Hydroperoxide-induced nucleotide degradation and adenosine formation in isolated rat cardiomyocytes

Andersson, Bo S.; Vidal, Ricardo F.; Sundberg, Monica; Rajs, Jovan; Sótonyi, Péter

doi:10.1016/0300-483x(95)03158-c

Cited by 13 publications

(7 citation statements)

References 20 publications

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“…tBHP consists of a tertiary butyl group and a hydridodioxygen group. As an organic hydroperoxide, tBHP is more stable than hydrogen peroxide (H 2 O 2 ), and it selectively inhibits mitochondrial function [Haidara et al, 2002; Drahota et al, 2005; Krivakova et al, 2007], induces membrane lipid peroxidation [Uchida et al, 1994; Gorbunov et al, 1998], and promotes nucleotide degradation and adenosine formation [Andersson et al, 1996]. When H9c2 cells are treated with tBHP, the morphology of their mitochondria changes from long filaments to small, round fragments [Sardao et al, 2007].…”

Section: Discussionmentioning

confidence: 99%

Mitochondrial accumulation under oxidative stress is due to defects in autophagy

Luo

Wang

et al. 2012

J of Cellular Biochemistry

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Mitochondrial dynamics maintains normal mitochondrial function by degrading damaged mitochondria and generating newborn mitochondria. The accumulation of damaged mitochondria influences the intracellular environment by promoting mitochondrial dysfunction, and thus initiating a vicious cycle. Oxidative stress induces mitochondrial malfunction, which is involved in many cardiovascular diseases. However, the mechanism of mitochondrial accumulation in cardiac myoblasts remains unclear. We observed mitochondrial dysfunction and an increase in mitochondrial mass under the oxidative conditions produced by tert-butyl hydroperoxide (tBHP) in cardiac myoblast H9c2 cells. However, in contrast to the increase in mitochondrial mass, mitochondrial DNA (mtDNA) decreased, suggesting that enhanced mitochondrial biogenesis may be not the primary cause of the mitochondrial accumulation. Therefore, we investigated changes in a number of proteins involved in autophagy. Beclin1, Atg12-Atg5 conjugate, Atg7 contents decreased but LC3-II accumulated in tBHP-treated H9c2 cells. Moreover, the capacity for acid hydrolysis decreased in H9c2 cells. We also demonstrated a decrease in DJ-1 protein under the oxidative conditions that deregulate mitochondrial dynamics. These results reveal that autophagy became defective under oxidative stress. We therefore suggest that defects in autophagy mediate mitochondrial accumulation under these conditions.

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Section: Discussionmentioning

confidence: 99%

Mitochondrial accumulation under oxidative stress is due to defects in autophagy

Luo

Wang

et al. 2012

J of Cellular Biochemistry

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“…Tert -butyl hydroperoxide (tBHP) is a membrane-permeant pro-oxidant agent used in several cell lines as a model to study the effects of oxidative stress on cellular function and cell death pathways [18,19,21,22]. Once inside cells, tBHP generates tert -butoxy radicals inducing several physiological alterations with consequent loss of cell viability via apoptosis or necrosis [28].…”

Section: Discussionmentioning

confidence: 99%

“…In cardiomyocytes, tBHP induced loss of cell shape, depletion of ATP, and formation of adenosine [21]. Other studies demonstrated that treatment with 1 mM tBHP lead to a rise in intracellular calcium concentration, hyper-contracture and loss of membrane integrity in cardiac myocytes isolated from rat ventricles [31].…”

Section: Discussionmentioning

confidence: 99%

“…Tert -butyl hydroperoxide (tBHP) is one of the most common pro-oxidant agents used to evaluate the effects of oxidative stress [18], and it has been found to induce cell death in several cell lines such as U937 [19], HepG2 [20], and primary cultures of cardiomyocytes [21] and hepatocytes [18,22]. According to the cell line used, induction of cell death by tBHP is characterized by cytochrome c release [23], increased expression of p53 [24], induction of the mitochondrial permeability transition pore [25], TUNEL-positive labeling, phosphatidylserine (PS) exposure and caspase 3 activation [26].…”

Section: Introductionmentioning

confidence: 99%

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Vital imaging of H9c2 myoblasts exposed to tert-butylhydroperoxide – characterization of morphological features of cell death

et al. 2007

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Background: When exposed to oxidative conditions, cells suffer not only biochemical alterations, but also morphologic changes. Oxidative stress is a condition induced by some pro-oxidant compounds, such as by tert-butylhydroperoxide (tBHP) and can also be induced in vivo by ischemia/ reperfusion conditions, which is very common in cardiac tissue. The cell line H9c2 has been used as an in vitro cellular model for both skeletal and cardiac muscle. Understanding how these cells respond to oxidative agents may furnish novel insights into how cardiac and skeletal tissues respond to oxidative stress conditions. The objective of this work was to characterize, through vital imaging, morphological alterations and the appearance of apoptotic hallmarks, with a special focus on mitochondrial changes, upon exposure of H9c2 cells to tBHP.

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“…Oxidative stress induced by t-BHP has been widely studied in isolated hepatocytes (Eklow et al, 1984;Jewell et al, 1986;Joyeux et al, 1990;Shertzer et al, 1994;Fernandes et al, 1995) as well as in isolated cardiomyocytes (Timerman et al, 1990;Daly et al, 1991;Vlessis et al, 1991;Castro and Bhatnagar, 1993;Andersson et al, 1996). Loss of cell viability, increase of intracellular free Ca 2 , nucleotide degradation, GSH oxidation and lipid peroxidation are the highlights of t-BHP effect.…”

Section: Introductionmentioning

confidence: 99%

Simultaneous determination of reduced and oxidized glutathione in freshly isolated rat hepatocytes and cardiomyocytes by HPLC with electrochemical detection

Remião

Carmo

Carvalho

et al. 2000

Biomed. Chromatogr.

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Glutathione and glutathione disulphide constitute an essential thiol redox system present in the cell. The balance in favour of the latter is an indication of oxidative stress. Glutathione and glutathione disulphide quantification in isolated cells may therefore be essential for the evaluation of mechanistic and comparative studies of toxic xenobiotics. In this study, a rapid and sensitive isocratic reverse-phase high-performance liquid chromatographic method using coulometric detection was implemented for the simultaneous detection of glutathione and glutathione disulphide, in freshly isolated hepatocytes and cardiomyocytes of the rat. The method implemented proved to be effective for the measurement of glutathione and glutathione disulphide in control conditions and for the detection of variations in this redox system, induced by tert-butylhydroperoxide. tert-Butylhydroperoxide is an organic peroxide, which has been used as a model molecule for inducing oxidative stress in isolated cells. A comparative study with a previously published HPLC-electrochemical detection method was performed.

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Hydroperoxide-induced nucleotide degradation and adenosine formation in isolated rat cardiomyocytes

Cited by 13 publications

References 20 publications

Mitochondrial accumulation under oxidative stress is due to defects in autophagy

Mitochondrial accumulation under oxidative stress is due to defects in autophagy

Vital imaging of H9c2 myoblasts exposed to tert-butylhydroperoxide – characterization of morphological features of cell death

Simultaneous determination of reduced and oxidized glutathione in freshly isolated rat hepatocytes and cardiomyocytes by HPLC with electrochemical detection

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