Selective Targeting of HUFAs Away from Cardiolipin and Beta- Oxidation Combine to Protect Mitochondrial Membranes against Oxidative Damage

2014 ◽  
pp. 166-175
Keyword(s):  
Oxidative Damage ◽  
Mitochondrial Membranes ◽  
Beta Oxidation ◽  
Selective Targeting

Some Observations on Intra-Mitochondrial Crystals

1977 ◽  
Vol 35 ◽  
pp. 406-407
Author(s):  
J. A. Clarke ◽  
D. N. Landon ◽  
P. R. Ward
Keyword(s):  
Cytochrome B ◽  
Mitochondrial Myopathy ◽  
Crystallographic Analysis ◽  
Mitochondrial Membranes ◽  
Electron Microscopes ◽  
Muscle Biopsies

Intra-mitochondrial crystals have been noted in muscle biopsies from patients in a wide variety of diseased states. As far as we are aware, none of these crystals have been subjected to detailed crystallographic analysis. Recently, similar crystals were observed in a biopsy from a patient with a mitochondrial myopathy, characterised by a deficiency in reducible cytochrome b (Morgan-Hughes, J. A., Darveniza, P., Kahn, S. N., Landon, D. N., Sherratt, R. M., Land, J. M. and Clark, J. B., 1977, Brain, In Press). Aldehyde-fixed, osmicated resin imbedded material was examined using Siemens, JEOL and Phillips electron microscopes with goniometer specimen stages. The crystals generally lay between the outer and inner mitochondrial membranes and measured 1 - 3 μm in length and 0.1 - 0.3 μm in width. Characteristically, these crystals revealed specific periodicities.

Erythrophagocytosis in the Liver in Hemolytic Anemias

1968 ◽  
Vol 26 ◽  
pp. 184-185
Author(s):  
O. T. Minick ◽  
E. Orfei ◽  
F. Volini ◽  
G. Kent
Keyword(s):  
Acid Phosphatase ◽  
Oxidative Damage ◽  
Phosphatase Activity ◽  
Kupffer Cells ◽  
Acid Phosphatase Activity ◽  
Common Type ◽  
Red Cell ◽  
Cell Fragments ◽  
Reticulo Endothelial System ◽  
Important Site

Hemolytic anemias were produced in rats by administering phenylhydrazine or anti-erythrocytic (rooster) serum, the latter having agglutinin and hemolysin titers exceeding 1:1000.Following administration of phenylhydrazine, the erythrocytes undergo oxidative damage and are removed from the circulation by the cells of the reticulo-endothelial system, predominantly by the spleen. With increasing dosage or if animals are splenectomized, the Kupffer cells become an important site of sequestration and are greatly hypertrophied. Whole red cells are the most common type engulfed; they are broken down in digestive vacuoles, as shown by the presence of acid phosphatase activity (Fig. 1). Heinz body material and membranes persist longer than native hemoglobin. With larger doses of phenylhydrazine, erythrocytes undergo intravascular fragmentation, and the particles phagocytized are now mainly red cell fragments of varying sizes (Fig. 2).

Intramitochondrial Viruses of Reptilian Cell Origin

1972 ◽  
Vol 30 ◽  
pp. 318-319
Author(s):  
Philip D. Lunger ◽  
H. Fred Clark
Keyword(s):  
Particle Production ◽  
Outer Zone ◽  
Density Variation ◽  
Core Region ◽  
Mitochondrial Membranes ◽  
Virus Particles ◽  
The Core ◽  
Vipera Russelli ◽  
Maturation Stages ◽  
Type Particle

In the course of fine structure studies of spontaneous “C-type” particle production in a viper (Vipera russelli) spleen cell line, designated VSW, virus particles were frequently observed within mitochondria. The latter were usually enlarged or swollen, compared to virus-free mitochondria, and displayed a considerable degree of cristae disorganization.Intramitochondrial viruses measure 90 to 100 mμ in diameter, and consist of a nucleoid or core region of varying density and measuring approximately 45 mμ in diameter. Nucleoid density variation is presumed to reflect varying degrees of condensation, and hence maturation stages. The core region is surrounded by a less-dense outer zone presumably representing viral capsid.Particles are usually situated in peripheral regions of the mitochondrion. In most instances they appear to be lodged between loosely apposed inner and outer mitochondrial membranes.

Structure of contact sites between the outer and inner mitochondrial membranes investigated by HVEM tomography

1996 ◽  
Vol 54 ◽  
pp. 966-967
Author(s):  
C.A. Mannella ◽  
K.F. Buttle ◽  
K.A. O‘Farrell ◽  
A. Leith ◽  
M. Marko
Keyword(s):  
Liver Mitochondrion ◽  
Adenine Nucleotide ◽  
Protein Complexes ◽  
Mitochondrial Membranes ◽  
Electron Microscopic ◽  
Contact Sites ◽  
Transmission Electron ◽  
Precursor Proteins ◽  
Membrane Contacts ◽  
And Function

Early transmission electron microscopy of plastic-embedded, thin-sectioned mitochondria indicated that there are numerous junctions between the outer and inner membranes of this organelle. More recent studies have suggested that the mitochondrial membrane contacts may be the site of protein complexes engaged in specialized functions, e.g., import of mitochondrial precursor proteins, adenine nucleotide channeling, and even intermembrane signalling. It has been suggested that the intermembrane contacts may be sites of membrane fusion involving non-bilayer lipid domains in the two membranes. However, despite growing interest in the nature and function of intramitochondrial contact sites, little is known about their structure.We are using electron microscopic tomography with the Albany HVEM to determine the internal organization of mitochondria. We have reconstructed a 0.6-μm section through an isolated, plasticembedded rat-liver mitochondrion by combining 123 projections collected by tilting (+/- 70°) around two perpendicular tilt axes. The resulting 3-D image has confirmed the basic inner-membrane organization inferred from lower-resolution reconstructions obtained from single-axis tomography.

