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Preuss Laboratory for Molecular Neuro-oncology, Brain Tumor Research Center, Departments of Neurological Surgery [C. S. C., K. D. A., M. A. I.] and Physiology [J. E. B., D. S. B.], University of California, San Francisco, California 94143
The nitric oxide synthases (NOS) are a family of related enzymes which regulate the production of NO, a free radical gas implicated in a wide variety of biological processes. Vasodilation and increased tumor blood flow, increased vascular permeability, modulation of host tumoricidal activity, and free radical injury to tumor cells and adjacent normal tissues are pathophysiological features of malignant tumors that may be mediated by NO. We examined human brain tumors for three NOS isoforms and NADPH diaphorase, a histochemical marker of NOS activity in the brain. We detected increased expression of the brain and endothelial forms of NOS [NOS I and NOS II, respectively (C. Nathan and Q. Xie. Cell, 78: 915–919, 1994)] in astrocytic tumors, and the highest levels of expression was found in higher grade tumors. Each of these two isoforms was found in tumor cells and tumor endothelial cells. The macrophage isoform of NOS (NOS III) was less frequently detected and expressed at a lower level, predominantly in tumor endothelial cells. NADPH diaphorase staining for NOS activity paralleled this pattern of NOS expression. Western blot analysis of tumor tissues for these NOS isoforms confirmed these observations. Our data indicate that malignant central nervous system neoplasms express unexpectedly high levels of NOS and suggest that NO production may be associated with pathophysiological processes important to these tumors.
1 This work was supported in part by NIH Grant 5 P20 NS31076 and grants from the Price Family Foundation, the Preuss Foundation, Ride for Kids Foundation, and the Betz Foundation.
2 To whom requests for reprints should be addressed, at Preuss Laboratory for Molecular Neuro-oncology, Brain Tumor Research Center, Department of Neurological Surgery, University of California, San Francisco, CA 94143-0520.
Received 10/31/94. Accepted 1/ 6/95.
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