ubiquinone and Adenocarcinoma

Pancreatic adenocarcinoma (PDAC) and lung cancer are expected to represent the most common cancer types worldwide until 2030. Under typical conditions, mitochondria provide the bulk of the energy needed to sustain cell life. For that inhibition of mitochondrial complex ΙΙ (CΙΙ) and ubiquinone oxidoreductase with natural treatments may represent a promising cancer treatment option. A naturally occurring flavonoid with biological anti-cancer effects is chyrsin. Due to their improved bioavailability, penetrative power, and efficacy, chitosan-chrysin nano-formulations (CCNPs) are being used in medicine with increasing frequency. Chitosan (cs) is also regarded as a highly versatile and adaptable polymer. The cationic properties of Cs, together with its biodegradability, high adsorption capacity, biocompatibility, effect on permeability, ability to form films, and adhesive properties, are advantages. In addition, Cs is thought to be both safe and economical. CCNPs may indeed be therapeutic candidates in the treatment of pancreatic adenocarcinoma (PDAC) and lung cancer by blocking succinate ubiquinone oxidoreductase.

Topics: Adenocarcinoma; Adenocarcinoma of Lung; Chitosan; Flavonoids; Humans; Lung Neoplasms; Nanoparticles; Pancreatic Neoplasms; Succinate Dehydrogenase; Ubiquinone

Fatigue is the most common and distressing symptom reported by cancer patients during and after treatment. Tumor growth increases oxidative stress and cytokine production, which causes skeletal muscle wasting and cardiac dysfunction. The purpose of this study was to determine whether treatment with the antioxidant ubiquinol improves muscle mass, cardiac function, and behavioral measures of fatigue in tumor-bearing mice.. Adult female mice were inoculated with colon26 tumor cells. Half the control and tumor-bearing mice were administered ubiquinol (500 mg/kg/day) in their drinking water. Voluntary wheel running (i.e., voluntary running activity [VRA]) and grip strength were measured at Days 0, 8, 14, and 17 of tumor growth. Cardiac function was measured using echocardiography on Day 18 or 19. Biomarkers of inflammation, protein degradation, and oxidative stress were measured in serum and heart and gastrocnemius tissue.. VRA and grip strength progressively declined in tumor-bearing mice. Muscle mass and myocardial diastolic function were decreased, and expression of proinflammatory cytokines was increased in serum and muscle and heart tissue on Day 19 of tumor growth. Oxidative stress was present only in the heart, while biomarkers of protein degradation were increased only in the gastrocnemius muscle. Ubiquinol increased muscle mass in the tumor-bearing and control animals but had no effect on the expression of biomarkers of inflammation, protein degradation, or oxidative stress or on behavioral measures of fatigue.

Topics: Adenocarcinoma; Animals; Antioxidants; Colonic Neoplasms; Fatigue; Female; Mice; Motor Activity; Muscle, Skeletal; Neoplasms, Experimental; Oxidative Stress; Ubiquinone

Skeletal muscle wasting is a prominent feature of cancer cachexia and involves decreased muscle protein synthesis and increased activity of the ubiquitin-proteasome pathway of protein degradation. We report that both indomethacin and ibuprofen improved body weight and weight of the gastrocnemius muscle in tumor-bearing mice. Ibuprofen increased the soluble protein content of the muscle without affecting muscle levels of phosphorylated p70 S6 kinase, a ribosomal kinase involved in protein synthesis. Paradoxically, indomethacin increased levels of ubiquitin-conjugated proteins. Further study is needed to understand the mechanism of action by which indomethacin and ibuprofen preserve body weight and muscle mass in the tumor-bearing mice. The data suggest that ibuprofen may have beneficial effects in the treatment of cancer cachexia.

Topics: Adenocarcinoma; Animals; Anti-Inflammatory Agents, Non-Steroidal; Body Weight; Cachexia; Colonic Neoplasms; Disease Models, Animal; Female; Ibuprofen; Indomethacin; Mice; Muscle, Skeletal; Neoplasms, Experimental; Ubiquinone

A multifunctional cell surface protein with NADH oxidase (NOX) activity and capable of oxidizing hydroquinones is located at the exterior of the cell and is shed in soluble form into sera. The oxidase appears to function as a terminal oxidase of a trans plasma membrane electron transport chain consisting of a NAD(P)H-ubiquinone reductase at the cytosolic membrane surface, possibly a b-type cytochrome, ubiquinone and the oxidase. Hyperactivity or conditions that interrupt ordered 2H+ + 2e- transport from NAD(P)H or hydroquinone to molecular oxygen and other acceptors at the external cell surface may result in the generation of superoxide. The latter may serve to propagate aging-related redox changes both to adjacent cells and circulating blood components. A circulating NOX activity form associated with aging and the reduction of cytochrome c by sera of aged patients that is partially inhibited by ubiquinone are described.

Topics: Adenocarcinoma; Breast; Breast Neoplasms; Cell Line; Cell Membrane; Cytochrome c Group; Electron Transport; Epithelial Cells; Female; HeLa Cells; Humans; Kinetics; Multienzyme Complexes; NADH, NADPH Oxidoreductases; Oxidation-Reduction; Oxidoreductases; Superoxides; Tumor Cells, Cultured; Ubiquinone; Ultraviolet Rays

Topics: Adenocarcinoma; Alkylating Agents; Animals; Cattle; DNA, Neoplasm; In Vitro Techniques; Mitochondria, Muscle; Mitomycins; Myocardium; NADH, NADPH Oxidoreductases; Neoplasm Proteins; Oxidation-Reduction; Quinones; RNA, Neoplasm; Sarcoma 180; Ubiquinone