Metal Ion Catalyzed Autoxidation Reactions: Kinetics and Mechanisms

Fábián, István; Csordás, Viktor

doi:10.1016/s0898-8838(03)54008-9

Cited by 19 publications

(5 citation statements)

References 157 publications

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“…for ALS [1640], atherosclerosis [106,764], cardiovascular disease [1641-1645], neuroprotection [1646], macular degeneration [1647], pre-eclampsia [1648-1652], critical care medicine [1653], aging [1165,1168,1654,1655], lung disease [1656], elective surgery involving ischaemia-reperfusion [1657], all-cause mortality [1637,1658], etc. One interpretation for these disappointing results, that is consistent with the general theme of this review, involves the recognition that a variety of anti oxidants can in fact act as pro -oxidants and thus actually promote the production of OH • radicals in the presence of inappropriately or inadequately liganded Fe(II) [130,528,1602,1604,1659,1660]. (One might also comment that the intracellular location of the anti oxidants may be an issue, and that the view that targeting them to mitochondria may well have considerable merit [1661-1663]. )…”

Section: Antioxidants As Therapeutic Agents? Should We Be Including Imentioning

confidence: 57%

Iron behaving badly: inappropriate iron chelation as a major contributor to the aetiology of vascular and other progressive inflammatory and degenerative diseases

2009

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Background: The production of peroxide and superoxide is an inevitable consequence of aerobic metabolism, and while these particular 'reactive oxygen species' (ROSs) can exhibit a number of biological effects, they are not of themselves excessively reactive and thus they are not especially damaging at physiological concentrations. However, their reactions with poorly liganded iron species can lead to the catalytic production of the very reactive and dangerous hydroxyl radical, which is exceptionally damaging, and a major cause of chronic inflammation.

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Section: Antioxidants As Therapeutic Agents? Should We Be Including Imentioning

confidence: 57%

Iron behaving badly: inappropriate iron chelation as a major contributor to the aetiology of vascular and other progressive inflammatory and degenerative diseases

2009

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“…While phlebotomy is a very traditional nostrum, often assumed or considered to have rather dubious or at best modest scientific support, there is in fact increasing literature implying its benefits in a variety of conditions (e.g. Aigner et al 2008 ; Beutler 2007 ; Broedbaek et al 2009 ; Brudevold et al 2008 ; Busca et al 2010 ; DePalma et al 2007 , 2010 ; Dereure et al 2008 ; Desai et al 2008 ; Dwyer et al 2009 ; Equitani et al 2008 ; Facchini et al 2002 ; Fargion et al 2002 ; Fernández-Real et al 2002 ; Fujita et al 2009 ; Fujita and Takei 2007 ; Hayashi et al 2006 ; Hayashi and Yano 2002 ; Heathcote 2004 ; Horwitz and Rosenthal 1999 ; Hua et al 2001 ; Kaito 2007 ; Kaito et al 2006 ; Kato et al 2001 , 2007 ; Kom et al 2006 ; Rajpathak et al 2009 ; Sullivan 2009 ; Sumida et al 2009 ; Tanaka et al 2007 , 2009 ; Toyokuni 2009b ; Zacharski et al 2008 ). Plausibly such benefits are due to its role in decreasing iron stores.…”

Section: Catalytic Behaviour Of Polypeptides and Proteinsmentioning

confidence: 99%

“…Anaemia can be caused by poor liganding as well as by an actual shortage of ‘iron’ itself . Note too that partial chelation in the presence of an antioxidant agent such as ascorbate (vitamin C) can in fact make ascorbate (or other reducing agent) act as a pro -oxidant and thus actually promote the production of OH • radicals in the presence of inappropriately or inadequately liganded Fe(II) (Allen and Cornforth 2009 ; Fábián and Csordás 2003 ; Halliwell 2009 ; Hininger et al 2005 ; Lachili et al 2001 ; Long et al 2000 ; Miller et al 1990 ; Reif 1992 ; Sugihara et al 1999 ). This very likely explains the often and indeed surprisingly disappointing clinical results obtained when using antioxidants alone (Bjelakovic et al 2008 ; Giustarini et al 2009 ; Kell 2009a ; Miller et al 2005 ).…”

