Abstract
Ovarian tumors are in second place (6–8%) from of all the female genital tumors. Benign forms are found in 75–80% of true ovarian tumors. Despite the fairly detailed knowledge of ovarian tumors, causes of origin and benign tumors of ovarian cysts remain open. Several studies have shown the important role of NO in ovarian physiology. It was shown that NO is synthesized locally ovaries and may play a role in the development of follicles, ovulation and luteal formation. Data on changes in the content NO derived and NOS activity in benign ovarian tumor are absent. The aim of the study was to investigate the characteristics of nitrosative status of benign epithelial cystic ovarian tumors of nonendometrioid origin. 220 patients of reproductive age were examined: 40 patients with ovarian follicular cysts, 60 – with serous cystadenomas, 60 – with mucinous cystadenomas, 30 – with cystadenocarcinomas of nonendometrioidnogo origin, 30 patients consist control group. NO x level of in the serum and in intracystic content, iNOS imunoreactivity in the walls of the remote masses were investigated. Study of NO x levels in biological fluids revealed the likely reduction of serum neutral NO metabolites in the cystadenocarcinomas, serous and mucinous cystadenomas in comparison with follicular cysts and control. Differences of intracystic NO x concentrations in mucinous, serous cystadenomas and follicular cysts was small. Immunohistochemical study of iNOS expression showed its small level in follicular cysts and benign cystadenomas, but high level in cystadenocarcinomas. Thus, NO and iNOS effect of on hyperproliferation processes in the ovaries is twofold. NO and iNOS reducing expression and their minor activity may impact on the cystic tumor formation and benign tumor formation in the ovaries. NO overexpression and iNOS increased activity associated with the malignancy processes in cystic formations of epithelial origin.
Highlights
IntroductionORCID: 0000-0002-8405-4457 biomedical research in this field is to elucidate the molecular mechanisms that regulate cell proliferation and apoptosis
Study of NOx levels in biological fluids of examined patients revealed the likely reduction of serum neutral nitric oxide (NO) metabolites in the cystadenocarcinomas (23.1 ± 0.6 mmol/l), serous (24.2 ± 0.3 mmol/l) and mucinous (23.9 ± 0.4 mmol/l) cystadenomas in comparison with follicular cysts (25.2 ± 0.3 mmol/l) and control (26.2 ± 0.2 mmol/l) (Figure 1)
At the same time the level of NOx in intracystic contents of cystadenocarcinomas exceeded that of the follicular cysts in 1.96 times (p < 0.01), in serous cystadenomas in 1.99 times (p < 0.01) and mucinous cystadenomas in 1.79 times (p < 0,01) (Table 2, Figure 2 і 3)
Summary
ORCID: 0000-0002-8405-4457 biomedical research in this field is to elucidate the molecular mechanisms that regulate cell proliferation and apoptosis. STUDY OBJECTIVE Recently there has been an avalanche increase in the number of scientific publications on the study of the role of nitric oxide. The goal of researchers was to study the so-called endothelial vascular relaxation factor (endothelium-derived relaxing factor). An unexpected and important discovery was the fact that this was a factor and nitric oxide (NO) [14]. NO is a biological messenger which is synthesized from L-arginine via nitric oxide synthase (NOS) [15]. Recent literature data show that NO, and NOS can modulate cancer-related events, including nitrozative, oxidative stress, apoptosis, cell cycle, angiogenesis, invasion and metastasis [21]
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