Background: Oleic acid (OA) is a monounsaturated compound with many health-benefitting properties such as obesity prevention, increased insulin sensitivity, antihypertensive and immune-boosting properties, etc. Within the untold benefits of this fatty acid is the novelty of anticancer property. OA can interact with cancer cell proteins and increase cancer cell proliferation-inhibiting factors; thus, turning down their potentials to spread to other tissues. Purpose: The proposal in the present work was to carry out a factual analysis on how oleic acid (OA) and some anticancer drugs offset nitropropionic acid-induced oxidative stress . Methods: Thirty Wistar rats were recruited and divided into five groups A, B, C, D and E; and made to take anticancer drugs in combination with OA in the following forms: Group A, (control) 0.9% of sodium chloride (NaCl); group B, oleic acid ( OA ) only ; group C, cyclophosphamide (CPP) + OA; group D, daunorrubicine (DRB) + OA; and group E , dexrazoxane (DXN) + OA. Every treatment was by intraperitoneal route and the administration was every 24 h for 5 days. The measurement of lipid peroxidation products, reactive oxygen species, sodium-potassium pump, antioxidants and amines were performed from brain extracts of the animals using TBARS, H 2 O 2 , Na+, K+ ATPase activity, GSH and dopamine (DA) respectively. Glucose hemoglobin and triglycerides were measured in blood. Results: In cortex, GSH increased in all groups, except in group B . Group C showed the highest increase of this biomarker. TBARS decrease and dopamine increase in all regions of groups C, D and E. H 2 O 2 increased only in cerebellum/medulla oblongata of group D and E. ATPase expression decreased in striatum of group C. Glucose increased in group E and hemoglobin increased in groups C and D. Conclusions: The boost in the amine (DA) and the antioxidant (GSH) generated by OA administration depicts that brain damage due to anticancer drugs could be ameliorated when jointly given with OA.