| PREFACENO is an important bioactive agent and signaling molecule that mediates a diverse array of actions such as vasodilation, neurotrans-mission, and iron metabolism. NO is cytotoxic toward viruses, bacteria , fungi, and protozoa. As a free radical, NO is highly reactive and reacts in biological systems with other free radicals, molecular oxygen , and heavy metals. In addition to its physiological roles, NO causes DNA damage by nitrosative deamination, DNA strand breakage by NO2, oxidative damage and DNA modifications by peroxynitite; NO may cause DNA modification by generating N - nitrosamines and by formadon of DNA - reative lipid - peroxidation - intermediates via peroxynitrite. NO also inhibites certain DNA repair activites.NO is endogenously produced by a family of enzymes known as NO synthases. Isoenzymes of NOS were originally classified into two types, constitutive and incible, based on initial observation of their expression characteristics. The constitutive type includes two types. Ca2+ - dependent isoform (NOS1or 3) were found to be constitutively expressed whereas a Ca + - dependent isoform required induction (iNOS or NOS2 ). NOS2 produces sustained, presumably up to mi-cromolar concentrations of NO, which we postulate, when compared to the rather pmolar range of Ca2+ - controlled NO production by NOS1and 3, may be able to exhaust the well - developed and normally very efficient cellar defense mechanisms.The activation of protooncogenes and inactivation of tumor suppressor genes in affected cells are considered as the core events that provide a selective growth advantage and clonal expassion during the multistep process of carcinogenesis. Somatic mutations, induced by exogenous mechanisms, were found to alter the normal functions of the p53 tumor suppressor gene. p53 is the most prominent example of tumor suppressor genes because it is mutated in about half of all human cancer. In contrast to other tumor suppressor genes like APC and RB, about 80% of p53 mutations are missense mutations that lead to amino acid substitutions in proteins and can alert the protein conformation and increase the stability of p53. These changes can also alter the sequence - specific DNA binding and transcription factor activity of p53. These abnormalities can abrogate p53 dependent pathways involved in important cellular functions like cell - cycle control, DNA repair, differentiation, genomic plasticity and programmed cell death,p53 was first discovered by several independent groups of scientists as a cellar 53 kDa protein that was bound to the large T antigen in SV40 DNA tumor virus transformed cells and expressed at high levels in certain murine or human cancer cell lines. The p53 gene was initially characterized as an oncogene because of its ability to efficiently induce neoplastic transformation of primary rodent cells when cotrans-fected with RAS and EIA. In fact, the p53 cDNA constructs, isolated earlier from human or murine tumor cells, were all missense mutants . the wild - type gene isolated from normal cells: failed to induce neoplastic transformation, inhibited tumor cells growth and blocked neoplastic transformation of primary rodent cells by a mutated in about50% of all human cancers. These facts then led to the reclassification of p53 and EIA as a tumor suppressor gene.In this study, we wanted to assess the correlation between muta-tional p53 and iNOS in ovarian neoplasm. We analyzed the pattern of immunohistochemical stain in 75 cases of paraffin - embeded resected ovarian neoplasm and healthy ovary using a rabbit polyclonal antibody to iNOS and p53.Material and MethodMaterialWe used cases from a ovarian neoplasm debase consisting of 49 paraffin - embeded malignant tumors and 15 paraffin - embeded benign ovarian tumors that had been collected in the Department of Pathology , the first clinical hospital china Medical University dating from 2000 to 2001. And 11 cases healthy ovarian operation specimen are collected as a control.Experiment methodUsing Immuno...
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