In many types of malignancy, ascites is a prognostic sign of advanced stage, with a survival rate of 11% for patients with ascites more than 6 months. Currently, combination therapy has become the base of cancer treatment. However, cytotoxicity to normal tissue is the major limitation of current combined drugs. In this study, Ehrlich ascites carcinoma (EAC) inoculated into mice was targeted with three consecutive doses of metformin, a safe drug with an anti-cancer effect. To test its suitability as a potential safe candidate against EAC cells for later combination therapy in comparable with cisplatin as a reference anti-neoplastic drug. The group that received metformin developed less malignant ascites than the control group. Metformin induced cellular quiescence in the EAC cells by upregulation of cyclin-dependent kinase inhibitor 1 (p21) expressions as cisplatin acted. Cell cycle analysis confirmed the quiescence state of the EAC cells treated with metformin or cisplatin. Furthermore, metformin-induced toxicity to EAC cells through elevation of reactive oxygen species levels (ROS). Therefore, metformin can be a suitable candidate for future combination with a low dose of cisplatin to treat the aggressiveness of EAC cells.
Background and objective Previous studies have demonstrated the anti-cancer effects of propolis. However, its use is limited because of its poor bioavailability. In the present study, the major objective was to improve propolis bioavailability using a nanosuspension formulation. The cytotoxic effect of propolis nanosuspension (PRO-NS) on the Ehrlich ascites carcinoma (EAC) in female Swiss albino mice was investigated in comparison to the free propolis. Materials and methods A propolis-loaded nanosuspension was formulated by applying solvent-antisolvent nano-precipitation technique. The prepared PRO-NS was characterized for average particle size, polydispersity index (PDI) and zeta potential. Also, the morphology of the nanosuspension particles was investigated using scanning electron microscopy (SEM). Moreover, PRO-NS cytotoxicity was tested using EAC bearing mice. The anticancer activity of Pro-NS was assessed by studying tumor volume, life span, viable and non-viable cell count, antioxidant, biochemical estimations and proliferation of EAC cells. Results The results revealed that propolis nanoparticles were relatively spherical in shape with rough surface. The tumor bearing mice treated with PRO-NS showed increased life span and inhibited tumor growth and the proliferation of EAC cells in comparison to the free propolis (p < 0.01). Moreover, Pro-NS ameliorated the increase in serum aspartate transaminase (AST) and alanine transaminase (ALT) activities, IgM and the level of creatinine and urea after implantation of EAC cells. In addition, PRO-NS improved the SOD activity and glutathione content of liver and EAC cells. Furthermore, PRO-NS inhibited the formation of lipid peroxidation products (MDA) and total IgG in EAC tumor bearing mice. Conclusions Our results indicate that PRO-NS has a strong inhibitory activity against growth of tumors in comparison to free propolis. The anti-tumor mechanism may be mediated by preventing oxidative damage, immune-stimulation and induction of apoptosis.
The formation of superoxide partially accounts for the well-known oxygen enhancement of radiation-induced biochemical changes and cell damage. Radioprotective effects of copper (II), manganese (IV) or vanadium (IV) complexes, of superoxide dismutase-mimetic activity, on body weight, survival rate and some biochemical parameters in pre-treated irradiated, untreated irradiated and treated non-irradiated female albino rats have been studied 24 h after whole body gamma-irradiation at a dose level of 6 Gy. Survival time, body weight, red blood cell (RBC) and white blood cell (WBC) counts, hemoglobin (Hb) concentration, percentage of hematocrit (Hct%), reduced glutathione (GSH), serum total protein, albumin, globulin (G), blood urea, creatinine and cholesterol were estimated, as well as the activities of blood superoxide dismutase (SOD), glutamate-oxaloacetic (GOT) and glutamate-pyruvic (GPT) transaminases, and alkaline phosphatase were assessed. A significant decline was shown in body weight, survival rate, the mean values of RBC and WBC counts, Hb and Hct percentages, and GSH concentration, as well as blood SOD activity, in whole body gamma-irradiated rats compared with the control non-irradiated rat group. The mean activity values of alkaline phosphatase, GOT and GPT, as well as the average values of blood urea, creatinine, total cholesterol, total protein and globulin were significantly elevated, while the average values of albumin and the albumin/globulin ratio were decreased in gamma-irradiated rats compared with the corresponding values of the normal control rat group. Pretreatment of rats with either manganese or vanadium complexes resulted in a significant increase in survival rate and body weight over that of the non-treated irradiated rat group. Pretreatment of rats with copper (II), manganese (IV) or vanadium (IV) complexes caused a significant increase in RBC and WBC counts, Hb concentration, HCt (%), GSH content and SOD activity in blood when compared to the irradiated rat group without treatment. The administration of copper (II), manganese (IV) or vanadium (IV) complexes prior to irradiation exposure resulted in a significant decrease in GOT and GPT activities in addition to blood urea, creatinine, cholesterol, globulin and total protein contents, while each complex exhibited a significant increase in plasma alkaline phosphatase, albumin, and the albumin/globulin ratio compared to the untreated irradiated rat group. Administration of vanadium (IV), manganese (IV) or copper (II) complexes in non-irradiated rats caused a significant increase in SOD activity without changing other biochemical parameters compared with the corresponding values of the normal control rat group. We conclude that these metallo-elements, particularly manganese (IV) and vanadium (IV) complexes of 2-methylaminopyridine, have radiation protection and radiation recovery. Furthermore, these metal complexes offer a new approach to overcome the pathological effects of ionizing radiation and suggest their use as a physiological approach ...
Background: Abnormalities in thyroid state may result in mental retardation. Oxidative stress and elevated serum inerleukin-6 (IL-6) levels have been identified as an important contributor to neurodegeneration. The aim: This work has been carried out to evaluate the interleukin-6, thyroid hormones as well as some parameters related to oxidative stress in mentally retarded patients with chromosomal abnormalities. Methods: karyotyping for blood, serum thyroid stimulating hormone (TSH), free thyroxin (FT4), superoxide dismutase (SOD), catalase(CAT), malondialdehyde (MDA) and interleukin-6 (IL-6) were measured in 60 mentally retarded patients and 30 healthy volunteers included as control groups. Results: Chromosomal abnormalities were studied in 60 mentally retarded patients, 50 of them were Down's syndromes and the other 10 consisted of (translocations, trisomies, ring chromosome, Edward's, Patau and Klinefelter syndromes). Thirty three subjects were euthyroid and 27 subjects were hypothyroid. In euthyroid group there was no significant difference in the values of TSH, FT4 and SOD whereas the values of MDA and CAT were significantly higher compared with control. On the other hand, IL-6 levels were highly significantly increased compared with the control group. In hypothyroid group there was a highly significant increase in TSH and IL-6 levels and a highly significant decrease in SOD, CAT, MDA and FT4 levels compared with those of the control group. Conclusion: Increased oxidative stress and IL-6 as well as hypothyroidism are common in mentally retarded individuals with chromosomal abnormalities. These findings are useful in supporting future antioxidant therapies and chemical inhibitors against the function of IL-6 to improve those patients.
scite is a Brooklyn-based organization that helps researchers better discover and understand research articles through Smart Citations–citations that display the context of the citation and describe whether the article provides supporting or contrasting evidence. scite is used by students and researchers from around the world and is funded in part by the National Science Foundation and the National Institute on Drug Abuse of the National Institutes of Health.
hi@scite.ai
10624 S. Eastern Ave., Ste. A-614
Henderson, NV 89052, USA
Copyright © 2024 scite LLC. All rights reserved.
Made with 💙 for researchers
Part of the Research Solutions Family.