Disease relevance of Cell Respiration

• In vitro intracellular changes of dissolved oxygen due to cell respiration were monitored, with gene gun injected PEBBLEs, in rat C6 glioma cells [1].
• Effects of adriamycin on Ehrlich Ascites cell respiration may depend on the presence of glucose [2].
• recA-dependent inhibition of cell division and cessation of cell respiration are not expressed in recA430 (formerly lexB) mutants of Escherichia coli after ultraviolet irradiation [3].
• In theory, this could further lead to ubiquinone deficiency in muscle cell mitochondria, disturbing normal cellular respiration and causing adverse effects such as rhabdomyolysis [4].
• Nevertheless, thymine deprivation is able to produce a normal induction of prophage and thymineless death in these same strains However, when these mutants are treated, in the presence of thymine, with UV-irradiation or bleomycin, they show a normal inhibition of cellular respiration and other SOS functions [5].

High impact information on Cell Respiration

• The fraction of mtDNA deletions is significantly higher in cytochrome c oxidase (COX)-deficient neurons than in COX-positive neurons, suggesting that mtDNA deletions may be directly responsible for impaired cellular respiration [6].
• Cytochrome c oxidase, the terminal enzyme of cellular respiration in mitochondria and many bacteria, reduces O(2) to water [7].
• Carbon monoxide (CO) can arrest cellular respiration, but paradoxically, it is synthesized endogenously by heme oxygenase type 1 (Ho-1) in response to ischemic stress [8].
• Myoglobin, an intracellular haemoprotein expressed in the heart and oxidative skeletal myofibres of vertebrates, binds molecular oxygen and may facilitate oxygen transport from erythrocytes to mitochondria, thereby maintaining cellular respiration during periods of high physiological demand [9].
• NO was also shown to alter cellular respiration and decrease the concentration of the antioxidant glutathione to a residual level of 15-20% in bacterial cells [10].

Chemical compound and disease context of Cell Respiration

• So it appears that the increased loss of oxypurines in HPI is caused by the impact of hypoxia, probably owing to be compromised cellular respiration with a subsequent general displacement of the purine metabolism in the catabolic direction [11].
• Recently we showed that J1 (L-melphalanyl-p-L-fluorophenylalanine ethyl ester), an alkylating nitrogen mustard-containing dipeptide, exhibited strong cytotoxic activity in fresh human tumor samples in addition to rapid and pronounced inhibition of macromolecular syntheses and cellular respiration in the human tumor lymphoma cell line U-937 GTB [12].
• During acute (< 30 min) hypoxia, cellular respiration is independent of the O2 concentration as long as PO2 remains above a critical value (5-10 Torr) [13].
• Lonidamine, a substituted indazole carboxylic acid that inhibits cellular respiration, was given in an escalating oral schedule to 20 evaluable patients with measurable extensive small cell carcinoma of the lung [14].

Biological context of Cell Respiration

• The presence and respiratory inhibition of MT in liver, but not heart, mitochondria suggest a hitherto unknown biological modulating activity of MT in cellular respiration and energy metabolism in a tissue-specific manner [15].
• Apoptosis was associated with a reduction in cell respiration but without impairment of respiratory chain function, without early changes in mitochondrial membrane potential and without cytochrome c release into the cytosol [16].
• Treatment with liposomal NAD(+) also preserved DeltaPsi(m) and cellular respiration during oxidative stress [17].
• By genomic Southern blot analysis and disruption of the COX8 chromosomal locus, we have shown that this gene is present in one copy per haploid genome and that its product, subunit VIII, is essential for maximal levels of cellular respiration and cytochrome c oxidase activity [18].
• COX8, the structural gene for yeast cytochrome c oxidase subunit VIII. DNA sequence and gene disruption indicate that subunit VIII is required for maximal levels of cellular respiration and is derived from a precursor which is extended at both its NH2 and COOH termini [18].

Anatomical context of Cell Respiration

• Three types of evidence that suramin rapidly inhibits cellular respiration or disrupts cellular energy balance in intact cells of the human prostate carcinoma cell line, DU145, are presented [19].
• The effects of exogenous changes in thyroid status on in vitro brown adipose tissue (BAT) cellular respiration and thermogenic enzymes (sodium-potassium ATP' ase and alpha-glycerophosphate dehydrogenase) were studied in fetal sheep [20].
• Suspensions of rat liver hepatocytes exposed to oxmetidine rapidly lose viability, an event preceded by a marked and rapid inhibition of cell respiration and depletion of ATP [21].
• Eugenol depressed cell respiration in homogenates of human dental pulp and in mouse fibroblast monolayers [22].
• Diazepam inhibits cell respiration and induces fragmentation of mitochondrial reticulum [23].

Associations of Cell Respiration with chemical compounds

• Cellular respiration was measured upon addition of nystatin (Nys) to maximally stimulate Na pump activity [24].
• Aspirin potentiated histamine-induced parietal cell respiration and aminopyrine uptake ratio but did not increase basal respiration or aminopyrine uptake, suggesting an apparent dissociation from aspirin-induced morphological changes [25].
• Sucrose deprivation led to structural changes in mitochondria, a decrease in mitochondrial volume, and a reduction in the rate of cellular respiration [26].
• Mitochondrial cytochrome c oxidase plays an essential role in aerobic cellular respiration, reducing dioxygen to water in a process coupled with the pumping of protons across the mitochondrial inner membrane [27].
• Cell respiration is catalyzed by the heme-copper oxidase superfamily of enzymes, which comprises cytochrome c and ubiquinol oxidases [28].

Gene context of Cell Respiration

• In comparison with wild-type COX2 expression, steady-state levels of T7-COX2 mRNA increase fivefold when transcription is driven by T7Pol expressed from the ADH1 promoter, yet COXII protein levels and cellular respiration rates decrease by about 50% [29].
• The basal formation of NO in mitochondria by a mitochondrial NOS seems to be one of the main regulators of cellular respiration, mitochondrial transmembrane potential, and transmembrane proton gradient [30].
• To study the link between FAS and cell respiration further, we also created a yeast strain that has FabI enoyl-ACP (acyl-carrier protein) reductase gene from Escherichia coli engineered to carry a mitochondrial targeting sequence in the genome, replacing the endogenous ETR1 gene [31].
• Analysis of an aegA mutant indicated that the aegA gene product is not essential for cell respiration or fermentation or for the utilization of ammonium or the amino acids L-alanine, L-arginine, L-glutamic acid, glycine, and DL-serine as sole nitrogen sources [32].
• UCP3 has been overexpressed at high levels in yeast systems, where it leads to the uncoupling of cell respiration, suggesting that UCP3 may indeed be capable of dissipating the mitochondrial proton gradient [33].

Analytical, diagnostic and therapeutic context of Cell Respiration

• Membrane-bound cytochrome c oxidase catalyzes cell respiration in aerobic organisms and is a primary energy transducer in biology [34].
• At 24 h after exposure to cisplatin, cellular respiration and viability decreased relative to controls and the amount of small DNA fragments, measured using quantitative agarose gel electrophoresis, was proportional to the concentration of cisplatin present during the drug exposure period [35].
• CONCLUSIONS: Given the uninfluenced parameters of the ileal mucosal microcirculation in our model of long-term porcine endotoxemia, selective iNOS inhibition probably improved the PCO(2) gap due to a redistribution of the microvascular perfusion within the gut wall and/or an amelioration of the cellular respiration [36].

References