Role of lipids, lipoproteins and vitamins in women with breast cancer
Introduction
Breast cancer is one of the most common cancers in women of developed and developing countries [1]. In India, it is the second most frequent cancer, which is estimated to be 19.3% of total female cancers with age standardized rate 17.5 per 100,000 [2]. The exact cause of breast cancer is not completely known, but presumably it represents a complex interplay of genetic susceptibility and environmental factors [3], [4]. Many studies have suggested that the relative risk of breast cancer is directly associated with the increase in dietary fat intake [5]. Animal studies have shown that increased quantities of fat fed during the initiation and promotion stages may increase the development of mammary tumors [6]. Lipids, lipoproteins and antioxidative vitamins have also been associated with the risk of breast cancer [7], [8]. Vitamin A is reported to play a vital role in suppressing carcinogenesis by increasing immunity to tumors through several mechanisms [9]. Because of their antioxidant properties, vitamin C and E neutralize reactive oxygen metabolites (ROMs), and reduce oxidative DNA damage and genetic mutations [10]. It has also been reported that vitamin C and E may enhance host immunologic functions [11]. Epidemiologic studies have indicated an inverse association between vitamin C intake and the risk of cancers [12]. It has been suggested that vitamin C readily scavenges ROMs and provides definite protection against oxidative DNA damage at normal physiologic concentration [13]. Studies also indicate that cancer cells synthesize an increased amount of DNA, RNA and proteins as compared to normal cells [14], which may be controlled by the administration of vitamins [15]. A recent study from our laboratory has reported higher lipid peroxidation (LPO) and ROMs (superoxide anions; O2.-, hydrogen peroxide; H2O2) production, and lower enzyme antioxidant (catalase). Higher superoxide dismutase (SOD) and glutathione peroxidase (GPx) were also reported [16]. O2.- is reduced to H2O2 by the catalytic activity of SOD. Both GPx and catalase again convert H2O2 into H2O. However, accumulation of O2.- and H2O2 results in the formation of hydroxyl radical (·OH), which oxidizes lipids giving rise to LPO [17]. Although ROMs production in our earlier study was higher, however, only on the basis of lower catalase activity, we did not conclude an oxidative stress hypothesis in breast cancer. The present study was conducted to investigate the status of total cholesterol (TC), high-density lipoprotein cholesterol (HDL-C), low-density lipoprotein cholesterol (LDL-C), triglycerides (TG), vitamin A, C, E, and retinol-binding protein (RBP) in females with breast cancer in relation to different clinical stages and menopausal status. Aim of the study was to evaluate the role of lipids and lipoproteins and vitamins, and to find out possible oxidative stress in breast cancer.
Section snippets
Methods
We selected 54 female breast cancer patients admitted to Sucheta Kripalini Hospital, Lady Hardinge Medical College, New Delhi, India. Patients did not receive any chemo- or radiotherapy before blood collection. Ages of patients ranged between 24 and 70 yr (mean 46.9 yr). They were categorized as stage II, III, and IV as well as pre- and postmenopausal patients. The clinical staging of breast cancer was done according to the TNM-UICC classification [18]. Tumor grading was done according to the
Results
In present case-control study, lipids (TC and TG), lipoproteins (HDL-C and LDL-C), vitamins (A, C and E) and RBP were estimated among breast cancer patients in relation to different clinical stages and menopausal status. Of 54 breast cancer patients, 28 were premenopausal and 26 postmenopausal. Out of the total breast cancer patients, 17 (31.5%) were of stage II, 21 (38.9%) of stage III, 16 (29.6%) of stage-IV. Table 1 depicts the status of biochemical parameters studied in breast cancer
Discussion
Oxygen is essential for aerobic life process. However, cells under aerobic condition are threatened with the insult of ROMs that are efficiently taken care of by the powerful antioxidant system in human body. The improper balance between ROMs production and antioxidant defenses results in oxidative stress, which deregulates the cellular functions leading to various pathologic conditions including cancer [26]. Clinical and epidemiologic findings have indicated the role of ROMs in the etiology of
Acknowledgments
The authors wish to thank Prof. S. Ashok, Department of Surgery, Sucheta Kripalini Hospital, Lady Hardinge Medical College, New Delhi, India, for providing patient materials. The work was supported by the grants from All India Council for Technical Education (AICTE) New Delhi (File No. 8017/RDH/BIO/207/98).
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