Singlet oxygen-induced arrhythmias. Dose- and light-response studies for photoactivation of rose bengal in the rat heart.

Kusama, Yoshiki; Bernier, Michèle; Hearse, David J.

doi:10.1161/01.cir.80.5.1432

Cited by 58 publications

(27 citation statements)

References 28 publications

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“…An ischaemic period is followed by rapid re-oxygenation [225] and radical fluxes, as well as by potentially damaging leucocyte infiltration. Elegant systems for studying oxidative affronts to the heart and to cardiac cells have been developed, some using photosensitizers to localize oxidation, and\or to permit "O # production [226]. Thus, after perfusion of hearts with the photosensitizer Rose Bengal, subsequent illumination leads, within seconds, to alterations in membrane transport and arrhythmias [227].…”

Section: Oxidized Proteins and Toxicity To The Host Organismmentioning

confidence: 99%

Biochemistry and pathology of radical-mediated protein oxidation

Dean

Stocker

et al. 1997

Biochemical Journal

1,551

982

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Radical-mediated damage to proteins may be initiated by electron leakage, metal-ion-dependent reactions and autoxidation of lipids and sugars. The consequent protein oxidation is O2-dependent, and involves several propagating radicals, notably alkoxyl radicals. Its products include several categories of reactive species, and a range of stable products whose chemistry is currently being elucidated. Among the reactive products, protein hydroperoxides can generate further radical fluxes on reaction with transition-metal ions; protein-bound reductants (notably dopa) can reduce transition-metal ions and thereby facilitate their reaction with hydroperoxides; and aldehydes may participate in Schiff-base formation and other reactions. Cells can detoxify some of the reactive species, e.g. by reducing protein hydroperoxides to unreactive hydroxides. Oxidized proteins are often functionally inactive and their unfolding is associated with enhanced susceptibility to proteinases. Thus cells can generally remove oxidized proteins by proteolysis. However, certain oxidized proteins are poorly handled by cells, and together with possible alterations in the rate of production of oxidized proteins, this may contribute to the observed accumulation and damaging actions of oxidized proteins during aging and in pathologies such as diabetes, atherosclerosis and neurodegenerative diseases. Protein oxidation may also sometimes play controlling roles in cellular remodelling and cell growth. Proteins are also key targets in defensive cytolysis and in inflammatory self-damage. The possibility of selective protection against protein oxidation (antioxidation) is raised.

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Section: Oxidized Proteins and Toxicity To The Host Organismmentioning

confidence: 99%

Biochemistry and pathology of radical-mediated protein oxidation

Dean

Stocker

et al. 1997

Biochemical Journal

1,551

982

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“…Through the development of a perfusion chamber surrounded by an array of 200 fiber optic cables, it is possible to photosensitize rose bengal in situ and thereby study the dose and light dependency of the electrocardiographic consequences of bursts of oxidant stress under aerobic conditions. Using low (nanomolar) concentrations of rose bengal, we have demonstrated [57] extremely rapid electrocardiographic changes (they can occur in under 5 seconds), which lead to severe arrhythmias in less than 30 seconds.…”

Section: Reperfusion-induced Arrhythmiasmentioning

confidence: 99%

“…Recently, the author and his colleagues [54][55][56][57][58] have addressed the issue of the rapidity with which oxidant stress can induce electrophysiologic injury. This we have achieved by exploiting the photodynamic properties of rose bengal [59][60][61].…”

Section: Reperfusion-induced Arrhythmiasmentioning

confidence: 99%

Reperfusion-induced injury: A possible role for oxidant stress and its manipulation

