Role of hydroxyl radical in superoxide induced microsomal lipid peroxidation: Protective effect of anion channel blocker

1996 ◽  
Vol 21 (1) ◽  
pp. 35-43 ◽  
Author(s):  
Salil K. Ghosh ◽  
Tapati Chakraborti ◽  
Arun B. Banerjee ◽  
Sujata Roychoudhury ◽  
Sajal Chakraborti
Keyword(s):  
Lipid Peroxidation ◽  
Protective Effect ◽  
Hydroxyl Radical ◽  
Channel Blocker ◽  
Anion Channel ◽  
Microsomal Lipid Peroxidation ◽  
Anion Channel Blocker

Protective Effect of Carvedilol on Paracetamol-induced Hepatotoxicity; Role of Modulation Inflammation and Lipid Peroxidation

2016 ◽  
Vol 13 (1) ◽  
pp. 33-43 ◽  
Author(s):  
Heba M. Mahmoud ◽  
Amira M. Abo-Yousse ◽  
Ali A. Abo-Saif
Keyword(s):  
Lipid Peroxidation ◽  
Protective Effect

The role of phospholipase A2 in microsomal lipid peroxidation induced with t-butyl hydroperoxide

1989 ◽  
Vol 158 (3) ◽  
pp. 1021-1028 ◽  
Author(s):  
Stephen M. Borowitz ◽  
Catherine Montgomery
Keyword(s):  
Lipid Peroxidation ◽  
Phospholipase A2 ◽  
Butyl Hydroperoxide ◽  
Microsomal Lipid Peroxidation

Antimalarial Drugs Exacerbate Rat Liver Microsomal Lipid Peroxidation in the Presence of Oxidants

2001 ◽  
Vol 21 (3) ◽  
pp. 353-359 ◽  
Author(s):  
E. Olatunde Farombi ◽  
Stanley Adoro ◽  
Samuel Uhunmwangho
Keyword(s):  
Lipid Peroxidation ◽  
Rat Liver ◽  
Lipid Hydroperoxide ◽  
Antimalarial Drugs ◽  
Oxygen Species ◽  
Radical Chain ◽  
Microsomal Lipid Peroxidation ◽  
Hydroperoxide Formation ◽  
Chain Breaking

The study was undertaken to evaluate the effect of prior treatment of rats with the antimalarial drugs amodiaquine (AQ) mefloquine (MQ) and halofantrine (HF) on rat liver microsomal lipid peroxidation in the presence of 1 mM FeSO4, 1 mM ascorbate and 0.2 mM H2O2 (oxidants). Ingestion of α-tocopheral, a radical chain-breaking antioxidant was also included to assess the role of antioxidants in the drug treatment. In the presence of oxidants AQ, MQ and HF elicited 288%, 175% and 225% increases in malondialdehyde (MDA) formation while the drugs induced 125%, 63% and 31% increases in the absence of oxidants respectively. Similarly, AQ, MQ and HF induced lipid hydroperoxide formation by 380%, 256%, 360% respectively in the presence of oxidants and 172%, 136% and 92% in the absence of exogenously added oxidants respectively. α-tocopherol reduced AQ, MQ and HF-induced MDA formation by 40%, 55% and 52% respectively and lipid hydroperoxide formation by 53%, 59% and 54% respectively. Similarly, α-tocopherol attenuated the AQ, MQ and HF-induced MDA formation by 49%, 51% and 51% in the presence of oxidants and lipid hydroperoxide formation by 61%, 62% and 47% respectively. The results indicate that rat liver microsomal lipid peroxidation could be enhanced by antimalarial drugs in the presence of reactive oxygen species and this effect could be ameliorated by treatment with antioxidants.

Role of cytochrome P-450 in CCl4-induced microsomal lipid peroxidation

1978 ◽  
Vol 27 (15) ◽  
pp. 1983-1985 ◽  
Author(s):  
Yasusuke Masuda ◽  
Tadashi Murano
Keyword(s):  
Lipid Peroxidation ◽  
Microsomal Lipid Peroxidation ◽  
Cytochrome P 450

scholarly journals Neuroprotective effects of volume-regulated anion channel blocker DCPIB on neonatal hypoxic-ischemic injury

