Liver diseases are often associated with hyperglycemia, inflammation, and oxidative stress. These conditions, commonly associated with diabetes mellitus and obesity, facilitate the formation of advanced glycation end products (AGEs). These products are known to impair protein function and promote inflammation. Accumulation of AGEs such as N(ε)-(carboxymethyl)lysine (CML) is related to chronic liver diseases and their severity. Although several reports suggest a crucial role of AGEs in liver failure, there is little investigation on the direct effects of reducing sugars, precursors of AGEs, and on the onset and progression of liver failure. In this work, we investigate the effects of intravenously administrated glycolaldehyde (GA), a short-chain aldehyde, on oxidative parameters in the liver of Wistar rats. Animals received a single injection of GA (10, 50, or 100 mg/kg) and were sacrificed after 6, 12, or 24 hours. Levels of protein carbonyl, lipid peroxidation, and reduced thiol were quantified. The activities of catalase, superoxide dismutase, and glyoxalase I were also assessed. The amount of CML was quantified with specific antibody. There was an increase in oxidative stress markers in the liver of GA-treated rats. Glycolaldehyde induced a decrease in the activities of all enzymes assayed. Also, all tested doses led to an increase in CML content. Our data suggest that GA might play an important role in liver diseases through the impairment of antioxidant defenses and generation of AGEs.