Objective: Ischemia-reperfusion (I-R) injury is defined as the paradoxical exacerbation of cellular dysfunction and death following restoration of blood flow to ischemic tissues. In our study, it was aimed to examine the potential DNA injury effects of liver IR injury with an experimental animal model. Material and Methods: In the study, modeling was done with seven male New Zealand rabbits. Blood samples were taken before the experimental IR model, 30 minutes after ischemia, and 60 minutes after reperfusion. The DNA damage in the blood of the rabbits was measured using Tail Length, Intensity, and Moment techniques. Statistical significance was determined using one-way analysis of variance (ANOVA) and Tukey's post hoc test. Results: There are significant differences between control-ischemia, control-reperfusion and I-R groups in all 3 measurements. Tail length; increased by 51.84%, 54.16% after ischemia and reperfusion, respectively. Tail length increased by 134.09% between control and reperfusion. Similarly, tail density and tail moment were increased by 78.95% (after ischemia), 77.96% (after reperfusion), 85.54% (after ischemia), 165.52% (after reperfusion) respectively. Conclusion: Tissue blood flow disruption is known to occur tissue hypoxia that triggers anaerobic respiration. Restoring blood flow to a hypoxic-tissue results in an increase in reactive oxygen species production. Literature stated I/R-related DNA damage may result from the formation of oxygen radicals during the reperfusion period. Moreover, it induces oxidative damage and exceeds the antioxidative capacity of circulating leukocytes, leading to DNA damage. In our study, DNA lesions characteristic of DNA damage mediated by free radicals were detected at a significantly increased level during reperfusion.