cytochrome oxidase/neoplasms

This study is aimed at evaluating the inhibitory effects of the association of hematoporphyrin and ultrasound at variable intensities with a fixed frequency of 1.1MHz in tumor nodules. Specifically, the effects were studied both in solid and ascitic S180 tumors transplanted in mice by clinical,

The activity of a group of respiratory enzymes was studied in normal menopausal as well as benign and malignant tumours. A decrease in the activity of succinic dehydrogenase, diphosphopyridine nucleotide diaphorase and cytochrome oxidase in malignant tumours especially in spindle cell sarcoma and

Activity of cytochrome oxidase, incorporated into the lipoprotein vesicles /proteoliposomes/ in the course of self assembly procedure, was studied. For this purpose the lipids were used, which were isolated from mitochondria of rat liver tissue and of hepatoma 27. The enzymatic activity was

We used McPeek's (1995a) method of evolutionary contrasts, and phylogenetic trees derived from maximum-parsimony, neighbor-joining, and maximum-likelihood analyses of data from the cytochrome oxidase I (COI) gene to evaluate the hypothesis that macroevolutionary changes in habitat use have driven

The effect of t-butyl-4-hydroxyanisole (BHA), a widely used food antioxidant additive, on the culture growth, oxygen consumption, and redox state of some electron carriers of intact TA3 and 786A ascites tumor cells has been studied. BHA inhibited culture growth and respiration of these two tumor

The classic association between cancer and mitochondrial dysfunction is actually considered as a role of mitochondria in cellular signalling. It is understood that mitochondria, mitochondrial oxidative damage and NO and H2O2 diffusion are involved in the progression of human colorectal cancer.

Metabolic studies in tumor cells have indicated that bioenergetic regulatory mechanisms geared to acute changes in oxygen availability are abnormal. In the present studies we have examined bioenergetic adaptations to chronic oxygen depletion in culture maintained tumor cells in comparison to normal

Cancer and treatments may induce cognitive impairments in cancer patients, and the causal link between chemotherapy and cognitive dysfunctions was recently validated in animal models. New cancer targeted therapies have become widely used, and their impact on brain functions and quality of life needs

BACKGROUND Statins, 3-hydroxy-3 methylglutaryl coenzyme A (HMG-CoA) reductase inhibitors, are currently the most widely used cholesterol-lowering drugs. Previous epidemiological studies have suggested that there may be be an association between statin use and decreased risk of prostate cancer

The effect of lonidamine, an antispermatogenic and antitumor drug, on the oxygen consumption, ATPase activity, and redox state of the electron carriers of Ehrlich ascites tumor mitochondria has been studied. Lonidamine inhibits ADP- and uncoupler-stimulated respiration on various NAD- and FAD-linked

Cancer cells have a proliferative advantage by utilizing intermediates of aerobic glycolysis (Warburg effect) for their macromolecule synthesis. Although the exact causes of this Warburg effect are unclear, high osmotic stress in solid tumor microenvironment is considered one of the important

BACKGROUND The unique metabolism of tumors was described many years ago by Otto Warburg, who identified tumor cells with increased glycolysis and decreased mitochondrial activity. However, "aerobic glycolysis" generates fewer ATP per glucose molecule than mitochondrial oxidative phosphorylation, so

The activation of the nuclear receptor peroxisome proliferator-activated receptor-γ (PPAR-γ) is known to exert anti-inflammatory and neuroprotective effects and PPAR-γ agonists are considered potential therapeutic agents in brain diseases including those affecting myelin. In demyelinating diseases

Oxidative stress can impair mitochondrial function and fuel utilization and is closely linked with the development of insulin resistance in skeletal muscle in diabetes mellitus as well as fatty liver disease. In vitro data indicate that cellular levels of reactive oxygen species depend on the