Effects of Medetomidine-Butorphanol and Medetomidine-Buprenorphine on Oxidative Stress and Vital Parameters in Dogs Undergoing Ovariohysterectomy.

Oxidative stress (OS) is caused by an imbalance between the production of oxygen-containing free radicals and their elimination. General anesthesia increases the production of reactive oxygen species (ROS) and therefore causes oxidative stress. Our objective was to determine the effects of medetomidine-butorphanol (MEDBUT) and medetomidine-buprenorphine (MEDBUP) on oxidative stress and cardiorespiratory parameters in dogs undergoing ovariohysterectomy (OHE).

Phosphorylation-dependent allosteric regulation of Cx43 gap junction inhibitor potency.

Physiological and pathological processes such as homeostasis, embryogenesis, development, tumorigenesis, and cell movement depend on the intercellular communication through gap junctions (GJIC). Connexin (Cx)-based GJ channels are formed of two apposing hemichannels in the contiguous cells and provide a direct pathway for electrical and metabolic intercellular communication. The main modulators of GJ conductance are transjunctional voltage, intracellular pH, Ca, Mg, and phosphorylation.

Cranberry and black chokeberry extracts isolated with pressurized ethanol from defatted by supercritical CO pomace inhibit colorectal carcinoma cells and increase global antioxidant response of meat products during in vitro digestion.

Berry phenolics are considered as phytochemicals, which might mitigate development of degenerative diseases, including cancer. Many studies demonstrated their antiproliferative effects in various cancer cell lines while the studies with real foods are rather scarce. We report antiproliferative properties of unique extracts, which were obtained from the defatted by supercritical CO cranberry (CrE) and black chokeberry (ChoE) pomace using pressurized ethanol, and global antioxidant response of meat products enriched with berry polyphenolics during in vitro digestion.

Salinomycin and dichloroacetate synergistically inhibit Lewis lung carcinoma cell proliferation, tumor growth and metastasis.

Drug combination is considered to be the cornerstone of cancer treatment. Simultaneous administration of two or more drugs but at lower doses not only increases cytotoxic effects on tumor cells, but also reduces side effects and possibly overcomes drug resistance. Salinomycin is a well-known cancer stem cell killer, and dichloroacetate is a pyruvate dehydrogenase kinase inhibitor that exclusively targets cells with altered mitochondrial activity, a characteristic being common to most of the cancer cells.

Fatty Acid Synthesis and Degradation Interplay to Regulate the Oxidative Stress in Cancer Cells.

Both cytosolic fatty acid synthesis (FAS) and mitochondrial fatty acid oxidation (FAO) have been shown to play a role in the survival and proliferation of cancer cells. This study aimed to confirm experimentally whether FAS and FAO coexist in breast cancer cells (BCC). By feeding cells with C-labeled glutamine and measuring labeling patterns of TCA intermediates, it was possible to show that part of the cytosolic acetyl-CoA used in lipid synthesis is also fed back into the mitochondrion via fatty acid degradation.

Dichloroacetate and Salinomycin Exert a Synergistic Cytotoxic Effect in Colorectal Cancer Cell Lines.

In the present study, we examined a hypothesis that dichloroacetate, a metabolic inhibitor, might efficiently potentiate the cytotoxic effect of salinomycin, an antibiotic ionophore, on two human colorectal cancer derived cell lines DLD-1 and HCT116. First, we performed a series of dose response experiments in the 2D cell culture by applying mono- and combination therapy and by using the Chou-Talalay method found that salinomycin in combination with dichloroacetate acted synergistically in both cell lines. Secondly, in order to recapitulate the in vivo tumor architecture, we tested various doses of these compounds, alone and in combination, in the 3D multicellular spheroid culture.