Inhibition of lipid peroxidation by a novel compound (CV-2619) in brain mitochondria and mode of action of the inhibition

Suno, Masahiro; Nagaoka, Akinobu

doi:10.1016/0006-291x(84)91389-5

Cited by 89 publications

(43 citation statements)

References 19 publications

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“…This could be one of the explanations for vitamin E-induced increase in cellular energy levels upon hypoglycemia-like conditions. Similarly, idebenone incorporates easily in the membranes and was also proposed to interfere with lipid peroxidation in brain mitochondria [49]. Neither vitamin E or idebenone influenced significantly the formation of intracellular ROS (Table 2 or 3), that may be explained by scavenging properties of these lipophilic antioxidants at the membrane level and not in the aqueous medium, where oxidation of DCFH 2 or DHR 123 takes place.…”

Section: Formation Of Ros and Protection By Vitamin E And Idebenonementioning

confidence: 99%

“…Idebenone, a benzoquinone derivative, seems to act both as a lipid radical scavenger and as an electron trapping agent. The antioxidant properties of idebenone were determined by the inhibition of lipid peroxidation through its free radical scavenger activity [49]. Furthermore, the protective effects of idebenone are also attributed to an improvement in cerebral energy metabolism [50,51].…”

Section: Formation Of Ros and Protection By Vitamin E And Idebenonementioning

confidence: 99%

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Influence of the antioxidants vitamin E and idebenone on retinal cell injury mediated by chemical ischemia, hypoglycemia, or oxidative stress

Rego

Santos

Oliveira

1999

Free Radical Biology and Medicine

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Abstract-A role for the antioxidants vitamin E and idebenone in decreasing retinal cell injury, after metabolic inhibition induced by chemical ischemia and hypoglycemia, was investigated and compared with oxidative stress conditions. Preincubation of the antioxidants, vitamin E (20 M) and idebenone (10 M), effectively protected from retinal cell injury after oxidative stress or hypoglycemia, whereas the protection afforded after postincubation of both antioxidants was decreased. Delayed retinal cell damage, mediated by chemical ischemia, was attenuated at 10 or 12 h postischemia, only after exposure to the antioxidants during all the experimental procedure. An antagonist of the N-methyl-D-aspartate (NMDA) receptors, an inhibitor of nitric oxide synthase (NOS) or a blocker of L-type Ca 2ϩ channels were ineffective in reducing cell injury induced by chemical ischemia, hypoglycemia or oxidative stress. Oxidative stress and hypoglycemia increased (about 1.2-fold) significantly the fluorescence of the probe DCFH 2 -DA, that is indicative of intracellular ROS formation. Free radical generation detected with the probe dihydrorhodamine 123 (DHR 123) was enhanced after oxidative stress, chemical ischemia or hypoglycemia (about 2-fold). Nevertheless, the antioxidants vitamin E or idebenone were ineffective against intracellular ROS generation. Cellular energy charge decreased greatly after chemical ischemia, was moderately affected after hypoglycemia, but no significant changes were observed after oxidative stress. Preincubation with vitamin E prevented the changes in energy charge upon 6 h posthypoglycemia. We can conclude that irreversible changes occurring during chemical ischemia mainly reflect the alterations taking place at the ischemic core, whereas hypoglycemia situations may reflect changes occurring at the penumbra area, whereby vitamin E or idebenone may help to increase cell survival, exerting a beneficial neuroprotective effect.

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Section: Formation Of Ros and Protection By Vitamin E And Idebenonementioning

confidence: 99%

Section: Formation Of Ros and Protection By Vitamin E And Idebenonementioning

confidence: 99%

Influence of the antioxidants vitamin E and idebenone on retinal cell injury mediated by chemical ischemia, hypoglycemia, or oxidative stress

Rego

Santos

Oliveira

1999

Free Radical Biology and Medicine

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“…The benzoquinone ring participates in redox reactions. Idebenone is able to function as an antioxidant by inhibition of lipid peroxidation and protection of cell membranes and mitochondria from oxidative stress [81][82][83]. It is also able to interact with the respiratory chain and electron balance in the mitochondria [76,84].…”

Section: Idebenonementioning

confidence: 99%

Clinical and pharmacological aspects of bath salt use: A review of the literature and case reports