Hearse

1991

Cardiovasc Drug Ther

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While some investigators recognize "reperfusion-induced injury" as an important component of the overall injury that occurs during ischemia and reperfusion, others question its existence. Resolution of this controversy is of considerable importance, particularly in an era of thrombolysis, since reperfusion-induced injury might be amenable to treatment. Although reperfusion is an absolute prerequisite for the recovery of ischemic tissue, it undoubtedly has some unfavorable effects. The identification of four (possibly sequential) components of reperfusion-induced injury helps to clarify the situation: a) Reperfusion after brief periods of ischemia can trigger arrhythmias in tissue that is potentially salvable; there is abundant experimental and clinical evidence for this form of reperfusion injury. b) Reperfusion may also be associated with "myocardial stunning"; however, given sufficient time, this prolonged postischemic contractile and metabolic dysfunction will recover. There is good experimental evidence and some clinical evidence for the existence of this type of reperfusion-induced injury. c) Reperfusion is commonly thought to cause lethal injury in cells that, until the time of reperfusion, were potentially salvable. However, conclusive evidence that reperfusion can kill cells does not yet exist. d) Reperfusion may alter the nature of necrotic processes in tissue that has already sustained lethal injury, while not altering the number of cells that die this may change the manner in which they die; this form of reperfusion injury could lead to differences in scar formation and vulnerability to aneurysm. There is considerable evidence for the existence of this form of reperfusion-induced injury. Many candidate mechanisms have been proposed for each form of reperfusion injury. Ionic disturbances (particularly for calcium) are often cited and, most recently, free radical-induced induced injury (oxidant stress) has been suggested as important. Considerable evidence exists that oxidant stress is involved in stunning and in reperfusion-induced arrhythmias, and characterization of underlying mechanisms might lead to novel therapeutic principles, such as antioxidant therapy. However, much remains to be learned.

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“…Other proposed causes of reperfusion arrhythmias include free radical formation, which could also mediate effects via an increase of cytosolic calcium. Kusama et al (1989) have shown that the rapid generation of singlet oxygen can cause arrhythmias in the isolated heart. At the same time, they have also shown that such singlet oxygen can damage the subcellular structures linking the sarcoplasmic reticulum with the T tubules, and the inference is that free radicals can act adversely on calcium cycles in the myocardium (Figure 1).…”

Section: Cytosolic Calcium On Reperfusionmentioning

confidence: 99%

“…Thereby excess cytosolic calcium is predisposed to, with the consequence of calcium-mediated arrhythmias. Direct proof of this hypothesis would await measurements of cytosolic calcium during the application of rapidly induced changes in free radical output, such as the induction of singlet oxygen arrhythmias (Kusama et al, 1989).…”

Section: Cytosolic Calcium On Reperfusionmentioning

confidence: 99%

Role of calcium and other ions in reperfusion injury

Opie

1991

Cardiovasc Drug Ther

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Calcium-related mechanisms may play a role in several aspects of reperfusion injury. One proposal is that internal cytosolic calcium concentration is elevated early in the reperfusion period and that excess oscillations of calcium can very significantly contribute to reperfusion ventricular arrhythmias. Alternate hypotheses, such as those involving free radicals and the local tissue renin-angiotensin system, can be married to the existing hypothesis. Furthermore, the hypothesis allows for a role of the sodium-calcium exchange system and the proton-sodium exchanger. The hypothesis also provides an explanation for "stunning," as it is proposed that early excessive cytosolic calcium damages the organelles regulating the contractile cycle, which subsequently develops into imperfect functioning of the contractile apparatus. Calcium antagonist drugs given during the ischemic period may lessen reperfusion injury by decreasing the severity of ischemic damage. When given at the time of reperfusion, results are complex and to some extent conflicting. The biggest challenge is to understand how relatively low doses of calcium antagonists given after the onset of reperfusion help to decrease delayed reperfusion "stunning." A logical but untested proposal is that calcium antagonists help to prevent delayed contraction-band necrosis, one of the causes of delayed no-reflow.

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Singlet oxygen-induced arrhythmias. Dose- and light-response studies for photoactivation of rose bengal in the rat heart.

Cited by 58 publications

References 28 publications

Biochemistry and pathology of radical-mediated protein oxidation

Biochemistry and pathology of radical-mediated protein oxidation

Reperfusion-induced injury: A possible role for oxidant stress and its manipulation

Role of calcium and other ions in reperfusion injury

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