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Introduction: Nanomedicine has recently been known as an emerging research area with promising applications in cancer diagnosis and treatment. Aside from this, gold nanoparticles (AuNPs), as one of the important components of nanomedicine, have attracted considerable attention due to their special physicochemical properties and lower toxicity than other nanoparticles. Despite the impressive advantages of AuNPs, it has not been yet determined whether oxidative stress contributes to the toxicity of AuNPs on bladder cancer. Aim: The aim of this study was to address this issue by conducting experiments in order to investigate the effects of 20 nm AuNPs on human bladder cancer 5637 cells. Materials and methods: The viability of 5637 cells was evaluated upon 24 hour exposure to different concentrations of AuNPs (0- 50&nbsp;&micro;g/ml) by 3-(4,&nbsp;5-dimethylthiazol, 2-yl)-2, 5-diphenyl tetrazolium bromide (MTT) assay. In order to evaluate oxidative stress status, total antioxidant capacity (TAC), total oxidant status (TOS), malondialdehyde (MDA) and also activities of antioxidant enzymes including glutathione peroxidase (GPx), catalase (CAT) and superoxide dismutase (SOD) were all determined by colorimetric assay kits. Results: The results from our experiment showed that the cytotoxicity caused by AuNPs was dose-dependent and the IC50 value was found to be 43.14&nbsp;&micro;g/ml after 24-hour exposure. Furthermore, MDA and TOS levels were significantly increased in treated cells compared to untreated cells (p<0.05). In contrast, TAC level and the activities of SOD, GPx, CAT were significantly decreased in AuNPstreated groups as compared with the untreated cells (p<0.05). Conclusions: Overall, AuNPs decrease the cell viability and increase oxidative stress in bladder cancer 5637 cells.

Background. Pharmacotherapy with medicinal plants is a promising approach to treat cancer. Cinnamon is a medicinal plant whose properties have been proven in various fields of medical sciences. Among its biological activities, its antioxidant and antiviral effects can be mentioned. In this study, the antitumor effects of Cinnamon with a focus on glucose metabolism in bladder cancer carcinoma cell-line 5637 were investigated. Methods. Aqueous extract of Cinnamon was prepared from Cinnamon bark. Bladder cancer 5637cell line were treated with different concentrations of aqueous extract of Cinnamon. MTT was used to evaluate cell viability at 24, 48, and 72 h. The concentration of 1.25, 2.50, and 5 mg/ml was used. Apoptosis was assessed with Hochest33258 staining. For evaluating of aqueous extract of Cinnamon effect on glycolysis, the gene expression of epidermal growth factor receptor 2 (ErbB2), heat shock protein transcription factor1 (HSF1), and lactate dehydrogenase A (LDHA), as well as protein levels of HSF1 and LDHA, LDH activity, glucose consumption, and lactate production, were measured. Results. Aqueous extract of Cinnamon significantly decreased ErbB2, HSF1, and LDHA gene expression and also decreased the protein level of HSF1 and LDHA, LDH activity, glucose consumption, and lactate production dose-dependently ( p < 0.05 ). Conclusion. Our finding showed that the aqueous extract of Cinnamon can inhibit proliferation in 5637 cells by inhibition of glycolysis and induction of apoptosis.

Some reports emphasize that zinc oxide nanoparticles (ZnO NPs) are detrimental to the reproductive organs of animals. As such, this research aimed at exploring the apoptotic potential of ZnO NPs on testis along with the beneficial role of Vitamins (V) A, C, and E against ZnO NP-induced damage. To this aim, a population of 54 healthy, male Wistar rats were used in this work and then assigned into nine groups of 6 rats as G1: Control 1 (Water); G2: Control 2 (Olive oil); G3: VA (1000 IU/kg), G4: VC (200 mg/kg), G5: VE (100 IU/kg), G6: ZnO NPs exposed animals (200 mg/kg); and G7, 8 and 9: ZnO NPs-exposed animals that were pre-treated with either VA, C, or E. Apoptosis rates were estimated by measuring the level of apoptotic regulatory markers including Bcl-2-associated X (Bax) and B-cell lymphoma protein 2 (Bcl-2) using western blotting and qRT-PCR assays. The data indicated that ZnO NPs exposure elevates the level of Bax protein and gene expression, whereas the protein and gene expression of Bcl-2 was reduced. Further, the activation of caspase-3,7 occurred after exposure to ZnO NPs, while the above alterations were significantly alleviated in the rats that were co-treated with VA, C, or E and ZnO NPs relative to the rats in the ZnO NPs group. In summary, VA, C, and E exerted anti-apoptotic functions in the testis of rats following administration of ZnO NPs.

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