2,3-Butanedione monoxime does not protect cardiomyocytes under oxidative stress

Przygodzki, Tomasz; Лапшина, Е. А.; Заводник, И. Б.; Sokal, Adam; Bryszewska, Maria

doi:10.1002/cbf.1277

Cited by 4 publications

(1 citation statement)

References 34 publications

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“…Peculiarly, the caspase 3 activity showed an intermediate activity with the LIRM solution compared to the two other solutions. None of the solutions demonstrated cytotoxicity in cell culture, a finding that is not often reported in the literature regarding cardioplegic solutions [ 15 , 16 ] .…”

Section: Discussionmentioning

confidence: 99%

Development of cardioplegic solution without potassium: experimental study in rat

Reichert¹,

Carmo²,

Lima³

et al. 2013

Revista Brasileira De Cirurgia Cardiovascular

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Introduction Myocardial preservation during open heart surgeries and harvesting for transplant are of great importance. The heart at the end of procedure has to resume its functions as soon as possible. All cardioplegic solutions are based on potassium for induction of cardioplegic arrest. Objective To assess a cardioplegic solution with no potassium addition to the formula with two other commercially available cardioplegic solutions. The comparative assessment was based on cytotoxicity, adenosine triphosphate myocardial preservation, and caspase 3 activity. The tested solution (LIRM) uses low doses of sodium channel blocker (lidocaine), potassium channel opener (cromakalin), and actin/myosin cross bridge inhibitor (2,3-butanedione monoxime). Methods Wistar rats underwent thoracotomy under mechanical ventilation and three different solutions were used for "in situ" perfusion for cardioplegic arrest induction: Custodiol (HTK), Braile (G/A), and LIRM solutions. After cardiac arrest, the hearts were excised and kept in cold storage for 4 hours. After this period, the hearts were assessed with optical light microscopy, myocardial ATP content and caspase 3 activity. All three solutions were evaluated for direct cytotoxicity with L929 and WEHI-164 cells. Results The ATP content was higher in the Custodiol group compared to two other solutions (P<0.05). The caspase activity was lower in the HTK group compared to LIRM and G/A solutions (P<0.01). The LIRM solution showed lower caspase activity compared to Braile solution (P<0.01). All solutions showed no cytotoxicity effect after 24 hours of cells exposure to cardioplegic solutions. Conclusion Cardioplegia solutions without potassium are promised and aminoacid addition might be an interesting strategy. More evaluation is necessary for an optimal cardioplegic solution development.

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Section: Discussionmentioning

confidence: 99%

Development of cardioplegic solution without potassium: experimental study in rat

Reichert¹,

Carmo²,

Lima³

et al. 2013

Revista Brasileira De Cirurgia Cardiovascular

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Characterization of the cellular effects of myeloperoxidase-derived oxidants on H9c2 cardiac myoblasts

Reyes

Hawkins

Rayner

2019

Archives of Biochemistry and Biophysics

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Myeloperoxidase impairs the contractile function in isolated human cardiomyocytes

Kalász

Pásztor

Fagyas

et al. 2015

Free Radical Biology and Medicine

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We set out to characterize the mechanical effects of myeloperoxidase (MPO) in isolated left-ventricular human cardiomyocytes. Oxidative myofilament protein modifications (sulfhydryl (SH)-group oxidation and carbonylation) induced by the peroxidase and chlorinating activities of MPO were additionally identified. The specificity of the MPO-evoked functional alterations was tested with an MPO inhibitor (MPO-I) and the antioxidant amino acid Met. The combined application of MPO and its substrate, hydrogen peroxide (H2O2), largely reduced the active force (Factive), increased the passive force (Fpassive), and decreased the Ca(2+) sensitivity of force production (pCa50) in permeabilized cardiomyocytes. H2O2 alone had significantly smaller effects on Factive and Fpassive and did not alter pCa50. The MPO-I blocked both the peroxidase and the chlorinating activities, whereas Met selectively inhibited the chlorinating activity of MPO. All of the MPO-induced functional effects could be prevented by the MPO-I and Met. Both H2O2 alone and MPO + H2O2 reduced the SH content of actin and increased the carbonylation of actin and myosin-binding protein C to the same extent. Neither the SH oxidation nor the carbonylation of the giant sarcomeric protein titin was affected by these treatments. MPO activation induces a cardiomyocyte dysfunction by affecting Ca(2+)-regulated active and Ca(2+)-independent passive force production and myofilament Ca(2+) sensitivity, independent of protein SH oxidation and carbonylation. The MPO-induced deleterious functional alterations can be prevented by the MPO-I and Met. Inhibition of MPO may be a promising therapeutic target to limit myocardial contractile dysfunction during inflammation.

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2,3-Butanedione monoxime does not protect cardiomyocytes under oxidative stress

Cited by 4 publications

References 34 publications

Development of cardioplegic solution without potassium: experimental study in rat

Development of cardioplegic solution without potassium: experimental study in rat

Characterization of the cellular effects of myeloperoxidase-derived oxidants on H9c2 cardiac myoblasts

Myeloperoxidase impairs the contractile function in isolated human cardiomyocytes

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