2012 ◽  
Vol 34 (1) ◽  
pp. 113-118 ◽  
Author(s):  
Ammar Alibrahim ◽  
Li-yan Zhao ◽  
Christine You-jin Bae ◽  
Andrew Barszczyk ◽  
Christopher Lf Sun ◽  
...  
Keyword(s):  
Channel Blocker ◽  
Ischemic Injury ◽  
Anion Channel ◽  
Neuroprotective Effects ◽  
Anion Channel Blocker ◽  
Hypoxic Ischemic Injury

scholarly journals Anion Channel Blockers Inhibit the Acrosome Reaction of Echinoderm Sperm. (anion channel blocker/acrosome reaction/acid release/stafish/sea urchin)

1985 ◽  
Vol 27 (4) ◽  
pp. 461-468 ◽  
Author(s):  
ICHIRO NISHIYAMA ◽  
HAJIME SASAKI ◽  
TAEI MATSUI ◽  
MOTONORI HOSHI
Keyword(s):  
Sea Urchin ◽  
Acrosome Reaction ◽  
Channel Blocker ◽  
Anion Channel ◽  
Channel Blockers ◽  
Acid Release ◽  
Anion Channel Blocker

scholarly journals Melatonin Inhibits Benzene-Induced Lipid Peroxidation in Rat Liver

2010 ◽  
Vol 61 (1) ◽  
pp. 11-18 ◽  
Author(s):  
Seema Sharma ◽  
Suresh Rana
Keyword(s):  
Lipid Peroxidation ◽  
Single Dose ◽  
Rat Liver ◽  
Treated Group ◽  
Melatonin Treatment ◽  
Liver Histopathology ◽  
Microsomal Lipid Peroxidation ◽  
Significant Difference ◽  
Mitochondrial Lipid

Melatonin Inhibits Benzene-Induced Lipid Peroxidation in Rat LiverWe studied the antioxidative role of melatonin against benzene toxicity in rat liver. The inhibition of mitochondrial and microsomal lipid peroxidation differed between 24-hour (single-dose), 15-day, and 30-day treatments. Inhibition of mitochondrial lipid peroxidation was the highest after the single dose of melatonin, whereas highest microsomal inhibition was recorded after 30 days of melatonin treatment. No significant difference was recorded between 15-day and 30-day treatments. Cytochrome P 4502E1 (CYP 4502E1) activity declined after the single-dose and 15-day melatonin treatment in the benzene-treated group, but it rose again, though not significantly after 30 days of treatment. Liver histopathology generally supported these findings. Phenol concentration in the urine samples declined in melatonin and benzene-treated rats. Our results show that melatonin affects CYP 4502E1, which is responsible for benzene metabolism. Inhibition of its metabolism correlated with lower lipid peroxidation. In conclusion, melatonin was found to be protective against lipid peroxidation induced by benzene.

Distinct Ca2+- and cAMP-dependent anion conductances in the apical membrane of polarized T84 cells

1998 ◽  
Vol 275 (2) ◽  
pp. C484-C495 ◽  
Author(s):  
Didier Merlin ◽  
Lianwei Jiang ◽  
Gregg R. Strohmeier ◽  
Asma Nusrat ◽  
Seth L. Alper ◽  
...  
Keyword(s):  
Channel Blocker ◽  
Apical Membrane ◽  
Anion Channel ◽  
Epithelial Cell Line ◽  
T84 Cells ◽  
Cell Monolayers ◽  
Anion Conductance ◽  
Anion Selectivity ◽  
Colonic Epithelial Cell Line ◽  
Anion Channel Blocker

Monolayers of the human colonic epithelial cell line T84 exhibit electrogenic Cl− secretion in response to the Ca2+ agonist thapsigargin and to the cAMP agonist forskolin. To evaluate directly the regulation of apical Cl−conductance by these two agonists, we have utilized amphotericin B to permeabilize selectively the basolateral membranes of T84 cell monolayers. We find that apical anion conductance is stimulated by both forskolin and thapsigargin but that these conductances are differentially sensitive to the anion channel blocker DIDS. DIDS inhibits thapsigargin-stimulated responses completely but forskolin responses only partially. Furthermore, the apical membrane anion conductances elicited by these two agonists differ in anion selectivity (for thapsigargin, I− > Cl−; for forskolin, Cl− > I−). However, the DIDS-sensitive component of the forskolin-induced conductance response exhibits anion selectivity similar to that induced by thapsigargin (I− > Cl−). Thus forskolin-induced apical anion conductance comprises at least two components, one of which has features in common with that elicited by thapsigargin.

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