In Reply:—  We appreciate Dr. Xia’s comments regarding our article.1As far as we understand, the comments can be summarized into two issues, including why we did not adopt the term “superoxide production” in the title of our article and why we focused our study on levels of superoxide, but not hydrogen peroxide, induced by the high concentration of glucose. We agree with Dr. Xia’s concern that oxidative stress results from an imbalance between the formation and the neutralization of oxidants. This is why we mentioned in the title of our article that propofol confers a decrease in oxidative stress, but not superoxide production, because we did not find definite evidence to support whether the effect of propofol on levels of superoxide in the rat brain slice is due to the inhibitory effect of this intravenous anesthetic on the formation or the neutralization of superoxide. Whether short- or long-term, exposure to high glucose reportedly increases superoxide levels within human tissues including vascular smooth muscle cells.2,3Considering these previous results, we conducted our study to evaluate the involvement of superoxide in the malfunction of cerebral microvessels induced by high glucose.1It is also crucial to note that chronic hyperglycemia predisposes to exaggerated inflammatory response and leukocyte dysfunction corresponding with superoxide production induced by nicotinamide adenine dinucleotide phosphate oxidase.4Therefore, it seems difficult to draw the conclusion that hydrogen peroxide solely contributes to all inflammatory processes induced by hyperglycemia and/or diabetes mellitus.

*Wakayama Medical University, Wakayama, Japan.

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Kinoshita H, Azma T, Nakahata K, Iranami H, Kimoto Y, Dojo M, Yuge O, Hatano Y: Inhibitory effect of high concentration of glucose on relaxations to activation of ATP-sensitive K+channels in human omental artery. Arterioscler Thromb Vasc Biol 2004; 24:2290–5
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