Section: Introductionmentioning

confidence: 99%

Towards a unifying, systems biology understanding of large-scale cellular death and destruction caused by poorly liganded iron: Parkinson’s, Huntington’s, Alzheimer’s, prions, bactericides, chemical toxicology and others as examples

2010

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Exposure to a variety of toxins and/or infectious agents leads to disease, degeneration and death, often characterised by circumstances in which cells or tissues do not merely die and cease to function but may be more or less entirely obliterated. It is then legitimate to ask the question as to whether, despite the many kinds of agent involved, there may be at least some unifying mechanisms of such cell death and destruction. I summarise the evidence that in a great many cases, one underlying mechanism, providing major stresses of this type, entails continuing and autocatalytic production (based on positive feedback mechanisms) of hydroxyl radicals via Fenton chemistry involving poorly liganded iron, leading to cell death via apoptosis (probably including via pathways induced by changes in the NF-κB system). While every pathway is in some sense connected to every other one, I highlight the literature evidence suggesting that the degenerative effects of many diseases and toxicological insults converge on iron dysregulation. This highlights specifically the role of iron metabolism, and the detailed speciation of iron, in chemical and other toxicology, and has significant implications for the use of iron chelating substances (probably in partnership with appropriate anti-oxidants) as nutritional or therapeutic agents in inhibiting both the progression of these mainly degenerative diseases and the sequelae of both chronic and acute toxin exposure. The complexity of biochemical networks, especially those involving autocatalytic behaviour and positive feedbacks, means that multiple interventions (e.g. of iron chelators plus antioxidants) are likely to prove most effective. A variety of systems biology approaches, that I summarise, can predict both the mechanisms involved in these cell death pathways and the optimal sites of action for nutritional or pharmacological interventions.

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“…The kinetics and mechanisms of metal-catalyzed autoxidation reactions, including Mn systems, have been recently reviewed . Aerobic catechol oxidation catalysis has been reported by Funabiki et al for a bis(μ-oxo)dimanganese(III,III) complex via a manganese(II) semiquinonato intermediate …”

Section: Introductionmentioning

confidence: 99%

Biomimetic Oxidation of 3,5-Di-tert-butylcatechol by Dioxygen via Mn-Enhanced Base Catalysis

et al. 2006

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The 6-coordinate dioximatomanganese(II) complex [Mn(HL)(CH3OH)]+ (2, where H2L is [HON=C(CH3)C(CH3)=NCH2CH2]2NH), formed by instant solvolysis of [Mn2(HL)2](BPh4)2 (1) in methanol, accelerates the triethylamine (TEA)-catalyzed oxidation of 3,5-di-tert-butylcatechol (H2dtbc) by O2 to the corresponding o-benzoquinone. Significantly, 2 alone has no catalytic effect. The observed rate increase can be explained by the interaction of 2 with the hydroperoxo intermediate HdtbcO2- formed from Hdtbc- and O2 in the TEA-catalyzed oxidation. The kinetics of the TEA-catalyzed and Mn-enhanced reaction has been studied by gas-volumetric monitoring of the amount of O2 consumed. The initial rate of O2 uptake (V(in)) shows a first-order dependence on the concentration of 2 and O2 and saturation kinetics with respect to both H2dtbc and TEA. The observed kinetic behavior is consistent with parallel TEA-catalyzed and Mn-enhanced oxidation paths. The 3,5-di-tert-butylsemiquinone anion radical is an intermediate detectable by electron spin resonance (ESR) spectroscopy. The dimeric catalyst precursor has been characterized by X-ray diffraction and electrospray ionization mass spectrometry and the monomeric catalyst by ESR spectroscopy.

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Metal Ion Catalyzed Autoxidation Reactions: Kinetics and Mechanisms

Cited by 19 publications

References 157 publications

Iron behaving badly: inappropriate iron chelation as a major contributor to the aetiology of vascular and other progressive inflammatory and degenerative diseases

Iron behaving badly: inappropriate iron chelation as a major contributor to the aetiology of vascular and other progressive inflammatory and degenerative diseases

Towards a unifying, systems biology understanding of large-scale cellular death and destruction caused by poorly liganded iron: Parkinson’s, Huntington’s, Alzheimer’s, prions, bactericides, chemical toxicology and others as examples

Biomimetic Oxidation of 3,5-Di-tert-butylcatechol by Dioxygen via Mn-Enhanced Base Catalysis

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