Glutathione <i>S</i>-transferase overexpression protects against anthracycline-induced H9C2 cell death

L’Ecuyer, Thomas; Allebban, Zuhair; Thomas, Ronald; Heide, Richard Vander

doi:10.1152/ajpheart.00778.2003

Cited by 72 publications

(60 citation statements)

References 48 publications

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“…[44][45][46] Moreover, DXR has been also reported to induce oncosis in different cells types, such as human endothelial cells, 15 melanoma 47 and myocytes. 48 Depletion of the glycogen content in ORS cells, which was clearly evident in our samples from T7 (data not shown) and T10, has been reported as one of the side effects of DXR. 49,50 Glycogen metabolism is very important in the epidermis and, in particular, within the hair follicle.…”

Section: Epithelial Compartmentsupporting

confidence: 56%

Epithelium–mesenchyme compartment interaction and oncosis on chemotherapy-induced hair damage

Selleri

Arnaboldi

Vizzotto

et al. 2004

Laboratory Investigation

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It is known that chemotherapy induces alopecia in humans, with important psychological and social implications in spite of its reversibility. Among chemotherapeutic drugs, anthracyclines are widely used, yet cause severe alopecia. One of the causes for the elevated sensibility of hair follicles to anthracyclines, and to drugs in general, is the high proliferation rate of follicular epithelium and the long duration of the growth phase (up to 7 years in humans). To clarify the mechanism of anthracycline toxicity, we used a rat model and focused our attention on the morphological alterations in hair follicles induced by doxorubicin. We observed the progression of hair follicle degeneration in the epithelial and mesenchymal compartments until alopecia arose, by both light and electron microscopy. As a first sign of damage, significant apoptosis was detected in the proximal perifollicular connective tissue sheath and sporadically in the matrix, near the interface between matrix and follicular papilla. We propose the apoptotic remodeling of the mesenchymal compartment as a process that is fundamental to the progression of events leading to alopecia. Regarding the epithelial compartment, it is important to note that oncosis was observed in a large number of follicular cells in the outer root sheath during the last stages of hair follicle regression. This indicates that oncosis is involved in a major way in the damage of epithelial cells.

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Section: Epithelial Compartmentsupporting

confidence: 56%

Epithelium–mesenchyme compartment interaction and oncosis on chemotherapy-induced hair damage

Selleri

Arnaboldi

Vizzotto

et al. 2004

Laboratory Investigation

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“…46) Cardioprotective effects were also found due to the overexpressions of GST, CuZn-SOD/Mn-SOD and catalase in both in vitro cardiac gene transfer and in transgenic mice models. [47][48][49] Interestingly, PU alone dose dependently increased tGSH, catalase, and SOD activity to levels substantially higher than those of controls and these effects remained in the presence of DOX. On the other hand, the antioxidants VIT C and NAC at the dose used did not similarly enhance tGSH levels and catalase/SOD enzyme activation.…”

Section: )mentioning

confidence: 89%

Antioxidative and Cardioprotective Effects of Phyllanthus urinaria L. on Doxorubicin-Induced Cardiotoxicity

Chularojmontri

Wattanapitayakul

Herunsalee

et al. 2005

Biological & Pharmaceutical Bulletin

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Doxorubicin (DOX) is an effective and broadly used agent to treat a variety of malignacies, such as leukemias, breast and ovarian cancer, and Hodgkin and non-Hodgkin lymphoma. The major limitation of clinical use is the development of cardiotoxicity. The adverse effects are dose dependent and can vary from transient electrocardiographic abnormalities to cardiomyopathy and heart failure. Recent studies have suggested that the mechanism of DOX-induced cardiotoxicity involves the generation of reactive oxygen species (ROS), especially superoxide anion and hydrogen peroxide.1-3) The main cellular damage caused by ROS includes lipid peroxidation, protein cross-linking, and DNA fragmentation. These may lead to cardiac dysfunction, apoptosis, and development of cardiomyopathy. 4-7)Although protection or alleviation of DOX toxicity can be achieved by administration of antioxidant vitamins such as ascorbic acid and vitamin E, their cardioprotective effects remain controversial. [8][9][10] It is well established that there is no universal "best" antioxidant. For example, ascorbic acid efficiently protects against lipid damage but not against protein damage.11) Thus alternative naturally occurring antioxidants may potentially be candidates for antioxidant therapy.It has been shown in many studies that traditionally used plant extracts protect against oxidative damage caused by a wide array of insults including DOX.12-16) Among traditional herbs, Phyllanthus spp. (Euphorbiaceae) has been used in Aryuvedic medicine for more than 2000 years and in Thai folk medicine for the treatment of many diseases, such as diarrhea, hepatitis, diabetes, abdominal pain, and kidney disease. 17,18) The antioxidant effects of plant species in the genus Phyllanthus have been reported. For example, Phyllanthus amarus (synonym: Phyllanthus niruri) reduced oxidative damage from radiation 19) and protected against hepatotoxicity induced by CCl 4 . 20) Phyllanthus emblica protected rat hearts from oxidative stress induced by ischemic-reperfusion injury.21) Phyllanthus urinaria L. is another medicinal plant that has attracted research attention in the treatment of several diseases. Substantial progress in determining its phytochemical and pharmacologic properties has been made. Several potential antioxidant compounds (e.g., polyphenols, lignans, flavonoids, gallic acid, ellagic acid, etc.) have been isolated from this plant. [22][23][24][25][26] However, to the best of our knowledge, there has been no report on the potential antioxidant effects of Phyllanthus urinaria. Therefore the purpose of this study was to investigate the antioxidant effects of Phyllanthus urinaria for the protection of cardiac cells from DOX cardiotoxicity. Cardiac toxicity is a major adverse effect caused by doxorubicin (DOX) therapy. Many recent studies have shown that DOX toxicity involves generation of reactive oxygen species (ROS). Although protection or alleviation of DOX toxicity can be achieved by administration of antioxidant vitamins such as ascorbic acid and vitamin ...

