• Ewa Romuk, Wioletta Szczurek, Przemysław Nowak, Marta Skowron, Bernard Prudel, Edyta Hudziec, Ewa Chwalińska, and Ewa Birkner.
• Department of Biochemistry, Medical University of Silesia, School of Medicine with the Division of Dentistry, Zabrze, Poland.
• Postepy Hig Med Dosw (Online). 2016 Dec 31; 70 (0): 1441-1450.

IntroductionPropofol is an intravenous sedative-hypnotic agent that is commonly used to induce and maintain general anaesthesia. This drug has antioxidant properties, which are partly caused by a phenolic structure similar to α-tocopherol. The present study aimed to evaluate the effect of propofol on the level of oxidative stress biomarkers in the frontal cortex, striatum, thalamus, hippocampus and cerebellum in rats with experimental Parkinson's disease (PD).Material/MethodsThe experiment was performed on 24 male Wistar rats assigned to the following groups: 1 - control; 2 - PD; 3 - PD with propofol. The dopaminergic systems were damaged with 6-hydroxydopamine (6-OHDA) administered to each lateral ventricle (2x15 μg/5 μl). 60 mg/kg of propofol was later given to the 8-week-old rats intraperitoneally. The activities of superoxide dismutase (SOD) and its enzymes Cu/ZnSOD and MnSOD, together with the malondialdehyde (MDA) concentration, total oxidative status (TOS) and total antioxidant capacity (TAC), were measured.ResultsIn the 2nd group, a significant increase in MDA concentration in the striatum, hippocampus and thalamus, and an increase of TOS in the striatum, thalamus and cerebellum were noted, along with a TAC decrease in the cortex, striatum and thalamus. Propofol caused a significant decrease in MDA levels in the cortex, striatum, hippocampus and thalamus, and a decrease in TOS levels in the cortex, striatum and cerebellum, with increased TAC in all evaluated structures.ConclusionsA shortage of natural antioxidants is observed in PD, along with an increase in pro-oxidants in many brain areas. Propofol inhibits oxidative stress in the brain, which shows its neuroprotective properties against oxidative damage.

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