Fenofibrate with its well established safety profile could offer an inexpensive, safe and effective prophylactic therapy for JEV infection. Apigenin were evaluated following acute exposure through intraperitoneal route to understand the dose dependent effects in Swiss mice. Intraperitoneal route of exposure enables the maximum bioavailability of Apigenin in liver. Doses of Apigenin were equivalent to the human exposure of flavones based on the equivalent body Chlorpropamide surface area index. Male Swiss mice were used in the present study to avoid any sex dependent variations in toxic effects in female mice due to the estrogenic action of Apigenin. Significantly increased serum ALT, AST and ALP in 100 and 200 mg/kg Apigenin treated groups indicate the insults to liver as increased ALT, AST and ALP in serum are typical indicators of damaged liver. Escitalopram Oxalate Galati also reported 4-fold increased plasma ALT in CD-1 mice following of intraperitoneal injection of flavonoids like EGCG, propyl gallate, gallic acid and tannic acid. Normal liver histoarchitecture of Apigenin treated animals supports the serum findings and suggestive of non toxic effects at these doses. Hydropic changes along with ballooning and degeneration of hepatocytes treated groups are the signs of adverse effects on mouse liver. Previous studies also demonstrated ROS production by Apigenin. LPO is initiated by the attack of free radicals on fatty acid or fatty acyl side chain of any chemical entity and is regarded as one of the basic mechanism of tissue damage.The increase of LPO level in Apigenin treated mice at 100 and 200 mg/kg indicates free radical generation showing the pro-oxidant nature of Apigenin. Similar nature of Apigenin is also demonstrated in the presence of high iron concentration in rat hepatocytes. Decreased GSH and increased ratio of GSSG and GSH in mice liver further supports this view. Similar observations were made by Kachadourian and Day in PC3 cells following Apigenin treatment. GSH is the functional anti-oxidative system in physiological conditions; its depletion might be due to its direct involvement in scavenging ROS in the process of neutralization and subsequent protection of essential thiol groups from oxidation. ROS are scavenged by cellular antioxidant defence system which includes intracellular enzymes such as SOD, CAT, GPx and GST. SOD activity and expression was decreased significantly following 100 and 200 mg/ kg Apigenin doses. As SOD dismutates superoxide into oxygen and H2O2 provides an important antioxidant defence in cells exposed to oxygen, its decrease infers excessive ROS generation. Significantly increased CAT activity in 200 mg/kg Apigenin treated mice clearly indicates H2O2 generation. Unaltered CAT in mice at 100 mg/kg dose may be due to more turnover of CAT in cells following Apigenin exposure. CAT is solely responsible for the destruction of H2O2 while GPx has a wide spectrum of activity and reduces lipid peroxides. In the lower dose groups CAT and GPx activities and mRNA level were not increased which might be due to insufficient ROS production in mice liver.