Inhibition of the TPNH-linked lipid peroxidation of liver microsomes by drugs undergoing oxidative demethylation

1964 ◽  
Vol 14 (4) ◽  
pp. 329-334 ◽  
Author(s):  
Stan Orrenius ◽  
Gustav Dallner ◽  
Lars Ernster
Keyword(s):  
Lipid Peroxidation ◽  
Liver Microsomes ◽  
Oxidative Demethylation

Antioxidant and Antifungal Properties of Benzimidazole Derivatives

2010 ◽  
Vol 65 (9-10) ◽  
pp. 537-542 ◽  
Author(s):  
Canan Kuş ◽  
Fatma Sözüdönmez ◽  
Benay Can-Eke ◽  
Tülay Çoban
Keyword(s):  
Lipid Peroxidation ◽  
Free Radical ◽  
Radical Scavenging ◽  
Liver Microsomes ◽  
Thiobarbituric Acid ◽  
Benzimidazole Derivatives ◽  
Rat Liver Microsomes ◽  
Inhibitory Effects ◽  
Stable Free Radical ◽  
Radical Scavenging Properties

Antioxidant and radical scavenging properties of a series of 2-[4-(substituted piperazin-/ piperidin-1-ylcarbonyl)phenyl]-1H-benzimidazole derivatives were examined. Free radical scavenging properties of compounds 11-30 and 33 were evaluated for the stable free radical 2,2-diphenyl-1-picrylhydrazyl (DPPH) and superoxide anion radical. In addition the inhibitory effects on the NADPH-dependent lipid peroxidation levels were determined by measuring the formation of 2-thiobarbituric acid reactive substances (TBARS) using rat liver microsomes. Compound 33 which has a p-fluorobenzyl substitutent at position 1 exhibited the strongest inhibition (83%) of lipid peroxidation at a concentration of 10-3 M, while the nonsubstituted analogue 13 caused 57% inhibition. This result is fairly consistent with the antimicrobial activity results against both Staphylococcus aureus and Candida albicans.

scholarly journals Stimulation of lipid peroxidation and hydroxyl-radical generation by the contents of human atherosclerotic lesions

1992 ◽  
Vol 286 (3) ◽  
pp. 901-905 ◽  
Author(s):  
C Smith ◽  
M J Mitchinson ◽  
O I Aruoma ◽  
B Halliwell
Keyword(s):  
Lipid Peroxidation ◽  
Copper Ions ◽  
Liver Microsomes ◽  
Rat Liver Microsomes ◽  
Atherosclerotic Lesions ◽  
Arterial Lesions ◽  
Human Cadavers ◽  
Radical Generation ◽  
Almost All

Lipid peroxidation within human arterial lesions is thought to play an important role in the development of atherosclerosis. Peroxidation can be accelerated by the presence of ‘catalytic’ iron or copper ions. Gruel samples from advanced atherosclerotic lesions in the abdominal aortae of human cadavers were tested for pro-oxidant properties. All samples contained bleomycin-detectable iron and phenanthroline-detectable copper. Almost all gruel samples stimulated peroxidation of rat liver microsomes, and this was usually inhibited by the iron-ion chelator desferrioxamine. Some samples stimulated formation of hydroxyl radicals from H2O2 in the presence of ascorbate, a reaction again inhibited by desferrioxamine. We conclude that the interior of human advanced atherosclerotic lesions is a highly pro-oxidant environment, and that the use of copper or iron ions to promote peroxidation of low-density lipoproteins in vitro may be a valid model for events in the arterial wall.

Rat lung microsomal lipid peroxidation: effects of vitamin E and reduced glutathione

1986 ◽  
Vol 61 (2) ◽  
pp. 785-790 ◽  
Author(s):  
D. P. Franco ◽  
S. G. Jenkinson
Keyword(s):  
Lipid Peroxidation ◽  
Vitamin E ◽  
Liver Microsomes ◽  
Sulfhydryl Group ◽  
Rat Lung ◽  
Active Components ◽  
Microsomal Lipid Peroxidation ◽  
Microsomal Membranes ◽  
High Concentrations

Lung microsomal membranes that contain the redox active components associated with the mixed-function oxidase system can be peroxidized in vitro. To investigate the characteristics of rat lung microsomal lipid peroxidation, we performed experiments using a variety of peroxidation initiators and microsomes obtained from normal and vitamin E-deficient rats. We found that lung microsomes obtained from normal rats are peroxidized much less than liver microsomes obtained from the same animals. Only initiation systems using very high concentrations of ferrous iron produced any significant peroxidation of normal rat lung microsomes. Lung microsomes obtained from vitamin E-deficient rats were found to be much more susceptible to peroxidation. Glutathione (GSH) was effective in inhibiting peroxidation when lung microsomes from normal rats were peroxidized. GSH was not effective in decreasing peroxidation when microsomes from vitamin E-deficient rats were peroxidized in the same system. We conclude that both GSH and vitamin E protect lung microsomal membranes from peroxidation. Glutathione protection appears to be related to the presence of a sulfhydryl group.

Lipid Peroxidation and Cherniluminescence during Naproxen Metabolism in Rat Liver Microsomes

1994 ◽  
Vol 13 (12) ◽  
pp. 831-838 ◽  
Author(s):  
Hiroyuki Yokoyama ◽  
Toshiharu Horie ◽  
Shoji Awazu
Keyword(s):  
Lipid Peroxidation ◽  
Singlet Oxygen ◽  
Rat Liver ◽  
Liver Microsomes ◽  
Thiobarbituric Acid ◽  
Rat Liver Microsomes ◽  
Oxygen Species ◽  
Thiobarbituric Acid Reactive Substances ◽  
Microsomal Suspension ◽  
Weight Protein

1 Rat liver microsomal suspension containing NADPH and MgCl2 was incubated at 37°C with naproxen, a non-steroidal anti-inflammatory drug. Thiobarbituric acid reactive substances (TBA-RS), high molecular weight protein aggregates and fluorescent substances were formed in the microsomal suspension. 2 Chemiluminescence was produced from the microsomal suspension. This chemiluminescence production was well correlated to the TBA-RS formation, indicating that the chemiluminescence production was closely associated with the lipid peroxidation. 3 The addition of SKF-525A to the microsomal suspension inhibited the production of TBA-RS, chemiluminescence and 6-demethylnaproxen (6-DMN), the oxidative product of naproxen. Further, the antioxidant, α-tocopherol and singlet oxygen quenchers like histidine, dimethylfuran and 1,4-diazabicyclo[2,2,2]octane strikingly inhibited the productions of chemiluminescence and TBA-RS. 4 Neither naproxen nor 6-DMN caused lipid peroxidation in the absence of NADPH. Thus, lipid peroxidation and chemiluminescence during the oxidation of naproxen in liver microsomes was suggested to be provoked by reactive oxygen species and an origin of chemiluminescence was shown to be singlet oxygen.

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