The consumption of ethanol disturbs oxidative-reductive balance in the liver leading to oxidative stress, which plays an important role in aging, but also in the pathogenesis of many diseases, including alcoholic liver disease. There are two types of antioxidants protecting cells from free radicals: antioxidant enzymes (including catalase, superoxide dismutase, glutathione peroxidase) and antioxidant low molecular-weight substances (including glutathione). The aim of the study was to define the effect of ethanol consumption on selected parameters of antioxidant defence in rodent models’ livers and to characterise the enzymatic and non-enzymatic mechanisms of antioxidant defence in the liver, based on the currently available literature. The presented data indicate that long-term ethanol consumption leads to decreased activity of superoxide dismutase (SOD) and level of glutathione, as well as increased activity of glutathione reductase, while in the case of catalase and glutathione peroxidise, depending on the study, there is either an increase or decrease of these enzymes activity in the liver. This may be due to the age and gender of animals, different experimental conditions, exposure time, ethanol solution dosage and concentration as well as the methods of administration of the ethanol solution. It should be noted that the experiments were conducted mainly on male rats or mice, which, compared to females, are less susceptible to alcohol-induced damage, and more to oxidative stress, which may have also affected the observed results.