The iron chelator pyridoxal isonicotinoyl hydrazone inhibits mitochondrial lipid peroxidation induced by Fe(II)–citrate

2001 ◽  
Vol 428 (1) ◽  
pp. 37-44 ◽  
Author(s):  
Natacha C.F Santos ◽  
Roger F Castilho ◽  
André R Meinicke ◽  
Marcelo Hermes-Lima
Keyword(s):  
Lipid Peroxidation ◽  
Iron Chelator ◽  
Pyridoxal Isonicotinoyl Hydrazone ◽  
Mitochondrial Lipid

Oxygen free radical-mediated selective endothelial dysfunction in isolated coronary artery

1992 ◽  
Vol 262 (3) ◽  
pp. H806-H812 ◽  
Author(s):  
K. Todoki ◽  
E. Okabe ◽  
T. Kiyose ◽  
T. Sekishita ◽  
H. Ito
Keyword(s):  
Lipid Peroxidation ◽  
Superoxide Dismutase ◽  
Free Radicals ◽  
Free Radical ◽  
Coronary Artery ◽  
Iron Chelator ◽  
Oxygen Free Radical ◽  
Alpha Tocopherol ◽  
Endothelium Dependent Relaxation ◽  
Iron Chelator Deferoxamine

To understand the direct involvement of free radicals causing reduction in endothelium-dependent relaxation of isolated canine coronary ring preparations, this study was undertaken to examine the effect of free radicals generated from dihydroxy fumarate (DHF) plus Fe(3+)-ADP or from H2O2 plus FeSO4. The vasodilators (acetylcholine, bradykinin, A23187, and nitroglycerin) were given after DHF/Fe(3+)-ADP or H2O2/FeSO4 was removed from the organ chamber. The earlier DHF/Fe(3+)-ADP exposure produced an attenuation of the relaxation of the rings induced by acetylcholine, bradykinin, or A23187 but not of the relaxation induced by nitroglycerin. The observed effect of previous DHF/Fe(3+)-ADP exposure was significantly protected in the vessels isolated from the dogs treated with alpha-tocopherol. In the experiments for assessing the effect of various scavengers, 1O2 scavenger histidine or iron chelator deferoxamine effectively protected the attenuation induced by DHF/Fe(3+)-ADP exposure of the relaxation elicited by acetylcholine; superoxide dismutase (SOD), catalase, or dimethyl sulfoxide (DMSO) had no effect on this system. Furthermore, the relaxation elicited by acetylcholine, but not nitroglycerin, was significantly attenuated by the earlier exposure to .OH generated by Fenton's reagent (H2O2+FeSO4); the attenuation was significantly protected by DMSO. These results are consistent with the view that .OH, 1O2, and/or iron-dependent reactive species selectively damage endothelium-dependent relaxation as opposed to endothelium-independent relaxation in endothelium-intact coronary ring preparations. It is also postulated that lipid peroxidation may be responsible for this effect.

Mitochondrial Lipid Peroxidation in Lung Damage and Disease

2014 ◽  
pp. 117-139 ◽  
Author(s):  
Sainath R. Kotha ◽  
Travis O. Gurney ◽  
Miles U. Magalang ◽  
Thomas J. Hund ◽  
Abhay R. Satoskar ◽  
...  
Keyword(s):  
Lipid Peroxidation ◽  
Lung Damage ◽  
Mitochondrial Lipid

Effects of Lercanidipine on Fe2+-Induced Mitochondrial Lipid Peroxidation

1997 ◽  
Vol 29 (Sup 1) ◽  
pp. S63-S72 ◽  
Author(s):  
Palmira Bernocchi ◽  
Claudio Ceconi ◽  
Anna Cargnoni ◽  
Paolo Pedersini ◽  
Antonella Boraso ◽  
...  
Keyword(s):  
Lipid Peroxidation ◽  
Mitochondrial Lipid

Inhibition of Mitochondrial Lipid Peroxidation by Bakuchiol, a Meroterpene from Psoralea corylifolia

Planta Medica ◽  
2000 ◽  
Vol 66 (6) ◽  
pp. 569-571 ◽  
Author(s):  
Hiroyuki Haraguchi ◽  
Junji Inoue ◽  
Yukiyoshi Tamura ◽  
Kenji Mizutani
Keyword(s):  
Lipid Peroxidation ◽  
Psoralea Corylifolia ◽  
Mitochondrial Lipid

scholarly journals Loss ofPLA2G6leads to elevated mitochondrial lipid peroxidation and mitochondrial dysfunction

Brain ◽  
2015 ◽  
Vol 138 (7) ◽  
pp. 1801-1816 ◽  
Author(s):  
Kerri J. Kinghorn ◽  
Jorge Iván Castillo-Quan ◽  
Fernando Bartolome ◽  
Plamena R. Angelova ◽  
Li Li ◽  
...  
Keyword(s):  
Lipid Peroxidation ◽  
Mitochondrial Dysfunction ◽  
Mitochondrial Lipid

scholarly journals Hepatotoxic Manifestations of Arsenic Trioxide Loaded Poly (Lactide-co-Glycolide) Nanoparticles in Wistar Rat

