Altered antioxidant capacity in human renal cell carcinoma: Role of glutathione associated enzymes

Plješa-Ercegovac, Marija; Mimic-Oka, Jasmina; Dragičević, Dejan; Savić-Radojević, Ana; Opačić, Miloš; Pljesa, Steva; Radosavljevic, R.; Simić, Tatjana

doi:10.1016/j.urolonc.2007.02.007

Cited by 41 publications

(48 citation statements)

References 35 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Same authors also observed a positive expression of AO enzymes in normal kidney tissue which corresponds to higher activity of these enzymes recorded in our study. We observed significantly lower activity of GPx in tumour tissue and this finding is in accordance with previous reports [9,12]. The impaired activity of CAT and GPx, the enzymes that have a role to eliminate H2O2 and organic peroxides, may increase lipid peroxidation caused by oxidative stress.…”

Section: Discussionsupporting

confidence: 93%

The Antioxidant Capacity of the Kidney Tissue in Patients With Renal Cell Carcinoma

Pavlović¹,

Todorović²,

Stojiljković³

et al. 2016

RAD Conference Proceedings

View full text Add to dashboard Cite

Abstract. Renal cell carcinoma is the most common and the most lethal type of kidney cancer with the highest incidence in developed countries. At the moment of diagnosis, many patients already have developed metastases. Tobacco smoking, obesity, hypertension and occupational exposure are established risk factors. Superoxide dismutase (SOD), catalase (CAT) and glutathione peroxidase (GPx) are antioxidant enzymes (AOE) that have a key role in protecting from reactive oxygen species (ROS) produced in pathological processes. We examined the antioxidant capacity of tumour tissue in patients with clear cell type of renal cell carcinoma. The results showed a significant decrease of AOE activities in the tumour tissue compared to the normal kidney tissue, indicating that the tumour tissue is under permanent oxidative stress. Renal cell carcinoma is highly resistant to radiation therapy, which is also associated with free radical production. Since the tumour tissue has impaired AO capacity, the findings of this study may contribute to the improvement of the potential therapeutic treatments.

show abstract

Section: Discussionsupporting

confidence: 93%

The Antioxidant Capacity of the Kidney Tissue in Patients With Renal Cell Carcinoma

Pavlović¹,

Todorović²,

Stojiljković³

et al. 2016

RAD Conference Proceedings

View full text Add to dashboard Cite

show abstract

“…In a study of antioxidant enzymes in RCC, catalase and selenium-dependent or selenium-independent glutathione peroxidase enzymes were shown to be low (Pljesa-Ercegovac et al, 2008). Another study showed that cytoplasmic superoxide dismutase and glutathione peroxidase activities were lower in RCC tissues than in normal tissues (Lusini et al, 2001).…”

Section: Discussionmentioning

confidence: 99%

Investigating paraoxonase-1 gene Q192R and L55M polymorphism in patients with renal cell cancer

Kara²,

Erol³

et al. 2011

Genet. Mol. Res.

View full text Add to dashboard Cite

ABSTRACT. Increased oxidative stress can help promote carcinogenesis, including development of renal cell carcinoma. The enzyme protects low-density lipoproteins from oxidation and can be a factor in this process. PON1 Q192R and L55M paraoxonase gene polymorphisms were assessed in 60 renal cell carcinoma patients and 60 healthy controls. Genotypes were examined by PCR; the restriction enzyme AlwI was used to examine the Q192R polymorphism and Hsp92II for the L55M polymorphism. Significant differences in the PON1 Q192R polymorphism were found between patients and controls. The Q allele was more frequent in the patient group than in controls, while the R allele was more frequent in the control group. No significant differences were found in the L55M polymorphism. Additionally, there were no significant differences in L and M allele frequencies. We conclude that the R allele may protect against renal cell carcinoma.

show abstract

“…The tumorigenicity of oxidative stress has been observed among various carcinomas, especially in RCC cells, which possess low antioxidant capacities as a consequence of the absence of peroxisomes and the changed redox status (20,21). The defective antioxidant capacity also produces a prooxidant environment in RCC cells and promotes the process of renal tumor genesis (20,22).…”

mentioning

confidence: 99%

Ectopic Expression of Human MutS Homologue 2 on Renal Carcinoma Cells Is Induced by Oxidative Stress with Interleukin-18 Promotion via p38 Mitogen-activated Protein Kinase (MAPK) and c-Jun N-terminal Kinase (JNK) Signaling Pathways

Chen

Dai

Kang

et al. 2012

Journal of Biological Chemistry

View full text Add to dashboard Cite

Background: Ectopically expressed MutS homologue 2 (hMSH2) is a ligand of ␥␦ T cells. Results: Oxidative stress induces ectopic expression of hMSH2 on renal carcinoma cells with IL-18 promotion via p38 MAPK and JNK pathways, promoting ␥␦ T cell-mediated lysis of renal tumor cells. Conclusion: Ectopically expressed hMSH2 is induced under stressful conditions. Significance: We reveal a mechanism of ectopic hMSH2 expression and its contribution to ␥␦ T cell-mediated immunosurveillance in stress.

show abstract

Altered antioxidant capacity in human renal cell carcinoma: Role of glutathione associated enzymes

Cited by 41 publications

References 35 publications

The Antioxidant Capacity of the Kidney Tissue in Patients With Renal Cell Carcinoma

The Antioxidant Capacity of the Kidney Tissue in Patients With Renal Cell Carcinoma

Investigating paraoxonase-1 gene Q192R and L55M polymorphism in patients with renal cell cancer

Ectopic Expression of Human MutS Homologue 2 on Renal Carcinoma Cells Is Induced by Oxidative Stress with Interleukin-18 Promotion via p38 Mitogen-activated Protein Kinase (MAPK) and c-Jun N-terminal Kinase (JNK) Signaling Pathways

Contact Info

Product

Resources

About