Glutathione peroxidase activity and selenium concentration in the hearts of doxorubicin-treated rabbits

Revis, N. W.; Marušić, Nives

doi:10.1016/0022-2828(78)90340-1

Cited by 71 publications

(17 citation statements)

References 12 publications

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“…5,6 Similar findings have also been reported in rabbits treated with 13.5 mg/kg of adriamycin in 3 weeks. 3 Because a single injection of adriamycin (15 mg/kg) did not have any influence on the activity of GSHPx, 21 it is likely that repeated administration of adriamycin over time is necessary to bring about a decrease in this activity. Furthermore, our data suggest that this decrease in the enzyme activity may be caused by the parallel decrease in the enzyme protein shown by the Western blots in the present study.…”

Section: And Singal Antioxidant Enzymes In Heart Failure 2107mentioning

confidence: 99%

“…1 However, a dose-dependent cardiotoxicity limits its clinical potential. 1,2 Adriamycin has been shown to cause myocardial antioxidant deficit in different animal species, [3][4][5] and probucol, a lipid-lowering drug and antioxidant, has been found to modulate these changes. 6 However, the molecular basis and early sequence of the changes in myocardial antioxidant enzyme activities due to adriamycin and probucol remain to be understood.…”

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confidence: 99%

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Adriamycin-Induced Early Changes in Myocardial Antioxidant Enzymes and Their Modulation by Probucol

2000

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Background-The clinical usefulness of adriamycin is restricted by the development of congestive heart failure. It has been suggested that probucol, a strong antioxidant, completely prevents adriamycin-induced cardiomyopathy without interfering with its antitumor properties. The present study investigated the effects of adriamycin and probucol on myocardial antioxidant enzyme activities and immunoreactive protein levels in rats. Methods and Results-Activities and protein levels of glutathione peroxidase (GSHPx) were significantly decreased from 2 to 24 hours, and those of manganese superoxide dismutase were decreased at 1 and 2 hours after adriamycin treatment. These changes were prevented by probucol. Catalase activity was increased from 2 to 24 hours after adriamycin treatment, but its protein levels were not significantly changed. Copper zinc superoxide dismutase activity and protein level were not changed at any time. Myocardial lipid peroxidation was found to be significantly higher at all time points, and this change was also prevented by probucol. Treatment with probucol alone increased GSHPx activity at 2 weeks, and in these hearts, lipid peroxidation was lower than the control value. Within 24 hours, there was no mortality in any of the groups. Conclusions-It is suggested that an early and persistent decrease in GSHPx activity and protein may play an important role in the pathogenesis of adriamycin-induced cardiomyopathy, worsening heart failure and mortality. (Circulation.

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Section: And Singal Antioxidant Enzymes In Heart Failure 2107mentioning

confidence: 99%

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confidence: 99%

Adriamycin-Induced Early Changes in Myocardial Antioxidant Enzymes and Their Modulation by Probucol

2000

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“…Robison et al (218) and Alderton et al (5) have found no change of glutathione peroxidase activity a week or more after the chronic weekly ANT treatments, while others have reported a slight, but significant, increase at this time point (279). A persistent decrease of expression and activity of this enzyme has been reported from compressed chronic ANT cardiotoxicity models where a total cumulative dose of DOX (13.5-15 mg/kg) was administered over 2-3 weeks only (163,215,249). The involvement of glutathione peroxidase in acute ANT cardiotoxicity has been probed using genetically modified organisms (69,298).…”

Section: Ant Cardiotoxicity and Myocardial Antioxidant Defensementioning

confidence: 99%

Oxidative Stress, Redox Signaling, and Metal Chelation in Anthracycline Cardiotoxicity and Pharmacological Cardioprotection

Štěrba

Popelová

Vávrová

et al. 2013

Antioxidants & Redox Signaling

283

192

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“…In a recent study, it was also shown that redox communication between peroxisomes and mitochondria may be important for ROS diffusion between subcellular compartments (Wang et al 2013). The liver due to the ADR metabolism may produce an important amount of ROS, but at the same time the antioxidant defence is a few times higher than, for example, that in the heart (Revis and Marusic 1978). Cytosolic ROS might be detoxified by these higher antioxidant activity in liver.…”

Section: Discussionmentioning

confidence: 99%

Recovery of adriamycin induced mitochondrial dysfunction in liver by selenium

Taşkın

Dursun

2014

Cytotechnology

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Adriamycin (ADR) is a chemotherapeutic drug. Its toxicities may associate with mitochondriopathy. Selenium (Se) is a trace element for essential intracellular antioxidant enzymes. However, there is lack of data related to the effect of selenium on the liver tissue of ADR-induced mitochondrial dysfunction. The study was to investigate whether Se could restore mitochondrial dysfunction of liver-exposed ADR. Rats were divided into four groups as a control, ADR, Se, co-treated ADR with Se groups. The biochemical measurements of the liver were made in mitochondrial and cytosol. ATP level and mitochondria membrane potential (MMP) were measured. Total oxidant (TOS), total antioxidant (TAS) status were determined and oxidative stress index (OSI) was calculated by using TOS and TAS. ADR increased TOS in mitochondria and also oxidative stress in mitochondria. ADR sligtly decreased MMP, and ATP level. Partial recovery of MMP by Se was able to elevate the ATP production in cotreatment of ADR with Se. TOS in mitochondria and cytosol was diminished, as well as OSI. We concluded that selenium could potentially be used against oxidative stress induced by ADR in liver, resulting from the restoration of MMP and ATP production and prevention of mitochondrial damage in vivo.

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Glutathione peroxidase activity and selenium concentration in the hearts of doxorubicin-treated rabbits

Cited by 71 publications

References 12 publications

Adriamycin-Induced Early Changes in Myocardial Antioxidant Enzymes and Their Modulation by Probucol

Adriamycin-Induced Early Changes in Myocardial Antioxidant Enzymes and Their Modulation by Probucol

Oxidative Stress, Redox Signaling, and Metal Chelation in Anthracycline Cardiotoxicity and Pharmacological Cardioprotection

Recovery of adriamycin induced mitochondrial dysfunction in liver by selenium

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