This study aimed to investigate the effect of glucocorticoid exposure on hepatic glutathione and adenosine contents in pregnant and non-pregnant rats. Rats were grouped into four groups (n=6/group) respectively; pregnant (PRE) and age-matched non-pregnant (NPR) rats received vehicle, pregnant (PRE+DEX) and non-pregnant (NPR+DEX) rats treated with dexamethasone (DEX) received glucocorticoid (DEX; 0.2mg/kg, per oral) between gestational days 14-19 and six days respectively. Statistical analysis was performed using SPSS software (Version 22; SPSS Inc. IL., USA) and data were expressed as mean ± SEM of 6 rats per group. Student’s t-test was used to compare the mean values of variables among the groups. Statistically significant differences were accepted at p<0.05. Data showed that GC exposure caused decreased hepatic glucose-6-phosphate dehydrogenase, glutathione peroxidase, GSH/GSSG ratio and adenosine content in both pregnant and non-pregnant rats. On the other hand, GC exposure led to elevated adenosine deaminase and xanthine oxidase activities, uric acid production, lactate dehydrogenase, aspartate aminotransferase, alanine transferase, alkaline phosphatase and gamma-glutamyltransferase. In sum, the present study indicates that liver damage caused by GC exposure is underlined by depleted hepatic adenosine and glutathione content and elevated markers of tissue inflammation and/or injury. The findings also suggest that the effects of GC exposure on hepatic health are not affected by pregnancy.