Improved antioxidant status by omega-3 fatty acid supplementation in breast cancer patients undergoing chemotherapy: a case series.

INTRODUCTION: Breast cancer is the second leading cause of cancer death in women worldwide and the third most common cancer in India. Various studies have reported that chemotherapy reduces the antioxidant status in patients with cancer. A diet rich in omega-3 fatty acids has been shown to offer protection against breast cancer through various mechanisms. However, there are no reports suggesting a relationship between consumption of omega-3 fatty acids during chemotherapy and antioxidant status in patients with breast cancer. Thus, the objective of this study was to evaluate whether fish oil supplementation could improve the antioxidant status of five women with breast cancer undergoing chemotherapy. CASE PRESENTATION: We report on the cases of five Indian women with breast cancer, in the age group of 34 to 60 years, who had poorly differentiated breast carcinoma and underwent modified radical mastectomy. Postsurgery, the patients were given fish oil capsules containing eicosapentaenoic acid (180 mg) and docosahexaenoic acid (120 mg)/capsule during their chemotherapy. Informed consent was obtained from each participant and they were followed-up to the completion of six chemotherapy cycles at 21-day intervals. CONCLUSIONS: The supplementation of fish oil significantly (p < 0.01) increased superoxide dismutases, glutathione reductase and catalase activity in red blood cells as well as the total plasma antioxidant status in the patients. This approach of using omega-3 fatty acids as an adjuvant treatment for breast cancer may help oncologists to manage the side effects of ongoing chemotherapy by improving the antioxidant status in patients.

Metabolic clock generates nutrient anticipation rhythms in mTOR signaling.

The mTOR signaling pathway modulates metabolic processes with respect to nutrient availability and other growth-related cues. According to the existing paradigm, mTOR complex 1 (mTORC1) activityin vivo is induced by food and gradually decreases during fasting. We found that mTORC1 activity is controlled by an internal clock mechanism different from the known light-entrainable circadian clock. We observed 24-hr rhythms in phosphorylation of mTORC1 downstream targets, which were entrained by food, persisted during fasting and could be uncoupled from oscillating expression of the canonical circadian clock genes. Furthermore, these rhythms were present in tissues of mice with disrupted light-entrainable circadian clock. We propose tissue-specific rhythms in the expression of tor and its negative regulator deptor as the molecular mechanism of the mTORC1 activity oscillation. Our data demonstrate the existence of at least two independent molecular circadian clocks: one providing metabolic adaptation to periodic light/darkness and the other - to feeding.