Acute and chronic stress can induce production of reactive oxygen species that can cause oxidative stress, which is recognized to be one of the key pathophysiological mechanism in liver and other diseases development. The aim of this study was to estimate the impact of acute and chronic stress on the oxidative stress development and antioxidative status of the liver in males (M), non-ovariectomized (NE-OVX) and ovariectomized (OVX) female rats. Seventy 16-week-old rats were included in the study and divided into nine groups: M, NE-OVX and OVX females that were exposed to acute stress; M, NE-OVX, and OVX females that were exposed to chronic stress; and M and NE-OVX females as a control groups. As an indicator of liver oxidative damage, lipid peroxidation levels expressed in terms of thiobarbituric acid reactive substances (TBARS) were determined, while liver antioxidative status was determined by catalase, superoxide dismutase, glutathione peroxidase, glutathione reductase, glutathione S-trasferase activities and oxidized/reduced glutathione (GSH/GSSG) ratio. Both acute and chronic stress significantly increased TBARS content in the liver of all groups relative to control groups. Results showed that acute and chronic stress lowered antioxidant defense capacity, as evaluated by the significant decrease in the GSH/GSSG ratio of some groups and decrease of some antioxidative enzymes activities. Ovariectomy itself resulted in the oxidative stress development. The analyzed data indicate that acute and chronic stress induced oxidative stress and decreased antioxidative capacity in rat liver. The oxidative and antioxidative response to acute and chronic stress were partially sex specific, while the intensity of the oxidative stress was the highest in the OVX females.