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“…H9c2 is a rat-derived cardiomyoblast cell line that exhibits morphological characteristics similar to those of immature embryonic cardiomyocytes, but preserves several elements of the electrical and hormonal signaling pathway found in adult cardiac cells (29,30). H9c2 cardiomyoblasts have been widely used to screen active components (31,32).…”

Section: Discussionmentioning

confidence: 99%

Effects of bpV(pic) and bpV(phen) on H9c2 cardiomyoblasts during both hypoxia/reoxygenation and H2O2-induced injuries

2011

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Abstract. Reactive oxygen species (ROS) are involved in myocardial injury. ROS are known to inactivate lipid phosphatase and tension homolog on chromosome 10 (PTEN), an enzyme that increases apoptosis in neonatal cardiomyocytes. BpV(pic) and bpV(phen), two bisperoxovanadium molecules and PTEN inhibitors, may be involved in limiting myocardial infarction. To compare the protective effects of bpV(pic) and bpV(phen) on ROS-induced cardiomyocyte injury and their possible mechanisms, we selected two popular models of hypoxia/reoxygenation (H/R) and H 2 O 2 -induced injury in H9c2 cardiomyoblasts to investigate their effects against injury. We found that pre-treatment with bpV(pic) and bpV(phen) increased the viability and protected the morphology of H9c2 cells under the conditions of H/R and H 2 O 2 by inhibiting LDH release, apoptosis and caspases 3/8/9 activities. However, their respective inhibitory abilities in the two models were different, suggesting that the quantity of ROS from the two models might be different. However, the conflict between ROS and PTEN may affect the action of bpV(pic) and bpV(phen). Taken together, the results demonstrate that bpV(pic) and bpV(phen) have inhibitory effects on oxidative stress-induced cardiomyocyte injury that may be partially modulated by the action of ROS on PTEN. IntroductionMyocardial ischemia/reperfusion injury (MIRI), which may lead to various complications, including myocardial infarction, cardiac contractile dysfunction and arrhythmia (1-4), has become an increasingly common problem in clinics. However, few strategies directed against MIRI have been tested under clinical conditions (5,6). Recently, a new finding showed that the pharmacological inhibition of lipid phosphatase and tension homolog on chromosome 10 (PTEN) limited myocardial infarct size and improved left ventricular function post-infarction (7). Moreover, protein tyrosine phosphatase inhibitors and bisperoxovanadium molecules (bpV) inhibited PTEN specifically at low concentrations (8). The protective effects of bpV(HOpic) on myocardial injury in vitro and in vivo have been observed in previous studies (7). However, other bpV molecules have not been studied and compared for their actions against MIRI.Based on the cellular mechanisms of ischemia/reperfusion injury that have been extensively explored (9-11), reactive oxygen species (ROS) generated with the re-admission of oxygen are considered the first and main cause of ischemia/ reperfusion injury (12). Thus, scavenging excessive ROS and restoring the reduction-oxidation (redox) balance in the body is an important strategy in inhibiting reperfusion injury, as the redox balance is the solid physiological condition in humans from birth (13,14), and, despite evolution, this balance has always been conserved in all organisms (15,16).Hydrogen dioxide (H 2 O 2 ), a famous ROS, inhibits the lipid phosphatase activity of the tumour suppressor PTEN enzyme (17), which suggests that when produced under pathological conditions, such as during MIRI or chronic inflamm...

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Glutathione S-transferase overexpression protects against anthracycline-induced H9C2 cell death

Cited by 72 publications

References 48 publications

Epithelium–mesenchyme compartment interaction and oncosis on chemotherapy-induced hair damage

Epithelium–mesenchyme compartment interaction and oncosis on chemotherapy-induced hair damage

Antioxidative and Cardioprotective Effects of Phyllanthus urinaria L. on Doxorubicin-Induced Cardiotoxicity

Effects of bpV(pic) and bpV(phen) on H9c2 cardiomyoblasts during both hypoxia/reoxygenation and H2O2-induced injuries

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