• Ken-ichi Chikutei, Tomohiro M Oyama, Shiro Ishida, Yoshiro Okano, Masako Kobayashi, Hiroko Matsui, Kanna Horimoto, Yumiko Nishimura, Shin-ya Ueno, and Yasuo Oyama.
• Department of Pharmaceutical Care and Clinical Pharmacy, Faculty of Pharmaceutical Sciences, Tokushima Bunri University, Tokushima 770-8512, Japan.
• Eur. J. Pharmacol. 2006 Jul 1; 540 (1-3): 18-23.

AbstractPropofol (2,6-diisopropylphenol) is a general anesthetic possessing a neuroprotective action against oxidative stress produced by H2O2. H2O2 induces an exposure of phosphatidylserine on outer surface of cell membranes, resulting in change in membrane phospholipid arrangement, in rat thymocytes. Since propofol is highly lipophilic, the agent is presumed to interact with membrane lipids and hence to modify the cell vulnerability to H2O2. Therefore, to test the possibility, we have examined the effect of propofol on rat thymocytes simultaneously incubated with H2O2. Although propofol (up to 30 microM) alone did not significantly affect the cell viability, the agent at 10 microM started to increase the population of dead cells in the presence of 3 mM H2O2 and the significant increase was observed at 30 microM. Propofol at clinically relevant concentrations (10-30 microM) facilitated the process of cell death induced by H2O2 in rat thymocytes. However, propofol protected rat brain neurons against the oxidative stress induced by H2O2 under same experimental condition. Therefore, the action of propofol may be dependent on the type of cells.

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