NADPH oxidases (NOX) are reactive oxygen species- (ROS-) generating enzymes regulating numerous redox-dependent signaling pathways. NOX are important regulators of cell differentiation, growth, and proliferation and of mechanisms, important for a wide range of processes from embryonic development, through tissue regeneration to the development and spread of cancer. In this review, we discuss the roles of NOX and NOX-derived ROS in the functioning of stem cells and cancer stem cells and in selected aspects of cancer cell physiology. Understanding the functions and complex activities of NOX is important for the application of stem cells in tissue engineering, regenerative medicine, and development of new therapies toward invasive forms of cancers.

This study shows for the first time that chemerin and vaspin serum concentrations are altered in patients with NAFLD. The analyzed adipokines appear to play a pivotal role in the pathogenesis of NAFLD, not only as regulators of insulin sensitivity, but also as mediators of the inflammatory process.

Chronic hepatitis C (CHC) is generally a slowly progressive disease, but some factors associated with rapid progression have been identified. Steatosis, independently of its metabolic or viral origin, leads to liver injury and fibrosis. It is suggested that hepatitis C virus may contribute to a wide spectrum of metabolic disturbances-namely, steatosis, insulin resistance, increased prevalence of impaired glucose tolerance, type 2 diabetes mellitus and lipid metabolism abnormalities. Adipokines, which are produced mainly by adipose tissue, may influence the inflammatory response and insulin sensitivity and contribute to the development of metabolic abnormalities in CHC and also regulate fibrogenesis and angiogenesis. Visfatin was described as an adipokine with immunomodulating and proinflammatory properties that promotes B-cell maturation and enhances activation of leukocytes, synthesis of adhesion molecules and production of proinflammatory cytokines. Visfatin exerts insulin-mimetic effects, decreases plasma glucose levels and regulates cell energy balance. Chemerin stimulates chemotaxis of dendritic cells, macrophages and natural killer (NK) cells toward the site of inflammation. On the other hand, it inhibits synthesis of proinflammatory mediators and enhances adiponectin production, influences adipocyte differentiation and maturation and regulates glucose uptake in adipocytes. Vaspin expression in human adipose tissue seems to be a compensatory mechanism associated with obesity and insulin resistance. Vaspin suppresses leptin, tumor necrosis factor (TNF)-α and resistin expression. Leptin protects against liver steatosis but accelerates fibrosis progression and exacerbates the inflammatory process. In contrast, adiponectin exerts a hepatoprotective effect. In this report, data indicating a possible role of these adipokines in the pathogenesis of chronic hepatitis are summarized.

Authors believe that metformin-based therapy, a cornerstone in diabetes therapy, not only improves the prognosis of diabetics by reducing blood glucose but also by reducing oxidative stress, inflammatory cytokine production and the shift toward alternative activation of macrophages.

Background. Propolis is a natural product widely consumed in folk medicine. Different biological activities, such as anticancer, antioxidant, anti-inflammatory, antibiotic and antifungal effects have been reported for propolis and its constituents.Objectives. An in vitro study focused on an evaluation of the biological activity of EEPP, including its anti-proliferative influence on selected neoplastic cells, considering qualitative-quantitative chemical characterization of Polish propolis. Material and Methods. Cytotoxicity was evaluated by means of the MTT and LDH assays. The apoptosis was determined using fluorescence microscopy with annexin V-FITC. Additional EEPP composition was analyzed by a High Performance Liquid Chromatography (HPLC) method. The antimicrobial activity was evaluated by minimal inhibitory concentrations (MIC) against Streptococcus aureus, Enetecoccus faecalis, Escherichia coli, Pseudomonas aeruginosa and Candida albicans.

