Mucosal mitochondrial function and antioxidant defences in patients with gastric carcinoma

C. E. Eapen, Madesh Muniswamy, K. A. Balasubramanian, A. Pulimood, M. Mathan, B. S. Ramakrishna

Research output: Contribution to journalArticle

30 Citations (Scopus)

Abstract

Background: Cancer cells have alterations in energy metabolism due to defective mitochondrial function. This may be due to generation of excessive free radicals and/or defective antioxidant enzyme systems. The aim of the present study was to assess mitochondrial function and antioxidant defences in the gastric mucosa of patients with gastric carcinoma (CA). Methods: Gastric mucosal mitochondrial function was assessed by means of the reduction of tetrazolium dye (MTT), and levels of antioxidants such as glutathione S- transferase (GST), catalase, superoxide dismutase (SOD), and thiols were measured in biopsy specimens taken from the tumour mucosa (TM) and tumour- free (TF) mucosa, 2 cm away from the tumour, in 49 patients with gastric CA and compared with that in 54 controls. In a further 10 patients with gastric CA, these studies were done on TM and TF mucosa 2 cm and ≤ 5 cm away from the turnout. In 10 patients and 5 controls, specimens were obtained for electron microscopy as well. Helicobacter pylori infection was diagnosed by means of histology. Results: MTT reduction and GST and SOD activities were significantly decreased in TM and TF mucosa in patients with CA compared with controls (P < 0.01). The levels of thiols and catalase activity were significantly increased in CA as compared with controls (P < 0.01). H. pylori positivity did not influence most of these variables but did give significant decrease in MTT reduction in CA (TF) mucosa (P = 0.01) and significant increase in thiol levels in CA (TM) mucosa (P = 0.04). Electron microscopy showed mitochondrial alterations in tumour cells in all patients and in adjacent mucosa of 10%-50% of the cells. Conclusions: 1) In gastric CA the cancer mucosal cells and the non-involved cells adjacent to the tumour have defective mitochondrial function, which may be due to altered antioxidant defences and possibly altered free radical formation. 2) Ultrastructural mitochondrial abnormalities are shown to parallel these biochemical abnormalities.

Original languageEnglish (US)
Pages (from-to)975-981
Number of pages7
JournalScandinavian Journal of Gastroenterology
Volume33
Issue number9
DOIs
StatePublished - Oct 7 1998
Externally publishedYes

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Stomach
Antioxidants
Mucous Membrane
Carcinoma
Neoplasms
Sulfhydryl Compounds
Glutathione Transferase
Helicobacter pylori
Catalase
Superoxide Dismutase
Free Radicals
Electron Microscopy
Helicobacter Infections
Gastric Mucosa
Energy Metabolism
Stomach Neoplasms
Histology
Coloring Agents
Biopsy
Enzymes

Keywords

  • Antioxidant enzymes
  • Gastric carcinoma
  • Mitochondrial abnormality

ASJC Scopus subject areas

  • Gastroenterology

Cite this

Mucosal mitochondrial function and antioxidant defences in patients with gastric carcinoma. / Eapen, C. E.; Muniswamy, Madesh; Balasubramanian, K. A.; Pulimood, A.; Mathan, M.; Ramakrishna, B. S.

In: Scandinavian Journal of Gastroenterology, Vol. 33, No. 9, 07.10.1998, p. 975-981.

Research output: Contribution to journalArticle

Eapen, C. E. ; Muniswamy, Madesh ; Balasubramanian, K. A. ; Pulimood, A. ; Mathan, M. ; Ramakrishna, B. S. / Mucosal mitochondrial function and antioxidant defences in patients with gastric carcinoma. In: Scandinavian Journal of Gastroenterology. 1998 ; Vol. 33, No. 9. pp. 975-981.
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AB - Background: Cancer cells have alterations in energy metabolism due to defective mitochondrial function. This may be due to generation of excessive free radicals and/or defective antioxidant enzyme systems. The aim of the present study was to assess mitochondrial function and antioxidant defences in the gastric mucosa of patients with gastric carcinoma (CA). Methods: Gastric mucosal mitochondrial function was assessed by means of the reduction of tetrazolium dye (MTT), and levels of antioxidants such as glutathione S- transferase (GST), catalase, superoxide dismutase (SOD), and thiols were measured in biopsy specimens taken from the tumour mucosa (TM) and tumour- free (TF) mucosa, 2 cm away from the tumour, in 49 patients with gastric CA and compared with that in 54 controls. In a further 10 patients with gastric CA, these studies were done on TM and TF mucosa 2 cm and ≤ 5 cm away from the turnout. In 10 patients and 5 controls, specimens were obtained for electron microscopy as well. Helicobacter pylori infection was diagnosed by means of histology. Results: MTT reduction and GST and SOD activities were significantly decreased in TM and TF mucosa in patients with CA compared with controls (P < 0.01). The levels of thiols and catalase activity were significantly increased in CA as compared with controls (P < 0.01). H. pylori positivity did not influence most of these variables but did give significant decrease in MTT reduction in CA (TF) mucosa (P = 0.01) and significant increase in thiol levels in CA (TM) mucosa (P = 0.04). Electron microscopy showed mitochondrial alterations in tumour cells in all patients and in adjacent mucosa of 10%-50% of the cells. Conclusions: 1) In gastric CA the cancer mucosal cells and the non-involved cells adjacent to the tumour have defective mitochondrial function, which may be due to altered antioxidant defences and possibly altered free radical formation. 2) Ultrastructural mitochondrial abnormalities are shown to parallel these biochemical abnormalities.

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