Oxidative Myocardial Injury and Cardiac-Derived Experimental Systems

Janero, David R.

doi:10.1016/b978-0-12-584552-6.50034-3

Cited by 4 publications

(8 citation statements)

References 175 publications

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“…In biological systems, oxidative stress carries with it the potential for polyunsaturated fatty acid peroxidation (Janero, 1990a). In heart-muscle tissue, as in the cardiomyocyte, polyunsaturated fatty acids are largely arachidonicacid esters of membrane phospholipid (Rogers, 1974;Janero and Burghardt, 1 9 8 9~) .…”

Section: H20-induced Degenerative Changes To Cardiomyocyte-membrane mentioning

confidence: 99%

“…Eagle's basal medium NJV'-diphenyl-l,4-phenylenediamine 5,5'-dithiobis-(2-nitrobenzoic acid) ethylene diaminetetraacetic acid reduced glutathione N-2-hydroxyethylpiperazine-N'-2'-ethanesulfonic acid high-pressure liquid chromatography hydrogen peroxide lactate dehydrogenase malondialdehyde nicotinamide adenine dinucleotide hydroxyl radical superoxide anion radical phosphate-buffered saline sodium dodecylsulfate superoxide dismutase thiobarbituric acid thiobarbituric acid-reactive substances trichloroacetic acid tris(hydroxymethy1)aminomethane reperfusion injury, the pathogenic relationships between individual species of partially reduced oxygen and cardiomyocyte necrosis remain obscure (Kloner et al, 1989;Janero, 1990a). Recent studies with heartmuscle tissue and isolated mammalian hearts ex vivo have provided compelling, albeit inferential, evidence that H,Oz is the primary form of partially reduced oxygen responsible for postischemic myocardial derangements (Meyers et al, 1985;Brown et al, 1989a,b;Konz et al, 1989;Kraemer et al, 1990;Shlafer et al, 1990).…”

Section: Abbreviationsmentioning

confidence: 99%

“…This report places particular emphasis on the degenerative changes in cardiomyocyte membranes with H,O,-induced oxidative stress and their pathogenic importance to irreversible cell injury. In these regards, alterations in membrane biochemistry and function have been observed under conditions of both tissue oxidative stress and cardiac ischemia-reperfusion, yet the role of such membrane derangements in the establishment of cardiomyocyte necrosis is a matter of considerable debate (Kloner et al, 1989;Janero, 1990a). Our results define a peroxidative mechanism for the pathogenesis of H,O,-.induced lethal cardiomyocyte injury involving the rapid transformation of H20, via iron-mediated reactions within the cardiomyocyte itself to products that initiate membrane lipid peroxidation.…”

Section: Abbreviationsmentioning

confidence: 99%

“…and the hydroxyl radical ('OH), and a nonradical inorganic hydroperoxide, hydrogen peroxide (HzOz) (Pryor, 1986). Tissue injury associated with partially-reduced oxygen reflects a state of "oxidative stress," under which bioactive oxidants present in excess of tissue detoxifying capabilities reach local levels sufficient to incite and promote tissue damage (Janero, 1990a). The myocardial content of partially-reduced oxygen increases dramatically with postischemic reperfusion of mammalian (Bolli et al, 1989) [including human (Davies et al, 199011 hearts.…”

mentioning

confidence: 99%

“…Species of partially-reduced oxygen are increasingly being implicated as causing tissue damage during myocardial ischemia-reperfusion (Kloner et al, 1989;Janero, 1990a). These nontetravalent reduction products of molecular oxygen are of two general types: "free radicals" containing an unpaired electron, such as the superoxide anion radical (O,?)…”

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confidence: 99%

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Hydrogen peroxide‐induced oxidative stress to the mammalian heart‐muscle cell (cardiomyocyte): Lethal peroxidative membrane injury

