Dietary effect of mead acid on DMBA‑induced breast cancer in female Sprague‑Dawley rats

In the present study, the dietary effects of mead acid (MA; 5,8,11‐eicosatrienoic acid) on 7,12‐dimethylbenz[a]anthra‐ cene (DMBA)‐induced breast cancer in female Sprague‐Dawley rats were examined. The 2.4 and 4.8% MA diets were commenced when the rats were 6 weeks of age. DMBA was administered by a single oral ingestion when the rats were 7 weeks of age, and the rats were maintained on the respective diets until 19 weeks of age. Tumor weight, histopathology, cell kinetics, and the fatty acid composition in breast tissue and serum were examined. In the control (CTR) group, the DMBA‐exposed rats were fed a basal diet (0% MA). The results revealed that there were no significant differences in tumor incidence, cell kinetics and in the N‐6/N‐3 ratio in breast tissue between the groups. Only the N‐6/N‐3 ratio of fatty acid composition in serum was significantly decreased in the 2.4% MA diet group. In previous studies, the 2.4% MA diet was shown to suppress N‐methyl‐N‐nitrosourea‐induced luminal A mammary cancer by decreasing cancer cell proliferation. The findings of the present study differ from those of previous studies with different breast cancer models. To further clarify the effects of MA against breast carcinogenesis, further investigations with different experimental breast cancer models are recommended. Introduction Breast cancer is the most frequent type of tumor occurring in women globally and its incidence has recently increased (1). Epidemiological investigations have demonstrated an associa‐ tion between the incidence of breast cancer and dietary habits. For example, a high‐fat diet has been shown to increase the risk of breast cancer (2,3). Notably, polyunsaturated fatty acids (PUFAs) are highly associated with mammary carcinogenesis. For example, n‐3 fatty acids, such as eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA) have been shown to suppress the growth of breast cancer in vitro and in vivo (4‐6). In contrast to these findings, n‐6 fatty acids, such as linoleic acid (LA) and arachidonic acid (AA) have been shown to promote the development of breast cancer (7,8). The asso‐ ciation between fatty acids and carcinogenesis thus needs to be clarified, in order to establish new dietary habits which may prevent cancers. The effects of n‐9 fatty acids on breast carcinogenesis are not yet well understood. Mead acid (MA) is a 20:3 n‐9 fatty acid (5,8,11‐eicosato‐ rienoic acid) that was characterized by Mead and Slaton (9). MA can be found in minor quantities in the plasma and tissues of adult mammals and is synthesized from oleic acid (OA;18:1 n‐9) by elongation and desaturation when essential n‐3 and n‐6 PUFAs are deficient (10,11). The anticancer effects of MA were previously investigated against luminal type A breast cancer (12). MA was found to suppress the growth of breast cancer cells (KPL‐1) in vitro. The dietary administration of MA was also shown to suppress the growth of transplanted KPL‐1 tumors in nude mice (12). In another previous in vivo study using female rats, breast cancer was induced by the carcinogen, N‐methyl‐N‐nitrosourea (MNU), and MA was shown to suppress the growth of breast tumor xenografts (13). In addition to the present study, to the best of our knowledge, only one previous study has been conducted to date reporting Dietary effect of mead acid on DMBA‐induced breast cancer in female Sprague‐Dawley rats YUICHI KINOSHITA1*, MASAHIRO YOSHIOKA2*, YUKO EMOTO3, TAKASHI YURI2, MICHIKO YUKI4, CHIHIRO KOYAMA5, AKIKO TAKENOUCHI5, KEI HAMAZAKI6, AIRO TSUBURA7 and KATSUHIKO YOSHIZAWA5 1Division of Central Laboratory of Medicine and Pathology, Wakayama Medical University Hospital, Wakayama 641‐8510; 2Department of Nutrition, Koshien University, Takarazuka, Hyogo 665‐0006; 3Ethics Review Center, Kansai Medical University, Hirakata, Osaka 573‐1010; 4Department of Pathology, Hyogo College of Medicine, Nishinomiya, Hyogo 663‐8501; 5Department of Innovative Food Sciences, School of Food Sciences and Nutrition, Mukogawa Women's University, Nishinomiya, Hyogo 663‐8558; 6Department of Public Health, Faculty of Medicine, University of Toyama, Toyama 930‐0194; 7Department of Pathology, Osaka Prefectural Saiseikai Izuo Hospital, Osaka 551‐0032, Japan Received June 22, 2020; Accepted August 31, 2020 DOI: 10.3892/ijfn.2020. 7 Correspondence to: Professor Katsuhiko Yoshizawa, Department of Innovative Food Sciences, School of Food Sciences and Nutrition, Mukogawa Women's University, 6‐46 Ikebiraki‐cho, Nishinomiya, Hyogo 663‐8558, Japan E‐mail: yoshizak@mukogawa‐u.ac. jp *Contributed equally