As novel promising anticancer candidates, the piano-stool type complexes of ruthenium, [RuCl(η-p-cymene)(N,S-L)]PF, K-, were synthesized from the reaction of the substituted benzo[b]thiophene based thiosemicarbazone ligands (L) with [{RuCl(η-p-cymene)}(μ-Cl)]. All complexes were fully characterized using elemental analysis, and spectroscopic methods such as FT-IR and H NMR. The molecular masses of the complexes were proved by MALDI-TOF analysis.
View Article and Find Full Text PDFOvarian cancer, which is one of the most diagnosed cancer types among women, maintains its significance as a global health problem. Several drug candidates have been investigated for the potential treatment of ovarian cancer. Nonsteroidal anti-inflammatory drugs (NSAIDs) demonstrated anti-cancer activity through the inhibition of cyclooxygenase 2 (COX-2) and by inhibiting COX-2-dependent prostaglandin (PG) production.
View Article and Find Full Text PDFExosomes released from cancer cells are involved in the reorganization of the tumor microenvironment which is the essential aspect of cancer pathogenesis. The intercommunications between cancer cells and diverse cell types in the microenvironment are accomplished by exosomes in ovarian cancer. Internalization pathway, intracellular fate, and biological functions in recipient cells mediated by exosomes released from cisplatin-resistant A2780cis have been studied.
View Article and Find Full Text PDFCisplatin is one of the most active cytotoxic agents in cancer treatment. To clarify the interaction with mitochondria, we hypothesize that the activities of mitochondrial electron transport chain (ETC) enzymes succinate dehydrogenase (SDH) and cytochrome c oxidase (COX), nucleotide levels, as well as levels of catalase (CAT) enzyme and membrane lipid peroxidation (LPO) can be affected by cisplatin. There was a significant decrease of both SDH and COX activities in the lung, heart, and brain tissues at the 1st day after cisplatin exposure, and the observed decreased levels of adenosine triphosphate (ATP) and adenosine diphosphate (ADP) in comparison with the control could be because of cisplatin-induced mitochondrial dysfunction.
View Article and Find Full Text PDFThe implication of oxidative stress as primary mechanism inducing doxorubicin (DOX) cardiotoxicity is still questionable as many in vitro studies implied supra-clinical drug doses or unreliable methodologies for reactive oxygen species (ROS) detection. The aim of this study was to clarify whether oxidative stress is involved in compliance with the conditions of clinical use of DOX, and using reliable tools for ROS detection. We examined the cytotoxic mechanisms of 2 μM DOX 1 day after the beginning of the treatment in differentiated H9c2 rat embryonic cardiac cells.
View Article and Find Full Text PDFCisplatin accumulates in mitochondria, which is a potent and widely used chemotherapeutic agent. In order to clarify the potential effect of cisplatin on electron transport chain (ETC), the variation of succinate dehydrogenase (SDH) and cytochrome c oxidase (COX) enzyme activities, nucleotide levels, as well as catalase (CAT) enzyme and membrane lipid peroxidation (LPO) level with respect to liver and kidney of cisplatin-exposed rats were studied. We found that cisplatin caused significant impairment in the SDH, COX, and CAT activities, and nucleotide levels associated with membrane LPO in isolated mitochondria.
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