significantly increased compared to control and low Pb and Cu treatments. In conclusion, this study indicates that Pb and Cu promote lipid peroxidation, disrupt membrane integrity, reduces growth and photosynthesis and inhibit mineral nutrition. Considering the potential for adverse human health effects associated with high concentrations of Pb and Cu contained in edible parts of citrus plants the study signals that it is important to conduct further research into the accessibility and uptake of the tested heavy metals in the soil and whether they pose risks to humans.

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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

Biochemical Journal ◽

10.1042/bj3520027 ◽

2000 ◽

Vol 352 (1) ◽

pp. 27-36 ◽

Cited By ~ 23

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+.

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Activation of Cellular Defense Mechanism by Organic-Inorganic Hybrid Molecules

YAKUGAKU ZASSHI ◽

10.1248/yakushi.14-00017-8 ◽

2014 ◽

Vol 134 (7) ◽

pp. 813-815

Author(s):

Tomoya Fujie ◽

Hiroshi Naka ◽

Chika Yamamoto ◽

Yasuhiro Shinkai ◽

Yoshito Kumagai ◽

...

Keyword(s):

Defense Mechanism ◽

Inorganic Hybrid ◽

Cellular Defense ◽

Hybrid Molecules

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APR-246 induces early cell death by ferroptosis in acute myeloid leukemia.

Haematologica ◽

10.3324/haematol.2020.259531 ◽

2021 ◽

Author(s):

Rudy Birsen ◽

Clement Larrue ◽

Justine Decroocq ◽

Natacha Johnson ◽

Nathan Guiraud ◽

...

Keyword(s):

Lipid Peroxidation ◽

Cell Death ◽

Acute Myeloid Leukemia ◽

Myeloid Leukemia ◽

Ex Vivo ◽

Lipid Peroxides ◽

Death Process ◽

Glutathione Biosynthesis ◽

Acute Myeloid

APR-246 is a promising new therapeutic agent that targets p53 mutated proteins in myelodysplastic syndromes and in acute myeloid leukemia. APR-246 reactivates the transcriptional activity of p53 mutants by facilitating their binding to DNA target sites. Recent studies in solid cancers have found that APR-246 can also induce p53-independent cell death. In this study, we demonstrate that AML cell death occurring early after APR-246 exposure is suppressed by iron chelators, lipophilic antioxidants and inhibitors of lipid peroxidation, and correlates with the accumulation of markers of lipid peroxidation, thus fulfilling the definition of ferroptosis, a recently described cell death process. The capacity of AML cells to detoxify lipid peroxides by increasing their cystine uptake to maintain major antioxidant molecule glutathione biosynthesis after exposure to APR-246 may be a key determinant of sensitivity to this compound. The association of APR-246 with induction of ferroptosis (either by pharmacological compounds, or genetic inactivation of SLC7A11 or GPX4) had a synergistic effect on the promotion of cell death, both in vivo and ex vivo.

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Cellular Cysteine Network and Neurodegeneration

Quality Control of Cellular Protein in Neurodegenerative Disorders - Advances in Medical Diagnosis, Treatment, and Care ◽

10.4018/978-1-7998-1317-0.ch012 ◽

2020 ◽

pp. 303-325

Author(s):

Shubhangi H. Pawar ◽

Vishal S. Gulecha ◽

Manoj S. Mahajan ◽

Aman B Upaganiawar ◽

Chandrashekhar D. Upasani

Keyword(s):

Oxidative Stress ◽

Defense Mechanism ◽

Free Radical Scavenger ◽

Cellular Damage ◽

Radical Scavenger ◽

Post Translational Modifications ◽

Cellular Defense ◽

Brain Antioxidants ◽

The Brain ◽

Oxidative Species

Oxidative stress is strongly linked to neurodegeneration and oxidative species can modify many amino acids and proteins in the brain. Cysteine amino acid is most susceptible to oxidative post-translational modifications (PTMs). Reversible or irreversible cysteine PTMs can cause dyshomeostasis, which further continued to cellular damage. Many cysteine dependent proteins and many non-proteins using cysteine as their structural components are affected by oxidative stress. Several cysteine dependent enzymes are acting as antioxidants. Cysteine is a major contributor to glutathione (GSH) and superoxide dismutase (SOD) synthesis. Cysteine precursor N-acetylcysteine (NAC) supplementation is proven as a potent free radical scavenger and increase brain antioxidants and subsequently potentiates the natural antioxidant cellular defense mechanism. Thus, in this chapter, the authors explore the linkage of cellular cysteine networks and neurodegenerative disorders.

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Prevention of lipid peroxidation does not prevent oxidant-induced myocardial contractile dysfunction

AJP Heart and Circulatory Physiology ◽

10.1152/ajpheart.1994.267.6.h2371 ◽

1994 ◽

Vol 267 (6) ◽

pp. H2371-H2377 ◽

Cited By ~ 1

Author(s):

Y. Kong ◽

E. J. Lesnefsky ◽

J. Ye ◽

L. D. Horwitz

Keyword(s):

Lipid Peroxidation ◽

Coronary Flow ◽

Systolic Function ◽

Lipid Peroxide ◽

Left Ventricular Pressure ◽

Lipid Peroxides ◽

Left Ventricular ◽

Contractile Dysfunction ◽

Myocardial Contractile ◽

Generating System

We tested whether, with exposure to an extraneous iron-catalyzed free radical-generating system, prevention of lipid peroxidation with U74006F, a 21-aminosteroid, could also prevent myocardial contractile dysfunction. Rabbits received either U74006F (10 mg/kg iv) or vehicle (V). Thirty minutes later the hearts were excised and perfused by a non-recirculating Langendorff technique. Six U74006F- and six V-treated hearts were exposed for 7.5 min to a .OH-generating system (H2O2 and Fe(2+)-ADP chelate). Myocardial lipid peroxides were measured by glutathione peroxidase-catalyzed oxidation of exogenous glutathione. With exposure to .OH, cytosolic lipid peroxide levels were increased threefold in V-treated hearts, but there was no increase in U74006F-treated hearts. After 30 min of recovery, developed pressure and maximum first derivative of left ventricular pressure were greater in U74006F-treated hearts than in V-treated hearts but were still 50 and 44% of levels in saline hearts, respectively. Coronary flow was markedly reduced after exposure to free radicals and was only slightly less depressed when U74006F was administered. When coronary flow following oxidant exposure was increased by nitroglycerin, U74006F again only modestly improved systolic function. Thus, although U74006F blocked lipid peroxidation, it only slightly improved the ventricular dysfunction caused by .OH. Therefore, factors other than lipid peroxidation play a major role in oxidant-induced myocardial stunning.

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