Lecithin: Cholesterol Acyltransferase and Na(+)-K(+)-ATPase Activity in Patients with Breast Cancer.
10.4048/jbc.2013.16.2.159
- Author:
Hilal Kiziltunc OZMEN
1
;
Seda ASKIN
Author Information
1. Department of Radiation Oncology, Ataturk University School of Medicine, Erzurum, Turkey. hkiziltuncozmen@hotmail.com
- Publication Type:Original Article
- Keywords:
Acytransferases;
Breast neoplasms;
Lecithins;
Na(+)-K(+)-ATPase;
Radiotherapy
- MeSH:
Breast;
Breast Neoplasms;
Cell Membrane;
Cholesterol;
Erythrocyte Membrane;
Humans;
Lecithins;
Lipid Metabolism;
Plasma;
Sterol O-Acyltransferase
- From:Journal of Breast Cancer
2013;16(2):159-163
- CountryRepublic of Korea
- Language:English
-
Abstract:
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 (RT) (p<0.001 and p<0.001, respectively). At the same time, emNaKATPs activity before RT was higher in the breast cancer patients than emNaKATPs activity after RT (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 RT 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 RT than control group. In addition, decreased emNaKATPs activity in breast cancer patients receiving radiotherapy may be due to decreased pLCAT concentrations and RT 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.
