Hepatobiliary Effects of Tertiary-Butylhydroperoxide (tBOOH) in Isolated Rat Hepatocyte Couplets

Ahmed-Choudhury, Jalal; Orsler, D J; Coleman, Roger

doi:10.1006/taap.1998.8495

Cited by 27 publications

(15 citation statements)

References 22 publications

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“…By its turn, t-BHP is a pro-oxidant agent widely used as an inducer of oxidative stress [26,31]. So, the effect of the compounds on t-BHP-induced oxidative stress on H9c2 cells was assessed by fluorescence microscopy, through the detection of oxidized dichlorofluorescein (DCF) form.…”

Section: Measurement Of Intracellular Reactive Oxygen Speciesmentioning

confidence: 99%

Nitrogen Compounds Prevent H9c2 Myoblast Oxidative Stress-Induced Mitochondrial Dysfunction and Cell Death

et al. 2010

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Oxidative stress has been connected to various forms of cardiovascular diseases. Previously, we have been investigating the potential of new nitrogen-containing synthetic compounds using a neuronal cell model and different oxidative stress conditions in order to elucidate their potential to ameliorate neurodegenerative diseases. Here, we intended to extend these initial studies and investigate the protective role of four of those new synthetic compounds (FMA4, FMA7, FMA762 and FMA796) against oxidative damage induced to H9c2 cardiomyoblasts by tert-butylhydroperoxide (t-BHP). The data indicates that FMA762 and FMA796 decrease t-BHP-induced cell death, as measured by both sulforhodamine B assay and nuclear chromatin condensation evaluation, at non-toxic concentrations. In addition, the two mentioned compounds inhibit intracellular signalling mechanisms leading to apoptotic cell death, namely those mediated by mitochondria, which was confirmed by their ability to overcome t-BHP-induced morphological changes in the mitochondrial network, loss of mitochondrial membrane potential, increased expression of the pro-apoptotic proteins p53, Bax and AIF and activation of caspases-3 and -9. Importantly, our results indicate that the compounds' ROS scavenging ability plays a crucial role in the protection profile, as a significant decrease in t-BHP-induced oxidative stress occurred in their presence. Data obtained indicates that some of the test compounds may clearly prove valuable in a clinical context by diminishing cardiac injury associated to oxidative stress without any toxicity.

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Section: Measurement Of Intracellular Reactive Oxygen Speciesmentioning

confidence: 99%

Nitrogen Compounds Prevent H9c2 Myoblast Oxidative Stress-Induced Mitochondrial Dysfunction and Cell Death

et al. 2010

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“…tert-Butyl hydroperoxide is a potent thiol oxidising agent that induces oxidative stress, with subsequent oxidation of intracellular glutathione, glutathione disulfide formation and changes to cellular membranes through lipid peroxidation [22]. It is used here as an alternative to H 2 O 2 for the induction of oxidative stress in an in vivo model.…”

Section: Discussionmentioning

confidence: 99%

“…There have been other reports of the effects of t BOOH on the liver. For example, treating cultured hepatocytes with 0.05 mM t BOOH induced lipid-signalled cell death [30] and exposure of isolated hepatocyte couplets to up to 200 mM t BOOH impaired biliary transport [22]. Higher doses, such as 0.4 mM t BOOH induced apoptosis of isolated hepatocytes [31].…”

Section: Discussionmentioning

confidence: 99%

The effects of oxidative stress on the liver sieve

Cogger

Müller

Fraser

et al. 2004

Journal of Hepatology

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“…The cholestatic agents, taurolithocholate [8], cyclosporin A [8,20] and β-oestradiol 17-(β-D-glucuronide) (17βEG) [8], as well as the oxidative-stress-inducers menadione [8,21] and t-butylhydroperoxide (tBOOH) [8,22], all increased tightjunctional permeability, as assessed by cVR of CLF, in a dose-dependent manner.…”

Section: Studies Of Alterations In Tight-junctional Integrity Using Hmentioning

confidence: 98%

Pathobiology and experimental therapeutics in hepatocellular cholestasis: lessons from the hepatocyte couplet model

et al. 2002

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Preparations of isolated liver cells, either freshly prepared or in culture, have been available for many years; however, because they lack the polarization of the cell in the tissue, their application to the study of processes involved in bile formation has been very limited. The hepatocyte couplet model offers a unique opportunity to study in vitro the intracellular processes involved: not only the physiology and pathophysiology of bile formation, but also the corresponding structural and molecular disturbances underlying different experimental models of cholestasis. In this review we describe the experimental data generated from this model in our laboratory over a period of years, including application of hepatocyte couplets to the study of cytoskeletal changes within the hepatocyte and mechanisms of hepatoprotection in experimentally induced, clinically relevant models of intrahepatic cholestasis.

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Hepatobiliary Effects of Tertiary-Butylhydroperoxide (tBOOH) in Isolated Rat Hepatocyte Couplets

Cited by 27 publications

References 22 publications

Nitrogen Compounds Prevent H9c2 Myoblast Oxidative Stress-Induced Mitochondrial Dysfunction and Cell Death

Nitrogen Compounds Prevent H9c2 Myoblast Oxidative Stress-Induced Mitochondrial Dysfunction and Cell Death

The effects of oxidative stress on the liver sieve

Pathobiology and experimental therapeutics in hepatocellular cholestasis: lessons from the hepatocyte couplet model

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