Amount Of 1O2 Research Articles

Oxidation of sulfites on vanadium-molybdenum oxides

The low temperature emission of 1O2 singlet oxygen from xV2O5 · yMoO3 binary oxides is investigated by means of flash desorption. Conditions for the generation of 1O2 on their surfaces are determined, along with the correlation between the amount of 1O2 and the degree of NaHSO3 conversion in the oxidation reaction. It is shown that on the surface of oxides there are oxygen species that upon decomposition produce 1O2 involved in the oxidation of HSO3−.

Studies on Production and Chemical Property of Singlet Oxygen and Superoxide Radical by Dyestuffs

There are several low lying singlet oxygen (1O2) and superoxide radical (O-2) which are important in photochemical oxidation. In our present analysis we are studying chemical property of singlet oxygen (1O2) and super oxide radical (O-2) and some dyestuffs species to produce reactive oxygen such as singlet oxygen 1O2 and superoxide radicals. Irradiation with sun light in vitro the dyestuff like benzanthrone, metanil yellow and p‐aminodiphenylamine were found to produce reactive oxygen species such as singlet oxygen (1O2) and/or superoxide radicals (O-2) .The dose response relationship between singlet 1O2 production when sunlight expose of those dyestuffs (0‐25 min), and (0‐12 min) for super oxide (O-2) production were studied. However benzanthrone produces detectable amount of 1O2, Although metanil yellow and p‐aminodiphenylamine (p‐ADPA) did not produce detectable amounts of 1O2 under similar conditions. The above dye stuffs are routinely used in textiles, cosmetics, detergents, leather industries as well as food additives and role of these activated oxygen species in the development of skin diseases.

The Release of Singlet Oxygen in the Reaction of Dioxiranes with AmineN-Oxides

The reactivity of dimethyldioxirane and methyl(trifluoromethyl)dioxirane towards the amine N-oxides 1a–13a and ammonium derivatives 13b–d has been investigated. In the dioxirane oxidation of the tertiary amines and nitrogen heteroarenes, the expected N-oxides are not always formed. Instead, the in situ generated N-oxides are deoxygenated by the dioxirane with the release of singlet oxygen (1O2) at comparable or even higher rates than the amine oxidation. The amount of 1O2 has been quantified by IR chemiluminescence and by chemical trapping with 9,10-dimethylanthracene. The nucleophilicity of the N-oxide determines the efficacy of the 1O2 release in the deoxygenation. Thus, for the less nucleophilic heteroaromatic N-oxides, the deoxygenation of the amine oxide competes ineffectively with the oxidation of the amine. The ammonium derivatives 13b–d do not promote the decomposition of the dioxiranes; as expected, they are epoxidized.

Direct detection and quantification of singlet oxygen during ischemia and reperfusion in rat hearts

To detect singlet oxygen (1O2) in postischemic reperfused hearts, 5,8-endoperoxide, an oxidation product of beta-carotene, was used as a marker for 1O2 generation and was quantified using high-performance liquid chromatography (HPLC). Isolated rat hearts were subjected to ischemia for 5, 10, 20, 30, and 60 min followed by 10 min of reperfusion with buffer containing 25 microM beta-carotene. The coronary effluent was collected, extracted, and injected into the HPLC unit. The production of 5,8-endoperoxide was maximum during the first 2 min of reperfusion. Maximal accumulated amount of 1O2 was observed in hearts subjected to 60-min ischemia (36.2 +/- 1.7 nmol.10 min-1.g-1) as compared with 10-min ischemia (6.2 +/- 1.0 nmol.10 min-1.g-1). There was a good correlation between the amount of 1O2 production and cardiac function. Treatment with 25 mM histidine significantly decreased 5,8-endoperoxide from 7.02 +/- 0.47 to 0.98 +/- 0.11 nmol.min-1.g-1 (P < 0.01) and improved cardiac function in the group with 60-min ischemia. This study demonstrates that 1) the present method is useful and reliable for the measurement of 1O2 in the heart, 2) 1O2 production during reperfusion is dependent on the duration of initial ischemia, and 3) 1O2 is one of the major factors in postischemic reperfusion injury.

Direct exposure of mammalian cells to pure exogenous singlet oxygen (1 delta gO2).

Mammalian cells attached to membrane filters or deposited on filters without attachment were exposed to gas-phase singlet oxygen (1O2) in the absence of any other reactants. Cells were exposed in a monolayer or less, in the absence of external medium, during steady-state 1O2 generation, ensuring that singlet oxygen impinged directly and equally on all cells simultaneously. The current methodology for cell exposure ensures that 1O2 is initially the only reactive species to which the cells are exposed. Results seen with this system can therefore be attributed solely and unambiguously to events initiated by 1O2. Further, all cells in the sample receive the same magnitude of exposure per surface area per time interval, which supports calculations of the amount of 1O2 required for irreversible cell damage, based on measured 1O2 flux and exposed cell surface area. Exposure to pure 1O2 irreversibly damaged a variety of cell types, including rat basophilic leukemia, human squamous carcinoma and Chinese hamster lung fibroblast cell lines, and murine primary hepatocytes. Cell survival curves following exposure to 1O2 followed apparent first-order kinetics. A large number of singlet oxygen collisions (approximately 10(12)-10(13) were required to inactivate a cell, on average, indicating a low probability that singlet oxygen collision will reduce cell survival. Regardless of cell type or the survival endpoint measured, lethal toxicity required a fairly constant number of 1O2 collisions per cell. This poses a serious caveat in the assignment of causality in correlating 1O2-initiated cellular damage with mechanism of death, i.e. most damage observed will not be related to death.(ABSTRACT TRUNCATED AT 250 WORDS)