2021 ◽  
Author(s):  
Yeshvandra Verma ◽  
Kavita Rana ◽  
Varsha Rani ◽  
Suresh VS Rana
Keyword(s):  
Lipid Peroxidation ◽  
Arsenic Trioxide ◽  
Human Health Risk ◽  
Wistar Rat ◽  
Point Of View ◽  
Glutathione S Transferase ◽  
Prime Concern ◽  
Different Types ◽  
Serum Transaminases ◽  
Mitochondrial Lipid

Abstract Present study reports on the hepatotoxic manifestations of arsenic trioxide loaded poly lactide-co-glycolide nanoparticles (As2O3-PLGA- NPs) in rats. As2O3-PLGA- NPs enhances the activity of serum transaminases. As2O3-PLGA-NPs are potential inducer of lipid peroxidation in mitochondria as well as microsomes. Mitochondrial lipid peroxidation was higher than the microsomal lipid peroxidation. CYP450 2E1 was lower in the liver of As2O3-PLGA- NPs treated rats in comparison to arsenic trioxide treated rats. GSH showed lower values than control rats and arsenic trioxide treated rats. Glutathione-S-transferase inhibited by arsenic trioxide, non significant increase was recorded in the liver of As2O3-PLGA- NPs treated rats. As2O3-PLGA- NPs readily accumulates in liver and induces peculiar histopathological changes viz. intracytoplasmic/intranuclear inclusions and apoptosis. Since As2O3-PLGA- NPs are being considered as a suitable chemo-preventive agent against different types of cancer, its toxicological properties are of prime concern from bio-safety point of view. Thus, present observations seem to be important from human health risk assessment point of view.

scholarly journals Hepatotoxic manifestations of arsenic trioxide loaded poly (lactide-co-glycolide) nanoparticles in wistar rat

2021 ◽  
Author(s):  
Yeshvandra Verma ◽  
Kavita Rana ◽  
Varsha Rani ◽  
S VS Rana
Keyword(s):  
Lipid Peroxidation ◽  
Arsenic Trioxide ◽  
Human Health Risk ◽  
Wistar Rat ◽  
Point Of View ◽  
Glutathione S Transferase ◽  
Prime Concern ◽  
Different Types ◽  
Serum Transaminases ◽  
Mitochondrial Lipid

Abstract Present study reports on the hepatotoxic manifestations of arsenic trioxide loaded poly lactide-co-glycolide nanoparticles (As2O3-PLGA- NPs) in rats. As2O3-PLGA- NPs enhances the activity of serum transaminases. As2O3-PLGA-NPs are potential inducer of lipid peroxidation in mitochondria as well as microsomes. Mitochondrial lipid peroxidation was higher than the microsomal lipid peroxidation. CYP450 2E1 was lower in the liver of As2O3-PLGA- NPs treated rats in comparison to arsenic trioxide treated rats. GSH showed lower values than control rats and arsenic trioxide treated rats. Glutathione-S-transferase inhibited by arsenic trioxide, non significant increase was recorded in the liver of As2O3-PLGA- NPs treated rats. As2O3-PLGA- NPs readily accumulates in liver and induces peculiar histopathological changes viz. intracytoplasmic/intranuclear inclusions and apoptosis. Since As2O3-PLGA- NPs are being considered as a suitable chemo-preventive agent against different types of cancer, its toxicological properties are of prime concern from bio-safety point of view. Thus, present observations seem to be important from human health risk assessment point of view.

Mechanisms of t-butyl hydroperoxide-induced toxicity to rabbit renal proximal tubules

1988 ◽  
Vol 255 (1) ◽  
pp. C28-C33 ◽  
Author(s):  
R. G. Schnellmann
Keyword(s):  
Lipid Peroxidation ◽  
Cell Death ◽  
Mitochondrial Dysfunction ◽  
Iron Chelator ◽  
Proximal Tubules ◽  
Butylated Hydroxytoluene ◽  
Specific Sequence ◽  
Lactate Dehydrogenase Activity ◽  
Renal Proximal Tubules ◽  
Butyl Hydroperoxide

This study examined the mechanisms of t-butyl hydroperoxide (TBHP)-induced oxidative injury to a suspension of rabbit renal proximal tubules. TBHP (0.25-1 mM) produced a specific sequence of intracellular events in the tubules. Initially, TBHP increased tubular glutathione disulfide content and lipid peroxidation. Subsequently, there was an increase in ouabain-sensitive oxygen consumption (indicative of an increase in intracellular sodium concentrations), mitochondrial dysfunction, and a decrease in glutathione content. Finally, cell death, as measured by a decrease in tubular retention of lactate dehydrogenase activity, began between 30 and 60 min. The toxicity was dependent on iron-mediated free radical formation, since the iron chelator, deferoxamine, and the antioxidants, promethazine, butylated hydroxytoluene, and dithiotreitol, prevented the lipid peroxidation, the mitochondrial dysfunction, and cell death. Further studies with the antioxidants provided evidence that lipid peroxidation plays an important role in TBHP toxicity in proximal tubules.

P.2.c.008 Increased mitochondrial lipid peroxidation in depression bipolar episode

2013 ◽  
Vol 23 ◽  
pp. S359-S360
Author(s):  
L. Jornada ◽  
A. Steckert ◽  
F. Scussel ◽  
G. Ferreira ◽  
E. Streck ◽  
...  
Keyword(s):  
Lipid Peroxidation ◽  
Mitochondrial Lipid
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