Superoxide generation by NADPH-cytochrome P-450 reductase: The effect of iron chelators and the role of superoxide in microsomal lipid peroxidation

Morehouse, Lee A.; Thomas, Craig E.; Aust, Steven D.

doi:10.1016/0003-9861(84)90552-6

Cited by 147 publications

(38 citation statements)

References 42 publications

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“…Disassociation of lipid peroxidation from hydroxyl radical generation has been observed by others [6,7,26]. Shaw et al [18] actually found an inverse relationship between lipid peroxidation and hydroxyl radical generation by mi~rosomes from ethanolfed rats.…”

Section: Resultsmentioning

confidence: 76%

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Effect of chronic ethanol consumption on microsomal lipid peroxidation

Krikun

Cederbaum

1986

FEBS Letters

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Microsomes isolated from chronic ethanol-fed rats displayed elevated rates of malondialdehyde production when compared to pair-fed controls, but lower rates when compared to chow-fed controls. These differences did not correlate with total content of cytochrome P-450 or activity of NADPH-cytochrome c reductase. Titration curves with the potent iron-chelating agent desferrioxamine revealed that the content of iron was greater in microsomes from the chow-fed and lowest in microsomes from the pair-fed control. However, other variables must also exist since even when excess iron was added to the microsomes, the order of malondialdehyde production remained chow-fed > chronic ethanol > pair-fed control. The variabilities associated with the different controls and the role and content of transition metals such as iron probably contribute towards the divergent effects of ethanol on lipid peroxidation. Lipidperoxidation Iron

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Section: Resultsmentioning

confidence: 76%

“…Carbon monoxide (2:l with respect to 02) did not inhibit malondialdehyde production in any of the microsomal preparations (not shown). The detailed studies of Aust and coworkers [6,7,26] have emphasized the importance of the reductase, and not-P-450, in microsomal lipid peroxidation.…”

Section: Resultsmentioning

confidence: 99%

Effect of chronic ethanol consumption on microsomal lipid peroxidation

Krikun

Cederbaum

1986

FEBS Letters

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“…[10][11][12] In particular, the induction of CYP1A1 leads to excessive generation of reactive oxygen species as a result of the depletion of cellular antioxidants. 13,14) A number of antioxidants have been tested as possible protectors against TCDD toxicity. Most notably, the protective effects of vitamins A and E have been demonstrated in experiments using TCDD-sensitive C57BL/6J female mice.…”

mentioning

confidence: 99%

Protective Effects of Tea Melanin against 2,3,7,8-Tetrachlorodibenzo-p-dioxin-Induced Toxicity: Antioxidant Activity and Aryl Hydrocarbon Receptor Suppressive Effect

Hung

Huang

Sava

et al. 2006

Biological & Pharmaceutical Bulletin

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We examined the protective ability of tea melanin against 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD)-induced toxicity in C57BL6J mice. Reduced tea melanin (RTM) and non-reduced tea melanin (NRTM) were incorporated to distinguish anti-oxidant activity from alternative pathways. The mice were given a single oral dose of TCDD (100 m mg/kg body weight) and then they were administered daily with NRTM or RTM (40 mg/kg, p.o.) for next 14 d. RTM protected the animals against TCDD-induced lipid peroxidation, inhibition of glutathione peroxidase, alteration in reduced and oxidized glutathione concentrations, loss of body weight, and increased relative liver weight. NRTM was less effective as compared to RTM because of its inferior antioxidant activity, but it still displayed a strong protective effect against TCDD toxicity owing to its similar suppression of the activity of the aryl hydrocarbon receptor. Both NRTM and RTM suppressed the expression of CYP1A1 gene and prevented the activation of cytochrome P450 isozyme in the livers of animals exposed to TCDD. These results suggest that tea melanin might be a potential agent offering dual protection against the development of TCDD-induced oxidative stress.

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“…Interruption of the CYP catalytic cycle after passage of the first electron results in OT• release and after passage of the second electron results in H202 release (Parkinson, 1996). OT• also can be produced by cytochrome P450 reductase (Aust et al, 1972;Morehouse et al, 1984).…”

Section: Polychlorinated Biphenylsmentioning

confidence: 99%

“…Neutrophils can be activated by PCBs, but only by ortho-substituted PCBs (Ganey et al, 1993). Finally, NADPHcytochrome P450 reductase can be induced by pHAH (Manjunath and Dufresne, 1988) and is a known source of ROS (Morehouse et al, 1984). While CYPlA is implicated as the source of ROS in in vitro studies, alterations in mitochondrial activities or reductase activity may contribute to the oxidative stress stimulated by more highly chlorinated pHAHs in vivo.…”

Section: Cyp Ia and Oxidative Stress In Vivomentioning

confidence: 99%

Involvement of Cytochrome P450 1A in the toxicity of aryl hydrocarbon receptor agonists : alteration arachidonic acid metabolism and production of reactive oxygen species

Schlezinger¹

1998

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Superoxide generation by NADPH-cytochrome P-450 reductase: The effect of iron chelators and the role of superoxide in microsomal lipid peroxidation

Cited by 147 publications

References 42 publications

Effect of chronic ethanol consumption on microsomal lipid peroxidation

Effect of chronic ethanol consumption on microsomal lipid peroxidation

Protective Effects of Tea Melanin against 2,3,7,8-Tetrachlorodibenzo-p-dioxin-Induced Toxicity: Antioxidant Activity and Aryl Hydrocarbon Receptor Suppressive Effect

Involvement of Cytochrome P450 1A in the toxicity of aryl hydrocarbon receptor agonists : alteration arachidonic acid metabolism and production of reactive oxygen species

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