Background and objective: Free radical chain reaction is a condition where there is an imbalance between free radicals and antioxidants in the body. This imbalance can lead to cellular and tissue damage, which is of particular concern in the context of cognitive decline associated with diabetes. The aim of this study was to identify molecular and cellular markers of oxidative stress in diabetic rats. Material and methods: The study involved 24 Wistar rats, classified into 3 groups, normal (GT), untreated diabetic (DTN) and treated with D-erythrodihydrosphingosine (inhibitor of Sphingosine kinases 1 and 2) (DTT), fed glucose and food to prevent hypoglycaemia, and subjected to the behavioural test including the 8-arm radial maze. RT-PCR was then used to assess the expression of pro-oxidant (8-hydroxydeoxyguanosine: 8-OHGD) and anti-oxidant (glutathione: GSH and superoxide dismutases: SOD) markers of oxidative stress. Results: The study compared GT with DTN and DTT in a maze task and showed that diabetes affects working memory in diabetic rats. GSH and SOD levels varied according to health status and treatments administered. High levels of GSH and SOD in DTT and DTN suggest high oxidative stress. Low levels in GTs indicate a normal state without significant oxidative stress. The study also found a significant difference between rat groups in the expression of 8-OHGD in the prefrontal cortex. Untreated diabetic rats had higher levels of 8-OHGD, indicating increased oxidative DNA damage due to the oxidative stress associated with diabetes. This shows that diabetes causes increased production of free radicals, leading to cell damage. Conclusion: This work shows that diabetes induces cognitive decline via oxidative stress.