Emamectin benzoate (EMB), which is used as a pesticide in agriculture, household, and veterinary medicine, can cause tissue damage with oxidative toxicity and can be considered as inducing apoptosis. In the present study, male mice were conducted by oral administration in EMB doses 25, 50, and 100 (mg/kg/day) for 14 days. Glutathione (GSH) and thiobarbituric acid reactive substance (TBARS) levels using spectrophotometric methods were measured. 8-hydroxy-2 '-deoxyguanosine (8-OHdG) which is DNA oxidation biomarker and, stress protein (HSP70) levels, caspase 3 enzyme activities were measured by ELISA techniques. This study shows that in vivo administration of EMB caused a marked induction of oxidative damage in liver tissue as demonstrated by an increased level of TBARS and reduced GSH level. The increase in HSP70 level did not prevent the apoptosis caused by the increase of caspase 3 enzyme activity. Toxicity caused by EMB also showed the formation of genotoxicity with an increase in DNA oxidation biomarker 8-OHdG levels. As a result of the study, the effects of toxicity caused by EMB on lipid; protein; and DNA, structural macromolecules in cells, and the importance of enzymatic and non-enzymatic bonds of the cell's protective systems were determined. Consequently, under experimental conditions, EMB exposure caused toxicity in the liver of male mice, and significant adverse effects were determined with biomarkers.