Mitochondrial cytochrome oxidase activity in renal cell carcinoma

Kirkali G., Gezer S., Sercan Z. Y., Akhunlar H., Sercan O., Kirkali Z.

Turkish Journal of Cancer, vol.30, no.1, pp.24-30, 2000 (Scopus) identifier

  • Publication Type: Article / Article
  • Volume: 30 Issue: 1
  • Publication Date: 2000
  • Journal Name: Turkish Journal of Cancer
  • Journal Indexes: Scopus, TR DİZİN (ULAKBİM)
  • Page Numbers: pp.24-30
  • Keywords: Cytochrome oxidase, Mitochondrial DNA, Mutation, Renal cell carcinoma
  • Dokuz Eylül University Affiliated: Yes


The reasons for not using oxidative phosphorylation (OXPHOS), and increased glycolysis in the malignant cell are still controversial. We used human renal cell carcinoma (RCC) tissue from 15 subjects and normal renal parenchyma of the same kidney. Thiobarbituric acid reactive substances (TBARS) level in RCC was significantly higher compared to normal tissue (p<0.001). However sulphydryl group (RSH) level was significantly lower in tumor than normal tissue (p<0.01). There were no mutations in cytochrome oxidase COX I, COX II and COX III genes. Cytochrome-c oxidase activity in tumor tissue was significantly lower compared to normal tissue (p<0.0003). Our data suggest that there may be a post-transcriptional dysfunction of mitochondrial complex genes or the mutations in the nuclear genes and/or tRNA and rRNA genes encoded by mitochondrial DNA that may be generalized to be a part of the multistage carcinogenesis process.