Oxygen deprivation

Employee Suffers Oxygen Deprivation, Safety Note No. DOE/EH-0110. U.S. Dept, of Energy. Washington, D.C., Oct. 1989. 

Early infiltration of polymorphonuclear leukocytes and monocyte/macro-phages into the transplanted organ occurs soon after reperfusion of the transplant is initiated. In the context of transplantation, oxygen deprivation and general tissue stress of the graft leads to the activation of proinflammatory cytokines and the upregulation of the adhesion molecules required for leukocyte... 

Branco-Price, C., Kawaguchi, R., Ferreira, R. B., and Bailey-Serres, J. (2005). Genomewide analysis of transcript abundance and translation in Arabidopsis seedlings subjected to oxygen deprivation. Ann. Bot. (Lond.) 96, 647—660. 

Weinberg, J.M. (1985). Oxygen deprivation-induced injury to isolated rabbit kidney tubules. J. Clin. Invest. 76 1193-2108. 

Bioprecursors provide relevant examples of chemotherapeutic agents whose activation occurs by reduction in oxygen-deprived cells. Bioprecursors certainly appear as a viable class of prodrugs, since they avoid potential toxicity problems caused by the carrier moiety (see below). In contrast, attention must be given here to metabolic intermediates. 

No human health effects have been detected at COHb blood levels below about 2% ( background levels in non-smokers average about 0.5%). Subtle effects on the nervous system, such as reduced ability to sense certain time intervals, have been reported at blood levels of 2.5%. At COHb levels of 5% certain cardiovascular changes are detectable, especially in patients with coronary heart disease. Heavy smokers exhibit COHb levels in the range of 5-6%, and if they happen to be pregnant, the fetus can suffer the effects of oxygen deprivation. 

Under Oxygen Deprivation. Ecology, Physiology and Biochemistry. The Hague SPB Academic Publishers, 267-282. 

Being inert, the noble gases are nontoxic. However, they can act as asphyxiant gases that can kill because of oxygen deprivations. 

The major effects observed in animals after exposure to 1,3-DNB are methemoglobin formation and testicular damage at doses that are higher than 1 mg/kg. Both effects are common to other nitroaromatic compounds. The biochemical changes that occur in the blood, primarily methemoglobin formation, lead to oxygen deprivation in the tissues, and then to cyanosis and neurotoxicity. 

Another early symptom of exposure to 1,3-DNB is cyanosis due to oxygen deprivation because of the presence of methemoglobin in the blood. These changes are also not specific for 1,3-DNB and may be produced by other nitrobenzene compounds and dinitrobenzene isomers. Therefore, cyanosis is not a good biomarker for 1,3-DNB exposure. 

Effect. Cyanosis is also an early symptom of exposure to 1,3-DNB (Okubo and Shigeta 1982) and is a result of oxygen deprivation due to the presence of methemoglobin in the blood. However, it is not specific and may occur after exposure to other nitrobenzene compounds or other non-related chemicals. 

The ACGIH has not assigned a numerical threshold limit value (TLV) for occupational exposure to ethane because the limiting factor is the available oxygen, the minimal content which should be 18% by volume under normal atmospheric pressure at concentrations below those required to produce severe oxygen deprivation, ethane presents an explosive hazard. ... 

Toxicology. Methane acts as a simple asphyxiant by causing oxygen deprivation at very high concentrations. 

To maintain hemostasis, blood must be retained in the vasculature as fluid. At the same time, blood components must be able to respond rapidly with a clot when a vascular injury occurs. To repair a vascular injury, platelets in blood first adhere as aggregates to the endothelial cells at the affected site and form an initial blood clot. Platelets then stimulate and activate coagulation factors found in plasma to form a more stable fibrin clot. As the injury is resolved and healed, the clot is degraded. Thrombosis is a pathological event wherein a blood clot occludes a blood vessel, resulting in ischemic necrosis of the tissue fed by the blood vessel. Ischemic necrosis involves local anemia and oxygen deprivation. Thrombosis of a coronary artery may lead to myocardial infarction or unstable angina [20]. 

Hypoxia is a deficiency of oxygen needed to maintain cellular homeostasis. It may be caused by a reduction in blood supply, namely ischemia, decreased cardiopulmonary function, and diminished oxygen-carrying capacity of the blood. Subsequent oxygen deficiency in tissues leads to depressed aerobic metabolism and, thus, insufficient ATP synthesis. Reductions in blood flow also exacerbate oxygen deprivation by impairing delivery of nutrients, such as glucose, and the removal of metabolic wastes, such as C02, from affected cells. 

In ischemic (oxygen-deprived) cells, a protein inhibitor blocks ATP hydrolysis by the ATP synthase operating in reverse, preventing a drastic drop in [ATP]. 

The pH within cells appears to be tightly controlled although small variations are sometimes observed. Red blood cells, thymocytes, liver, skeletal muscles, and intact hearts all maintain a pH in the range 7.0 - 7.3.b/h/1 However, the pH can fall to 6.2 within 13 minutes of oxygen deprivation (ischemia) and to 6.1 after exhaustive exercise.13 0 The 31P NMR technique permits the monitoring of pH as well as the state of the adenylate system (Section D) in human limbs suffering from circulatory insufficiency.0... 

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