Mj. Gonzalez et al., DIETARY FISH-OIL INHIBITS HUMAN BREAST-CARCINOMA GROWTH - A FUNCTION OF INCREASED LIPID-PEROXIDATION, Lipids, 28(9), 1993, pp. 827-832
Female athymic nude mice were implanted subcutaneously with human brea
st carcinoma MDA-MB231. Seven to ten days later, the mice were divided
into groups and fed a purified diet containing the following types of
fat (% of diet): (i) 20% corn oil (CO); (ii) 15% CO:5% fish (menhaden
) oil (FO); (iii) 10% CO:10% FO; (iv) 5% CO:15% FO; (v) 1% CO:19% FO;
and (vi) 1% CO:19% FO plus antioxidants (alpha-tocopherol acetate, 200
0 IU/kg diet and tertiary butylhydroquinone, 2% of total fat). The lin
oleic acid levels (% of diet) of the groups were 12.0, 9.1, 6.2, 3.3,
0.9 and 0.9%, respectively. After 6-8 wk, the carcinomas were assessed
for tumor volume (cm3) and assayed for thiobarbituric acid reactive s
ubstances (TBARS). Human breast carcinoma growth was suppressed in mic
e consuming FO diets without antioxidants as compared to mice fed CO;
the greater the amount of dietary FO fed, the greater the carcinoma gr
owth suppression (P < 0.05). The addition of antioxidants to the FO di
et significantly (P < 0.05) reversed the FO-induced carcinoma growth s
uppression. Concentrations of TBARS in the human breast carcinomas wer
e increased in all the FO (without antioxidants) fed mice, compared to
mice fed CO; the level of increase in TBARS was directly related to t
he increase in the level of FO fed (P < 0.05). The addition of antioxi
dants to the FO diet significantly (P < 0.05) reduced the concentratio
n of TBARS in the breast carcinomas. Thus, these results provide evide
nce that dietary FO can significantly suppress growth of human breast
carcinoma MDA-MB231, even in the presence of substantial amounts of li
noleic acid (3.3-9.1%). The inhibitory effect of FO on growth of these
carcinomas was associated with an increased concentration of TBARS in
the tumor tissue. In conclusion, dietary FO induced suppression of hu
man breast carcinoma growth is a function, at least in part, of an acc
umulation of lipid peroxidation products in the tumor tissues.