Lecithin: cholesterol acyltransferase and na(+)-k(+)-ATPase activity in patients with breast cancer.

Hilal Kiziltunc O., AŞKIN S.

Journal of breast cancer, cilt.16, sa.2, ss.159-63, 2013 (SCI-Expanded) identifier identifier identifier

  • Yayın Türü: Makale / Tam Makale
  • Cilt numarası: 16 Sayı: 2
  • Basım Tarihi: 2013
  • Doi Numarası: 10.4048/jbc.2013.16.2.159
  • Dergi Adı: Journal of breast cancer
  • Derginin Tarandığı İndeksler: Science Citation Index Expanded (SCI-EXPANDED), Scopus
  • Sayfa Sayıları: ss.159-63
  • Anahtar Kelimeler: Acytransferases, Breast neoplasms, Lecithins, Na+-K+-ATPase, Radiotherapy, PLATELET-ACTIVATING-FACTOR, PLASMA, RADIATION, PHOSPHOLIPIDS, ERYTHROCYTES, HYDROLYSIS, METABOLISM, MEN
  • Atatürk Üniversitesi Adresli: Evet

Özet

Purpose: The aim of this study was to determine whether plasma lecithin:cholesterol acyltransferase (pLCAT) and erythrocyte membrane Na+-K+-ATPase ase (emNaKATPs) activity have a correlation in breast cancer. This study compared these parameters at time points before and after treatment with radiotherapy. Methods: The levels of pLCAT and emNaKATPs were assessed in 30 patients with breast carcinoma and 20 control subjects. While emNaKATPs was measured with spectrophotometric method, pLCAT levels was measured using a specific enzyme-linked immunosorbent assay. Results: pLCAT levels, both before and after radiotherapy, were found to be decreased in breast cancer patients than in the controls groups (p<0.001 and p<0.001, respectively). Also, pLCAT levels after radiotherapy were found to be decreased in breast cancer patients than the pLCAT levels before radiotherapy (p<0.001). The emNaKATPs activity were higher in the control group than in the breast cancer patients before/after radiotherapy (RI) (p<0.001 and p<0.001, respectively). At the same time, emNaKATPs activity before RI was higher in the breast cancer patients than emNaKATPs activity after RI (p<0.001). There was a significant correlation between pLCAT and emNaKATPs activity in breast cancer patients receiving radiotherapy (r=0.63, p<0.001), but no correlation between in breast cancer patients before RI and control group (r=0.023, p>0.05). Conclusion: The results of the present study demonstrated that decreased pLCAT and emNaKATPs activity levels in breast cancer patients after/before RI than control group. In addition, decreased emNaKATPs activity in breast cancer patients receiving radiotherapy may be due to decreased pLCAT concentrations and RI beam. In our opinion, altered activities of pLCAT and emNaKATPs are linked to the treatment effect of radiotherapy. These data may clarify the development of cell membrane dysfunction and lipid metabolism in breast cancer patients receiving radiotherapy.