A mode of action of acetaminophen （APAP）-induced renal toxicity is supposedly via N-acetyl-p-benzoquinone imine. In this renal toxicity model we explored the inhibitory effects of mead acid （MA）, which is an n-9 PUFA of dietary supplementation. Seven week-old male SD rats received a single intraperitoneal injection of 500 mg/kg APAP and serum and kidney samples were collected at 24 and 48hrs after. Basal or 4.8% MA diets were given from one week before the APAP injection until sacrifice. Experimental groups were basal diet + vehicle, 4.8% MA diet + vehicle, basal diet + APAP, and 4.8% MA diet + APAP. Biomarkers of renal toxicity （blood urea nitrogen （BUN）, creatinine （CRE））, histopathology of kidney and immunohistochemistry for drug-metabolizing enzyme （cytochrome P4502E1（CYP2E1）） and oxidative stress （heme oxgenase （HO-1）, thymidine glycol （TG）） were performed. The diacron-reactive oxygen metabolites （d-ROMs） and bioantioxidant power （BAP） tests were conducted to detect oxidative stress and anti-oxidative activity in serum, respectively. In the basal diet+ APAP group, the BUN and CRE levels were significantly increased and acute necrosis and dilatation in the renal outer medullary area were present. Tubular necrosis was detected mainly in proximal tubules which was positive for CYP2E1. HO-1 and TG signals were also seen in these epithelia. In contrast, these tubular changes and expression of HO-1signal were reduced in the rats fed the MA diet. MA supplementation inhibited APAP induced renal toxicity via the decreased level of oxidative stress in kidney.

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.