Cancer is the most common cause of death worldwide. Annually, more than ten million new cancer cases are diagnosed, and more than six million deaths occur due to cancer. Nonetheless, over 80% of human cancer may be preventable through proper nutrition. Numerous nutritional compounds are effective in preventing cancer. Selenium and zinc are essential micronutrients that have important roles in reducing oxidative stress and protecting DNA from the attack of reactive oxygen species. Selenium is an essential trace element that possesses several functions in many cellular processes for cancer prevention. Meanwhile, zinc may have protective effects on tumor initiation and progression, and it is an essential cofactor of several mammalian proteins. Results show that both selenium and zinc provide an effective progression of DNA repair system; thus, cancer development that originated from DNA damage is decreased. Results mostly focus on the separate effects of these two elements on different cell types, tissues, and organs, and their combined effects are largely unknown. This review aimed to emphasize the joint role of selenium and zinc specifically on DNA repair for cancer prevention.
In this preliminary study, a new series of some cerium vanadate derivatives have been investigated as new type of inhibitors of xanthine oxidase (XO; E.C 1.17.3.2). XO is a superoxideproducing enzyme found normally in serum and the lungs, and its activity is concerned with several important health problems such as gout, severe liver damage, vascular dysfunction and injury, oxidative eye injury and renal failure. In this study, we present a critical overview of the effects of these novel type agents on XO with comparing the efficacy and safety profiles of allopurinol, the efficient classical inhibitor of XO.
Pathogenesis of cancer is a multi-step process containing a number of cellular alterations such as post-translational dysregulation of intracellular signaling proteins. These alterations control several functions in carcinogenesis such as angiogenesis, metastasis, evading growth suppressors, and sustaining proliferative signaling. Data of various studies has demonstrated that Phosphatidylinositol 3-kinase (PI3K/AKT) and Mitogen-activated protein kinase (ERK/MAPK) pathways are both abnormally activated in many cancer types, including neuroblastoma. ERK/MAPK and PI3K/AKT signaling pathways that are regulated by sequential phosphorylation upon extracellular stimulation have many important functions in cell cycle, migration, proliferation and apoptosis. Besides their aberrant phosphorylation/activation, there is a crosstalk between these two pathways resulting in an anti-apoptotic effect. In this chapter, carcinogenetic abnormalities in post-translational regulation of the activity of ERK/MAPK and PI3K/AKT pathways in neuroblastoma and other cancers will be summarized. In addition, several crosstalk nodes between two pathways will be briefly explained. All these concepts are not only crucial for thoroughly understanding the molecular basis of carcinogenesis but also choosing the appropriate molecular targets for effective diagnosis and treatment.
In this study, 9-benzylidene-9H-fluorene-substituted urea (5a-p) and thiourea derivatives (5q-v) were synthesized and their inhibitory effects on the activity of human carbonic anhydrase (hCA) I and II were evaluated. hCA I and II were purified from human erythrocytes using a Sepharose 4B-L-tyrosinesulphanilamide affinity column. All the synthesized compounds inhibited the activity of the hCA I and II isoenzymes. Among the synthesized compounds, 5f was found to be the most active (IC 50 = 21.4 μM) for inhibition of hCA I and 5s was the most active (IC 50 = 25.3 μM) for inhibition of hCA II. IN VITRO ИНХИБИЦИЈА НА ПРЕЧИСТЕНА ЧОВЕЧКА КАРБОНСКА АНХИДРАЗА I И II СО НОВИ ФЛУОРЕНСКИ ДЕРИВАТИВо оваа студија беа синтетизирани деривати на уреа (5a-p) и тиоуреа (5q-v) добиени со супституција на 9-безилиден-9H-флуорен и беше проценет нивниот инхибиторен ефект врз човечка карбонска анхидраза (hCA) I и II. HCA I и II беа пречистени од човечки еритроцити со употреба на афинитетната колона Sepharose 4B-L-тирозин-сулфаниламид. Сите синтетизирани соединенија ја инхибираа активноста на изоензимите на hCA I и II. Од синтетизираните соединенија, 5f се покажа најактивно (IC 50 = 21,4 μM) за инхибиција на hCA I, додека 5s беше најактивно (IC 50 = 25,3 μM) за инхибиција на hCA II.Клучни зборови: 9-безилиден-9H-флуорен; уреа; тиоуреа; карбонска анхидраза; инхибиција