Coffee is one of the most popular beverages worldwide. Coffee contains bioactive compounds that affect the human body such as caffeine, caffeic acid, chlorogenic acids, trigonelline, diterpenes, and melanoidins. Some of them have demonstrated potential anticarcinogenic effects in animal models and in human cell cultures, and may play a protective role against colorectal cancer. Colorectal cancer (CRC) is the third leading cause of cancer-related mortality in the USA and other countries. Dietary patterns, as well as the consumption of beverages, may reduce the risk of CRC incidence. In this review, we focus on published epidemiological studies concerning the association of coffee consumption and the risk of development of colorectal cancer, and provide a description of selected biologically active compounds in coffee that have been investigated as potential cancer-combating compounds: Caffeine, caffeic acid (CA), chlorogenic acids (CGAs), and kahweol in relation to colorectal cancer progression in in vitro settings. We review the impact of these substances on proliferation, viability, invasiveness, and metastasis, as well as on susceptibility to chemo- and radiotherapy of colorectal cancer cell lines cultured in vitro.

Visfatin has recently been established as a novel adipokine that is predominantly expressed in subcutaneous and visceral fat. Only few studies have investigated the effect of visfatin on prostate, breast, ovarian cancer as well as on astrocytoma cell biology. There have been no previous studies on antioxidative enzyme activities, proliferation processes or levels of DNA damage in malignant melanoma cells in response to visfatin stimulation. Here, we report that visfatin increases activity of selected antioxidative enzymes (SOD, CAT, GSH-Px) in culture supernatants of Me45 human malignant melanoma cells. Our findings suggest that visfatin triggers a redox adaptation response, leading to an upregulation of antioxidant capacity along with decreased levels of the lipid peroxidation process in Me45 melanoma cells. Moreover, visfatin led to a significantly increased proliferation rate in the study using the [(3)H]thymidine incorporation method. Unlike insulin, visfatin-induced melanoma cell proliferation is not mediated by an insulin receptor. Better understanding of the role of visfatin in melanoma redox states may provide sound insight into the association between obesity-related fat adipokines and the antioxidant defense system in vitro in melanoma progression.

Abstract:The biological activity of nanosize silver particles towards oral epithelium-derived carcinoma seems to be still underinvestigated. We evaluated the influence of low doses of nanosize scale silver particles on the proliferation and viability of malignant oral epithelial keratinocytes in vitro, alone and in conjunction with the plant alkaloid berberine. Cells of human tongue squamous carcinoma SCC-25 (ATCC CRL-1628), cultivated with the mixture of Dulbecco's modified Eagle's medium, were exposed to silver nanoparticles alone (AgNPs, concentrations from 0.31 to 10 µg/mL) and to a combination of AgNPs with berberine chloride (BER, 1/2 IC 50 concentration) during 24 h and 48 h. The cytotoxic activity of AgNPs with diameters of 10 nm˘4 nm was measured by 3-(4,5-dimethyl-2-thiazyl)-2,5-diphenyl-2H-tetrazolium bromide (MTT) assay. Cell cycle analysis was performed by treating cells with propidium iodide followed by flow-activated cell sorting. RT-QPCR reaction was used to assess expression of anti-apoptotic proteins Bcl-2 and pro-apoptotic protein Bcl-2-associated X protein Bax genes expression. Monodisperse silver nanoparticles at a concentration of 10 µg/mL arrested SCC-25 cells cycle after 48 h at the G0/G1 phase in a dose-and time-dependent manner through disruption G0/G1 checkpoint, with increase of Bax/Bcl-2 ratio gene expression. AgNPs exhibit cytotoxic effects on SCC-25 malignant oral epithelial keratinocytes, which is diminished when combined with BER. The AgNPs concentration required to inhibit the growth of carcinoma cells by 50% (IC 50 ) after 48 h was estimated at 5.19 µg/mL. AgNPs combined with BER increased the expression of Bcl-2 while decreasing the ratio of Bax/Bcl-2 in SCC-25 cells. Silver particles at low doses therefore reduce the proliferation and viability of oral squamous cell carcinoma cells. SCC-25 cells are susceptible to damage from AgNPs-induced stress, which can be regulated by the natural alkaloid berberine, suggesting that nanoparticles may be potentially used in a chemoprevention/chemotherapy by augmentation of action of standard anti-cancer drugs.