The effects of thymoquinone and quercetin on the toxicity of acrylamide in rat glioma cells.

Acrylamide is a neurotoxic agent forming in foods. Thymoquinone and quercetin are plant-derived antioxidants in various foods with known benefits. C6 cells are glioblastoma cells. In this study, we aimed at preventing acrylamide toxicity by thymoquinone and quercetin in the C6 cell line. In our study, first, toxic doses of acrylamide, nontoxic doses of thymoquinone and quercetin in C6 cells for 24 h were determined by MTT (3-[4,5-dimethylthiazol-2-yl]-2,5 diphenyl tetrazolium bromide) colorimetric test. After that, caspase 3/7 and annexin V tests were performed by flow cytometry to evaluate whether the apoptosis pathway was inducted. Furthermore, autophagy and oxidative stress were assessed by flow cytometry. The amount of Nrf2 (nuclear factor erythroid 2-related factor 2) was determined by immunocytochemistry. The morphological examination was performed by microscopic analyses. As a result, 4 mM of acrylamide was determined to be used to induce toxicity in C6 cells. The nontoxic doses of thymoquinone and quercetin were respectively determined as 3.9 and 2.0 µM. Thymoquinone and quercetin not only reduced acrylamide-induced apoptosis in annexin V and caspase 3/7 assays but also morphological deformations in microscopic examinations. In autophagy, it was revealed that acrylamide-induced autophagy was decreased by quercetin and thymoquinone pretreatments. As for Nrf2 expression, it was observed that acrylamide increased Nrf2 expression, and thymoquinone and quercetin pretreatments increased it even further. In conclusion, in the study, acrylamide demonstrated a damaging effect on C6 glioblastoma cells, and thymoquinone and quercetin pretreatments exerted a protective effect against acrylamide-induced damage in C6 cells.

Toward stimulating apoptosis in human lung adenocarcinoma cells by novel nano-carmofur compound treatment.

Lung cancer is one of the common and most fatal diseases worldwide. It has a high incidence in both men and women, in Turkey. Current antineoplastic drugs are reported to have limitations such as narrow therapeutic index and selectivity, toxicity, and antiproliferative effects on cancer cells. Thus, this study was aimed to investigate the potential cytotoxic, antiproliferative and apoptosis-triggering effects of a newly developed SLN-Carmofur compound on human lung adenocarcinoma A549 cells. The results of this study have shown that SLN-Carmofur significantly decreased the viability of A549 cells in a dose-dependent manner by short-time application. The IC50 value of the agent caused chromatin condensation, fragmentation of the nuclei, and holes on cytoskeleton; moreover, it altered the ultrastructure of the exposed cells with clear signs of apoptosis. Taken all our results together, it is indicated that SLN-Carmofur may be proposed for further research for drug development for cancer therapy, depending on the valuable potential in stimulating apoptosis in cancer cells.

Promising anti-growth effects of palladium(II) saccharinate complex of terpyridine by inducing apoptosis on transformed fibroblasts in vitro.

Fibrosarcoma is one of the fatal cancer types and there is still not satisfactory success in its treatment despite new drugs. Therefore, the search for a new compound has been going on. It is currently known that some palladium-based anti-cancer compounds seem to have powerful apoptosis-inducing effects in cancer cells. For this purpose, a palladium(II)-saccharinate complex containing terpyridine which was synthesized by our research group was investigated in terms of its anti-tumor effects against mouse embryonic fibroblast NIH/3T3 (normal cell line) and rat embryonic fibroblast 5RP7 (H-ras transformed cell line) in vitro. The MTT and ATP viability assays were used to determine anti-growth/cytotoxic effects. Cytotoxic activity was confirmed by real time cytotoxicity analysis system. Flow cytometry analysis was further used to determine the mode of cell death (apoptosis/necrosis). Apoptosis was confirmed by triple-staining the cells with Hoechst 33342/PI/Calcein-AM triple and evaluated with fluorescence microscopy. It was found that the compound showed significant anti-growth activity by inducing apoptosis in a dose dependent manner. In conclusion, taking into account the cytotoxic activity of the compound at even relatively lower doses, in vivo experiments to elucidate its potential use for the treatment of fibrosarcoma are warranted.