Glutathione peroxidase, glutathione reductase and protein oxidation in patients with glioblastoma multiforme and transitional meningioma

Tanrıverdi, Taner; Hanımoğlu, Hakan; Kacira, Tibet; Sanuş, Galip Zihni; Kemerdere, Rahşan; Atukeren, Pınar; Gümüştaş, Koray; Canbaz, Bülent; Kaynar, Mehmet Yaşar

doi:10.1007/s00432-007-0212-2

Cited by 33 publications

(18 citation statements)

References 22 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Expression levels and activities of GR and GPx were decreased in patients with glioblastoma multiforme (GBM) and transitional meningioma (TM), when compared with normal brain tissues. However, protein oxidation levels measured by protein carbonyl content were increased in GBM and TM, perhaps because of the decreases in other antioxidant systems (185). The role of GR in zincinduced toxicity was shown by studies in human lung cell lines and rat astrocytes (6,193).…”

Section: Distribution Of Redox Systems In Nucleimentioning

confidence: 96%

Redox Control Systems in the Nucleus: Mechanisms and Functions

Jones

2010

Antioxidants & Redox Signaling

176

125

View full text Add to dashboard Cite

Proteins with oxidizable thiols are essential to many functions of cell nuclei, including transcription, chromatin stability, nuclear protein import and export, and DNA replication and repair. Control of the nuclear thioldisulfide redox states involves both the elimination of oxidants to prevent oxidation and the reduction of oxidized thiols to restore function. These processes depend on the common thiol reductants, glutathione (GSH) and thioredoxin-1 (Trx1). Recent evidence shows that these systems are controlled independent of the cytoplasmic counterparts. In addition, the GSH and Trx1 couples are not in redox equilibrium, indicating that these reductants have nonredundant functions in their support of proteins involved in transcriptional regulation, nuclear protein trafficking, and DNA repair. Specific isoforms of glutathione peroxidases, glutathione Stransferases, and peroxiredoxins are enriched in nuclei, further supporting the interpretation that functions of the thiol-dependent systems in nuclei are at least quantitatively distinct, and probably also qualitatively distinct, from similar processes in the cytoplasm. Elucidation of the distinct nuclear functions and regulation of the thiol redox pathways in nuclei can be expected to improve understanding of nuclear processes and also to provide the basis for novel approaches to treat aging and disease processes associated with oxidative stress in the nuclei. Antioxid. Redox Signal. 13, 489-509.

show abstract

Section: Distribution Of Redox Systems In Nucleimentioning

confidence: 96%

Redox Control Systems in the Nucleus: Mechanisms and Functions

Jones

2010

Antioxidants & Redox Signaling

176

125

View full text Add to dashboard Cite

show abstract

“…Glioblastomas, like normal brain tissue, have low antioxidant activity. This is supported by several studies that have revealed depleted levels of ROS detoxification enzymes (gluthathione peroxidase and superoxide dismutase) in clinical glioblastomas examined from tumor patient explants (27–29). Additionally, glioblastomas have been shown to increase the expression levels of the ROS generator, xanthine oxidase.…”

Section: Discussionmentioning

confidence: 57%

1′-Acetoxychavicol acetate promotes caspase 3-activated glioblastoma cell death by overcoming enhanced cytokine expression

2013

View full text Add to dashboard Cite

The brain consumes ∼20% of the oxygen utilized in the human body, meaning that brain tumors are vulnerable to paradoxical physiological effects from free radical generation. In the present study, 1′-acetoxychavicol acetate (ACA), a naturally derived antioxidant that inhibits xanthine oxidase, was evaluated for its role as an anti-tumorigenic agent in glioblastomas. The study revealed that ACA inhibited glioblastoma cell proliferation as a consequence of promoting apoptotic cell death by enhancing caspase 3 activity. It was also shown that ACA impaired the migratory ability of glioblastoma cells by decreasing their adhesive properties. Additionally, ACA increased the protein expression levels of the pro-survival signaling cytokines, IL-6 and IL-1α, established cell protectors and survival molecules in brain tumors. Together, these results demonstrate that, despite enhanced expression of compensatory signaling molecules that contribute to tumor cell survival, ACA is an effective pro-apoptotic inducing agent in glioblastomas.

show abstract

“…The creation of glioma tumor is a complex process involved neoplastic changes of cells, resistance to apoptosis, lack of cell cycle control and angiogenesis (12). Many studies showed that OS has a substantial role in these processes and modulation of OS can have a therapeutic potential in treatment (13)(14). It is demonstrated that pro-inflammatory cytokine and OS could interact and provoke each other and contribute to the development and progression of some diseases such as diabetes and cancer.…”

Section: Discussionmentioning

confidence: 99%

Comparison of Prooxidant-antioxidant Balance between Patients with High Grade Gliomas (IV) and Control Group

Farajirad

Ghaemi

Khajavi

et al. 2015

IrJNS

View full text Add to dashboard Cite

Background & Aim: The most common primary brain tumors of the central nervous system are gliomas. Among a number of different biomolecular events, a strong relation between oxidative stress pathways and the development of this cancer has been proved. Oxidative stress (OS) is the consequence of an imbalance between pro-oxidants and antioxidants towards pro-oxidants. The pro-oxidants cause lipid peroxidation of cell membranes, protein, DNA oxidation and changes in brain cell growth. In this study, the pro-oxidant-antioxidant balance (PAB) was determined in patients with gliomas.Methods & Materials/Patients: Sera of 49 patients with high grade glioma (grade IV WHO) which is called glioblastoma multiform (GBM) and 49 healthy subjects were collected and PAB test was measured.Results: A significant increase of PAB value was observed in patients with GBM (158.10±85.71 HK unit) in comparison to control group (74.54±33.54 HK). Conclusion:The PAB assay showed the oxidative stress in glioblastoma. In further research, this easy elucidation of oxidative stress in these patients can be applied to evaluate the effectiveness of antioxidant therapies in patients with GBM

show abstract

Glutathione peroxidase, glutathione reductase and protein oxidation in patients with glioblastoma multiforme and transitional meningioma

Abstract: GPx and GRx decreased and POx increased significantly in both GBM and TM when compared to normal brain tissues. Further, clinical studies with a larger patient population are required to show the role(s) of antioxidant enzymes in brain tumors more accurately.

Cited by 33 publications

References 22 publications

Redox Control Systems in the Nucleus: Mechanisms and Functions

Redox Control Systems in the Nucleus: Mechanisms and Functions

1′-Acetoxychavicol acetate promotes caspase 3-activated glioblastoma cell death by overcoming enhanced cytokine expression

Comparison of Prooxidant-antioxidant Balance between Patients with High Grade Gliomas (IV) and Control Group

Contact Info

Product

Resources

About