Antioxidants vs Lung Disease

Roehm, J. N.

doi:10.1001/archinte.1971.00310190092011

Cited by 47 publications

(16 citation statements)

References 1 publication

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“…[27][28][29][30][31] band is formed at B1110 cm À1 that is characteristic of the peroxide C-O bond 32,33 of the secondary ozonide ring (1,2,4-trioxolane, SOZ) known to be formed in ozone-alkene reactions. 14,[34][35][36][37][38][39][40] New bands at B1385 and 1347 cm À1 are also assigned to the SOZ. 31,33 The peak at 1210 cm À1 is assigned to a C-O moiety, although the specific species is not known.…”

Section: Auger Spectroscopymentioning

confidence: 99%

A new mechanism for ozonolysis of unsaturated organics on solids: phosphocholines on NaCl as a model for sea salt particles

Karagulian

Lea

Dilbeck

et al. 2008

Phys. Chem. Chem. Phys.

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PERSPECTIVEThe ozonolysis of an approximately one monolayer film of 1-oleoyl-2-palmitoyl-sn-glycero-3-phosphocholine (OPPC) on NaCl was followed in real time using diffuse reflection infrared Fourier transform spectrometry (DRIFTS) at 23 1C. Matrix-assisted laser desorption/ionization (MALDI) mass spectrometry and Auger electron spectroscopy were used to confirm the identification of the products. Ozone concentrations ranged from 1.7 Â 10 12 to 7.0 Â 10 13 molecules cm À3 (70 ppb to 2.8 ppm). Upon exposure to O 3 , there was a loss of CQC accompanied by the formation of a strong band at B1110 cm À1 due to the formation of a stable secondary ozonide (1,2,4-trioxolane, SOZ). The yield of the SOZ was smaller when the reaction was carried out in the presence of water vapor at concentrations corresponding to relative humidities between 2 and 25%.

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Section: Auger Spectroscopymentioning

confidence: 99%

A new mechanism for ozonolysis of unsaturated organics on solids: phosphocholines on NaCl as a model for sea salt particles

Karagulian

Lea

Dilbeck

et al. 2008

Phys. Chem. Chem. Phys.

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“…In vitro experiments established that both gases are capable of oxidizing fatty acid methyl esters (65). The lungs of rats exposed to N0 2 (1 ppm for 4 hr) were analyzed for peroxidized polyenoic fatty acids (66).…”

Section: Lipid Peroxidation and Lung Injurymentioning

confidence: 99%

Chemicals, Drugs, and Lipid Peroxidation

Plaa¹,

Witschi²

1976

Annu. Rev. Pharmacol. Toxicol.

490

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“…Therefore the presence of the suggested enzymatic protective mechanism against lipid peroxidation damage may explain the following observations: (a) failure to detect any or to detect increasing amounts of lipid peroxide in nutritionally stressed animals (5); (b) development of tolerance by animals to oxidants, e.g., ozone and NO2, following prior sublethal exposure (15)(16)(17); (c) insignificant decrease of SH groups following ozone exposure (Chow and Tappel, unpublished); and (d) rapid metabolism of injected lipid peroxide by the animal (14). The same type of protective mechanism may also apply to lipid peroxidation induced by NO 2 exposure (19,20) and hyperoxia (42), as well as CC14 (43), ethanol (44) and other free radical inducing agents. While the glutathione peroxidase pathway appears to be a major protective mechanism, other types of protective mechanisms would work in parallel.…”

Section: Fig 2 Correlation Between Malonaldehyde Concentration and mentioning

confidence: 99%

“…The damaging effects of nitrogen dioxide and ozone are related to their oxidative reactions, including initiation of lipid peroxidation, which can be partially prevented by a-tocopherol and other antioxidants (18)(19)(20). To understand how animals respond biochemically under ozone stress, these studies investigated alterations of lung tissue enzyme activities that may be important in the detoxification of lipid peroxides.…”

Section: Introductionmentioning

confidence: 99%

An enzymatic protective mechanism against lipid peroxidation damage to lungs of ozone‐exposed rats

Chow

Tappel

1972

Lipids

328

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The effects of whole animal exposure to ozone and of dietary α‐tocopherol on the occurrence in rat lung of lipid peroxidation and alteration of the activity of enzymes important in detoxification of lipid peroxides were studied. Exposure to 0.7 and 0.8 ppm ozone continuously for 5 and 7 days, respectively, significantly elevated the concentration of TBA reactants, primarily malonaldehyde, produced by lipid peroxidation, as well as the activities of glutathione (GSH) peroxidase, GSH reductase and glucose‐6‐phosphate (G‐6‐P) dehydrogenase. As a logarithmic function of dietary α‐tocopherol (0, 10.5, 45, 150 and 1500 mg/kg), the increase in formation of malonaldehyde and the increase in activities of GSH peroxidase and G‐6‐P dehydrogenase were partially inhibited. The activity of GSH reductase was not affected by dietary α‐tocopherol. The concentration of malonaldehyde and the activity of GSH peroxidase in lung were linearly correlated (p<0.001). This study confirmed the occurrence of lipid peroxidation in the lung during ozone exposure and revealed an enzymatic mechanism against damage. An apparent compensation mechanism is that with increased lipid peroxides there is increased activity of GSH peroxidase, which in turn increases lipid peroxide catabolism. The increased activities of GSH reductase and G‐6‐P dehydrogenase also function in the protective chain by providing increased levels of GSH and NADPH, respectively.

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Antioxidants vs Lung Disease

Cited by 47 publications

References 1 publication

A new mechanism for ozonolysis of unsaturated organics on solids: phosphocholines on NaCl as a model for sea salt particles

A new mechanism for ozonolysis of unsaturated organics on solids: phosphocholines on NaCl as a model for sea salt particles

Chemicals, Drugs, and Lipid Peroxidation

An enzymatic protective mechanism against lipid peroxidation damage to lungs of ozone‐exposed rats

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