Protective effect of chitooligosaccharides on hydrogen peroxide-induced PC-12 cells death by inhibition of oxidative damage

2010 ◽  
Vol 34 (8) ◽  
pp. S27-S27
Author(s):  
Xueling Dai ◽  
Ping Chang ◽  
Ke Xu ◽  
Changjun Lin ◽  
Hanchang Huang ◽  
...  
Keyword(s):  
Hydrogen Peroxide ◽  
Oxidative Damage ◽  
Protective Effect ◽  
Pc 12 Cells ◽  
Cells Death

Aging and Oxidative Damage: Are Telomeres the Target?

2002 ◽  
Vol 7 (5) ◽  
pp. 295-313 ◽  
Author(s):  
Patricia A. McChesney ◽  
Lynne W. Elmore ◽  
Shawn E. Holt
Keyword(s):  
Oxidative Damage

Melatonin reduces high levels of lipid peroxidation induced by potassium iodate in porcine thyroid

2019 ◽  
pp. 1-7 ◽  
Author(s):  
Paulina Iwan ◽  
Jan Stepniak ◽  
Malgorzata Karbownik-Lewinska
Keyword(s):  
Lipid Peroxidation ◽  
Oxidative Damage ◽  
Membrane Lipids ◽  
Chemical Properties ◽  
Iodine Concentration ◽  
Free Radical Scavenger ◽  
Radical Scavenger ◽  
Protective Effects ◽  
Potassium Iodate ◽  
Hormone Synthesis

Abstract. Iodine is essential for thyroid hormone synthesis. Under normal iodine supply, calculated physiological iodine concentration in the thyroid is approx. 9 mM. Either potassium iodide (KI) or potassium iodate (KIO3) are used in iodine prophylaxis. KI is confirmed as absolutely safe. KIO3 possesses chemical properties suggesting its potential toxicity. Melatonin (N-acetyl-5-methoxytryptamine) is an effective antioxidant and free radical scavenger. Study aims: to evaluate potential protective effects of melatonin against oxidative damage to membrane lipids (lipid peroxidation, LPO) induced by KI or KIO3 in porcine thyroid. Homogenates of twenty four (24) thyroids were incubated in presence of either KI or KIO3 without/with melatonin (5 mM). As melatonin was not effective against KI-induced LPO, in the next step only KIO3 was used. Homogenates were incubated in presence of KIO3 (200; 100; 50; 25; 20; 15; 10; 7.5; 5.0; 2.5; 1.25 mM) without/with melatonin or 17ß-estradiol. Five experiments were performed with different concentrations of melatonin (5.0; 2.5; 1.25; 1.0; 0.625 mM) and one with 17ß-estradiol (1.0 mM). Malondialdehyde + 4-hydroxyalkenals (MDA + 4-HDA) concentration (LPO index) was measured spectrophotometrically. KIO3 increased LPO with the strongest damaging effect (MDA + 4-HDA level: ≈1.28 nmol/mg protein, p < 0.05) revealed at concentrations of around 15 mM, thus corresponding to physiological iodine concentrations in the thyroid. Melatonin reduced LPO (MDA + 4-HDA levels: from ≈0.97 to ≈0,76 and from ≈0,64 to ≈0,49 nmol/mg protein, p < 0.05) induced by KIO3 at concentrations of 10 mM or 7.5 mM. Conclusion: Melatonin can reduce very strong oxidative damage to membrane lipids caused by KIO3 used in doses resulting in physiological iodine concentrations in the thyroid.

Oxidative injury associated with stenting of asymptomatic carotid artery stenosis

VASA ◽  
2017 ◽  
Vol 46 (4) ◽  
pp. 268-274
Author(s):  
Erhan Saraçoğlu ◽  
Ertan Vuruşkan ◽  
Yusuf Çekici ◽  
Salih Kiliç ◽  
Halil Ay ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Carotid Artery ◽  
Oxidative Damage ◽  
Carotid Artery Stenosis ◽  
Artery Stenosis ◽  
Oxidative Stress Marker ◽  
Asymptomatic Carotid ◽  
Imaging Methods ◽  
Neurological Findings ◽  
Asymptomatic Carotid Artery Stenosis

Abstract. Background: After carotid artery stenting (CAS), neurological complications that cannot be explained with imaging methods may develop. In our study we aimed to show, using oxidative stress markers, isolated oxidative damage and resulting neurological findings following CAS in patients with asymptomatic carotid artery stenosis. Patients and methods: We included 131 neurologically asymptomatic patients requiring CAS. The neurological findings were evaluated using the modified Rankin Scale (mRS) prior to the procedure, one hour post-procedure, and two days after. Patients with elevated mRS scores but with or without typical hyperintense lesions observed on an MRI and with changes of oxidative stress marker levels at the time (Δtotal-thiol, Δtotal antioxidative status [TAS], and Δtotal oxidant status [TOS]) were evaluated. Results: In the neurological examination carried out one hour prior to the procedure, there were 92 patients with mRS = 0, 20 with mRS = 1, and 12 with mRS = 2. When Δtotal-thiol, ΔTAS, and ΔTOS values and the mRS were compared, it was observed that as the difference in oxidative parameters increased, clinical deterioration also increased proportionally (p = 0.001). Conclusions: We demonstrate a possible correlation between oxidative damage and neurological findings after CAS which could not be explained by routine imaging methods.

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