Janero¹,

Hreniuk²,

Sharif³

1991

Journal Cellular Physiology

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Oxidative stress induced by hydrogen peroxide (H2O2) may contribute to the pathogenesis of ischemic-reperfusion injury in the heart. For the purpose of investigating directly the injury potential of H2O2 on heart muscle, a cellular model of H2O2-induced myocardial oxidative stress was developed. This model employed primary monolayer cultures of intact, beating neonatal-rat cardiomyocytes and discrete concentrations of reagent H2O2 in defined, supplement-free culture medium. Cardiomyocytes challenged with H2O2 readily metabolized it such that the culture content of H2O2 diminished over time, but was not depleted. The consequent H2O2-induced oxidative stress caused lethal sarcolemmal disruption (as measured by lactate dehydrogenase release), and cardiomyocyte integrity could be preserved by catalase. During oxidative stress, a spectrum of cellular derangements developed, including membrane phospholipid peroxidation, thiol oxidation, consumption of the major chain-breaking membrane antiperoxidant (alpha-tocopherol), and ATP loss. No net change in the protein or phospholipid contents of cardiomyocyte membranes accompanied H2O2-induced oxidative stress, but an increased turnover of these membrane constituents occurred in response to H2O2. Development of lethal cardiomyocyte injury during H2O2-induced oxidative stress did not require the presence of H2O2 itself; a brief "pulse" exposure of the cardiomyocytes to H2O2 was sufficient to incite the pathogenic mechanism leading to cell disruption. Cardiomyocyte disruption was dependent upon an intracellular source of redox-active iron and the iron-dependent transformation of internalized H2O2 into products (e.g., the hydroxyl radical) capable of initiating lipid peroxidation, since iron chelators and hydroxyl-radical scavengers were cytoprotective. The accelerated turnover of cardiomyocyte-membrane protein and phospholipid was inhibited by antiperoxidants, suggesting that the turnover reflected molecular repair of oxidized membrane constitutents. Likewise, the consumption of alpha-tocopherol and the oxidation of cellular thiols appeared to be epiphenomena of peroxidation. Antiperoxidant interventions coordinately abolished both H2O2-induced lipid peroxidation and sarcolemmal disruption, demonstrating that an intimate pathogenic relationship exists between sarcolemmal peroxidation and lethal compromise of cardiomyocyte integrity in response to H2O2-induced oxidative stress. Although sarcolemmal peroxidation was causally related to cardiomyocyte disruption during H2O2-induced oxidative stress, a nonperoxidative route of H2O2 cytotoxicity was also identified, which was expressed in the complete absence of cardiomyocyte-membrane peroxidation. The latter mode of H2O2-induced cardiomyocyte injury involved ATP loss such that membrane peroxidation and cardiomyocyte disruption on the one hand and cellular de-energization on the other could be completely dissociated.(ABSTRACT TRUNCATED AT 400 WORDS)

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Section: H20-induced Degenerative Changes To Cardiomyocyte-membrane mentioning

confidence: 99%

Section: Abbreviationsmentioning

confidence: 99%

Section: Abbreviationsmentioning

confidence: 99%

mentioning

confidence: 99%

mentioning

confidence: 99%

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Hydrogen peroxide‐induced oxidative stress to the mammalian heart‐muscle cell (cardiomyocyte): Lethal peroxidative membrane injury

Janero¹,

Hreniuk²,

Sharif³

1991

Journal Cellular Physiology

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Hydrogen peroxide‐induced oxidative stress to the mammalian heart‐muscle cell (cardiomyocyte): Nonperoxidative purine and pyrimidine nucleotide depletion

Janero¹,

Hreniuk²,

Sharif³

1993

Journal Cellular Physiology

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Hydrogen peroxide (H2O2) overload may contribute to cardiac ischemia-reperfusion injury. We report utilization of a previously described cardiomyocyte model (J. Cell. Physiol., 149:347, 1991) to assess the effect of H2O2-induced oxidative stress on heart-muscle purine and pyrimidine nucleotides and high-energy phosphates (ATP, phosphocreatine). Oxidative stress induced by bolus H2O2 elicited the loss of cardiomyocyte purine and pyrimidine nucleotides, leading to eventual de-energization upon total ATP and phosphocreatine depletion. The rate and extent of ATP and phosphocreatine loss were dependent on the degree of oxidative stress within the range of 50 microM to 1.0 mM H2O2. At the highest H2O2 concentration, 5 min was sufficient to elicit appreciable cardiomyocyte high-energy phosphate loss, the extent of which could be limited by prompt elimination of H2O2 from the culture medium. Only H2O2 dismutation completely prevented ATP loss during H2O2-induced oxidative stress, whereas various free-radical scavengers and metal chelators afforded no significant ATP preservation. Exogenously-supplied catabolic substrates and glycolytic or tricarboxylic acid-cycle intermediates did not ameliorate the observed ATP and phosphocreatine depletion, suggesting that cardiomyocyte de-energization during H2O2-induced oxidative stress reflected defects in substrate utilization/energy conservation. Compromise of cardiomyocyte nucleotide and phosphocreatine pools during H2O2-induced oxidative stress was completely dissociated from membrane peroxidative damage and maintenance of cell integrity. Cardiomyocyte de-energization in response to H2O2 overload may constitute a distinct nonperoxidative mode of injury by which cardiomyocyte energy balance could be chronically compromised in the post-ischemic heart.

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Myocardial Ischemia–Reperfusion Injury and the Cardioprotective Potential of Natural Antioxidants

Janero¹

1994

Natural Antioxidants in Human Health and Disease

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Oxidative Myocardial Injury and Cardiac-Derived Experimental Systems

Cited by 4 publications

References 175 publications

Hydrogen peroxide‐induced oxidative stress to the mammalian heart‐muscle cell (cardiomyocyte): Lethal peroxidative membrane injury

Hydrogen peroxide‐induced oxidative stress to the mammalian heart‐muscle cell (cardiomyocyte): Lethal peroxidative membrane injury

Hydrogen peroxide‐induced oxidative stress to the mammalian heart‐muscle cell (cardiomyocyte): Nonperoxidative purine and pyrimidine nucleotide depletion

Myocardial Ischemia–Reperfusion Injury and the Cardioprotective Potential of Natural Antioxidants

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