〈Background〉 We reported on the characteristics of green tea extract (GTE)-induced hepatotoxicity in rats. Using this model, we explored the inhibitory effects of n-9 PUFA, mead acid (MA), by dietary supplementation. 〈Methods〉 7-week-old male Sprague-Dawley rats received a single intraperitoneal injection of 200 mg/kg GTE, serum and liver were collected 24, 48 hrs, and 7 days after the GTE injection. The control or 4.8% MA diets was given from one week before GTE injection to sacrifice. Control diet + saline, 4.8% MA diet + saline, control diet + GTE, and 4.8% MA diet + GTE groups were set. Serum biomarkers of hepatotoxicity [aspartate aminotransferase (AST), alanine aminotransferase (ALT)], liver histopathology, and immunohistochemistry of apoptosis (γH2A.X), oxidative stress (8-nitroguanosine) and hypoxia [hypoxia inducible factor (HIF)-1α] were examined. Fatty acid in serum and liver tissue of the control diet + saline and 4.8% MA diet+ saline groups were analyzed. 〈Results〉 In the control diet + GTE group, AST and ALT levels increased. Centrilobular hepatocellular necrosis was seen 24 and 48 hrs after GTE exposure. Furthermore, the levels of these changes decreased in the MA diet group. In the control diet + GTE group, γH2A.X, 8-nitroguanosine, and HIF-1α-positive hepatocytes appeared and peaked at 48 hrs. The level of these changes reduced by MA diet feeding. MA composition in the serum and liver significantly increased in the MA diet group, compared to the control diet group. 〈Conclusion〉The levels of GTE-induced liver damage, such as serum biomarkers, histology, and immunohistochemistry for hepatotoxicity were inhibited by MA diet feeding. This effect may be related to suppression of cell death via the pathway of oxidative stress and hypoxia in the liver.

In the present study, the dietary effects of mead acid (MA; 5,8,11‑eicosatrienoic acid) on 7,12‑dimethylbenz[a]anthracene (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.