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.