Katanin is a microtubule severing protein belonging to the ATPase family and consists of two subunits; p60‐katanin synthesized by the KATNA1 gene and p80‐katanin synthesized by the KATNB1 gene. Microtubule severing is one of the mechanisms that allow the reorganization of microtubules depending on cellular needs. While this reorganization of microtubules is associated with mitosis in dividing cells, it primarily takes part in the formation of structures such as axons and dendrites in nondividing mature neurons. Therefore, it is extremely important in neuronal branching. p60 and p80 katanin subunits coexist in the cell. While p60‐katanin is responsible for cutting microtubules with its ATPase function, p80‐katanin is responsible for the regulation of p60‐katanin and its localization in the centrosome. Although katanin has vital functions in the cell, there are no known posttranscriptional regulators of it. MicroRNAs (miRNAs) are a group of small noncoding ribonucleotides that have been found to have important roles in regulating gene expression posttranscriptionally. Despite being important in gene regulation, so far no microRNA has been experimentally associated with katanin regulation. In this study, the effects of miR‐124‐3p, which we detected as a result of bioinformatics analysis to have the potential to bind to the p60 katanin mRNA, were investigated. For this aim, in this study, SH‐SY5Y neuroblastoma cells were transfected with pre‐miR‐124‐3p mimics and pre‐mir miRNA precursor as a negative control, and the effect of this transfection on p60‐katanin expression was measured at both RNA and protein levels by quantitative real‐time PCR (qRT‐PCR) and western blotting, respectively. The results of this study showed for the first time that miR‐124‐3p, which was predicted to bind p60‐katanin mRNA by bioinformatic analysis, may regulate the expression of the KATNA1 gene. The data obtained within the scope of this study will make important contributions in order to better understand the regulation of the expression of p60‐katanin which as well will have an incontrovertible impact on the understanding of the importance of cytoskeletal reorganization in both mitotic and postmitotic cells.
Xanthine oxidase (XO), in purine metabolism is a flavoprotein containing molybdenum with a key role. It has biological functions such as regeneration of NAD+, iron absorption and mobilization, reduction of nitrates. In this study, xanthine oxidase enzyme was purified by Sepharose-4B-L-tyrosine-4-aminobenzamidine dihydrochloride gel according to affinity chromatography technique and immobilization on glutaraldehyde was investigated. XO purified by ammonium sulfate precipitation and affinity chromatography was obtained with an 11.5 % yield and 694.04 degrees of purity. The purity of XO was confirmed by SDS-PAGE and a single band of around 150 kDa was observed. Kinetic constants (KM and VMax) of the enzyme were determined 1.67x10-4 M and 0.56 U/mL.min respectively by using xanthine compound as a substrate. The in vitro effects of NH4F, NH4Cl, CaCl2, ZnCl2, HgCl2, Hg(NO3)2.H2O compounds and commercially named colchicum dispert, commonly used in the treatment of gout disease in the clinic, were investigated. The IC50 values of compounds showing inhibition effect were determined. Afterward XO was immobilized on glutaraldehyde, which was used as a solid support material. The highest XO activity was observed in the sample of the immobilized enzyme at a rate of 6 % glutaraldehyde. The kinetic constants (KM and VMax) of the immobilized enzyme were determined as 5.18x10-4 M and 0.73 U/mL.min respectively. These values revealed that the catalytic activity of the free enzyme was higher than the immobilized enzyme.
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