Miotto¹,

Striebel²,

Cho

et al. 2013

Drug and Alcohol Dependence

121

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Abstract:Reactive oxygen species (ROS) are widely believed to cause or aggravate several human pathologies such as neurodegenerative diseases, cancer, stroke and many other ailments. Antioxidants are assumed to counteract the harmful effects of ROS and therefore prevent or treat oxidative stress-related diseases. In this report, recent human studies exploring the efficiency of antioxidants in prevention and treatment of various diseases are reviewed. Few antioxidants including edaravone (for ischemic stroke in Japan), Nacetylcysteine (for acetaminophen toxicity), alfa-lipoic acid (for diabetic neuropathy) and some flavonoids (polyphenolic compounds present in dietary plants), such as micronized purified flavonoid fraction (diosmin and hesperidin) and oxerutins (for chronic venous insufficiency) as well as baicalein and catechins (for osteoarthritis) have found accepted clinical use. However, despite much enthusiasm in the 1980s and 1990s, many well-known agents such as antioxidant vitamins and also more recently developed compounds such as nitrones have not successfully passed the scrutiny of clinical trials for prevention and treatment of various diseases. This has given rise to a pessimistic view of antioxidant therapy, however, the evidence from human epidemiological studies about the beneficial effects of dietary antioxidants and preclinical in vitro and animal data are compelling. We have probably wasted too much time on agents like antioxidant vitamins instead of focusing on more disease specific, target-directed, highly bioavailable antioxidants. We here discuss possible reasons for the lack of success in some clinical trials and seek to provide some suggestions to be considered if antioxidant therapy is to succeed as an effective therapeutic strategy.

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“…DPI is known to inhibit NADPH oxidase (29) but could also affect mitochondrial complex I (36). However, rotenone, which inhibits mitochondrial complex I (26) and TTFA (mitochondrial complex II inhibitor (27)), had no effect. Myxothiazol and antimycin A (complex III inhibitors (28)) were able to suppress the effect of NS3 on human monocytic cells.…”

Section: Calcium Inflow Tyrosine Kinases and P38 Are Involved In P47mentioning

confidence: 99%

Nonstructural 3 Protein of Hepatitis C Virus Triggers an Oxidative Burst in Human Monocytes via Activation of NADPH Oxidase

Bureau

Bernad

Chaouche

et al. 2001

Journal of Biological Chemistry

147

121

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It has been shown that oxidative stress occurs in chronic hepatitis C. Release of reactive oxygen species (ROS) from sequestered phagocytes and activated resident macrophages represents the predominant component of oxidative stress in the liver. However, little is known about the ability of the monocyte to produce ROS in response to protein of hepatitis C virus. In this study, we investigated the ROS production in human monocytes stimulated by several viral proteins of hepatitis C virus. Human monocytes from healthy blood donors were incubated with recombinant viral protein: Core, NS3, NS4, and NS5. ROS production was measured by chemiluminescence. Only NS3 triggered ROS production in human monocytes. Generated ROS were mainly the anion superoxide. NS3 also induced a rapid and transient increase in intracellular calcium concentration measured by a video digital microscopy technique. By using different metabolic inhibitors, we showed that ROS production requires calcium influx, tyrosine kinases, and the stress-activated protein kinase, p38. The study of p47 PHOX phosphorylation and translocation showed that NADPH oxidase was activated and involved in ROS production induced by NS3. In a second experiment, NS3 inhibited the oxidative burst induced by phorbol 12-myristate 13-acetate. These results indicate that NS3 activates NADPH oxidase and modulates ROS production, which may be involved in the natural history of hepatitis C infection.

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Inhibition of lipid peroxidation by a novel compound (CV-2619) in brain mitochondria and mode of action of the inhibition

Cited by 89 publications

References 19 publications

Influence of the antioxidants vitamin E and idebenone on retinal cell injury mediated by chemical ischemia, hypoglycemia, or oxidative stress

Influence of the antioxidants vitamin E and idebenone on retinal cell injury mediated by chemical ischemia, hypoglycemia, or oxidative stress

Clinical and pharmacological aspects of bath salt use: A review of the literature and case reports

Nonstructural 3 Protein of Hepatitis C Virus Triggers an Oxidative Burst in Human Monocytes via Activation of NADPH Oxidase

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