Excessive production of nitric oxide in rat solid tumor and its implication in rapid tumor growth

✍ Scribed by Koichi Doi; Takaaki Akaike; Hidechika Horie; Youichiro Noguchi; Shigemoto Fujii; Toru Beppu; Michio Ogawa; Hiroshi Maeda

• Publisher: John Wiley and Sons
• Year: 1996
• Tongue: English
• Weight: 627 KB
• Volume: 77
• Category: Article
• ISSN: 0008-543X
• DOI: 10.1002/(sici)1097-0142(19960415)77:8<1598::aid-cncr27>3.0.co;2-u

✦ Synopsis

BACKGROUND.

Rapid tumor growth is caused by angiogenesis factors, growth factors, etc. We previously reported a possible connection between nitric oxide (NO) and enhanced vascular permeability in solid tumor. In the present experiment, the role of NO in solid tumor pathology was further investigated in animal tumor.

METHODS.

To identify NO formed in solid tumor (AH136B) implanted in the feet of rats, electron paramagnetic resonance (EPR) spectroscopy was performed directly on the frozen tumor tissue at 110K by measuring endogenous nitrosyl ironsulfur complexes, and by using exogenously added NO capturing agents, i.e., diethyldithiocarbamate (DETC)-Fe2' and N-(dithiocarboxy)sarcosine (DTCS)-Fe2' complexes. Induction of inducible isoform of nosymthase iNOS mRNA was examined with reverse transcriptase-polymerase chain reaction (RT-PCR) combined with Southern blot analysis. In addition, vascular permeability was assessed by measuring extravasation of "Cr-labeled bovine serum albumin in solid tumor.