Reaction of Ozone with Enzymes of Erythrocyte Membranes

Mudd, J.B.; Dawson, P.J.; Adams, J.R.; Wingo, John; Santrock, Jeffrey

doi:10.1006/abbi.1996.0492

Cited by 19 publications

(9 citation statements)

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“…Inactivation and/or denaturation upon exposure to ozone has been shown for lysozyme [14,15], glutamine synthetase [16], glyceraldehyde-3-phosphate dehydrogenase (G3PDH) [17], and acetylcholine esterase (AChE) [18]. Biomolecular targets also exist in atmosphere, either within viable cells (bacteria, fungal spores, etc.)…”

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confidence: 99%

Peptide ozonolysis: Product structures and relative reactivities for oxidation of tyrosine and histidine residues

Lloyd

Spraggins

Johnston

et al. 2006

J. Am. Soc. Mass Spectrom.

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Angiotensin II (DRVYIHPF) and two analogs, (DRVYIAPA and DRVAIHPA), were used as model systems to study the ozonolysis of peptides containing tyrosine and histidine residues. The ESI mass spectrum of angiotensin II following exposure to ozone showed the formation of adducts containing one, three, and four oxygen atoms. CID and SID spectra of these adducts were consistent with formation of Tyr ϩ O and His ϩ 3O as expected from previous work with amino acids. However, several fragment ions observed in the CID and SID spectra suggested formation of a rather unexpected adduct, Tyr ϩ 3O, and a small amount of the Phe ϩ O adduct. These findings were confirmed by examining two angiotensin analogs. Exposure of DRVYIAPA to ozone resulted in the addition of either one or three oxygen atoms on Tyr, while DRVAIHPA showed only the addition of three oxygen atoms-all on His. Other noteworthy minor oxidation products were observed from these analogs including Tyr ϩ 34 Da, His ϩ 5 Da, His ϩ 34 Da, and His ϩ 82 Da. The reaction rates of the peptides with ozone were found to be similar: second-order rate coefficients are 274 Ϯ 3, 379 Ϯ 6, and 439 Ϯ 34 M Ϫ1 s Ϫ1 for DRVYIAPA, DRVAIHPA, and angiotensin II, respectively. The relative rates indicate (1) an isolated His residue has a slightly greater ozone reactivity than an isolated Tyr residue, and (2) the reaction rates of isolated residues are not additive when both residues are present in the same

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confidence: 99%

Peptide ozonolysis: Product structures and relative reactivities for oxidation of tyrosine and histidine residues

Lloyd

Spraggins

Johnston

et al. 2006

J. Am. Soc. Mass Spectrom.

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“…Lipid peroxidation in vivo has been claimed to be of basic importance in aging, damage to cells by air pollution and in oxygen toxicity (Tappel 1973). On the other hand, studies suggest that radiation hazards (Inouye et al 1979) or influence of various environmental pollutants (Mudd & Freeman 1977) are closely related to lipid peroxidation. The effects of sulfur oxides on living organisms in an experimental model have shown that sulfite oxidation is remarkably accelarated by superoxide anion radical (0;) and Mn", suggesting sulfite radical formation in oxidation process (Inouye e t a / .…”

Section: Discussionmentioning

confidence: 99%

Air Pollutant Sulfur Dioxide‐induced Alterations on the Levels of Lipids, Lipid Peroxidation and Lipase Activity in Various Regions of the Rat Brain

Haider

Hasan

Khan

1982

Acta Pharmacologica et Toxicologica

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The exposure of rats to SO2 (10 p.p.m.) for one hour daily for 30 days caused depletion of total lipids in all brain areas. The contents of phospholipid were elevated in cerebellum and brain stem, but were depleted in cerebral hemisphere. Cholesterol levels showed an increase in various brain regions. On the other hand, gangliosides were increased in cerebellum and brain stem, but were decreased in cerebral hemisphere. Interestingly, cholesterol/phospholipid ratio was increased in different regions of the brain. Lipase activity was elevated in cerebral hemisphere. Lipid peroxidation showed marked increment in whole brain and in all the brain areas studied. The results suggest that SO2‐exposure induces degradation of lipids. Interestingly, the lipid contents are affected differentially in the various parts of the brain.

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“…Therefore many of the pulmonary and all of the nonpulmonary effects of ozone must arise from the production of initial ozonation products as ozone enters the lung^air interface and the subsequent reactions of these initial ozonation products. The initial ozonation products are known to include molecules formed from the ozonation of lipids (Goldstein and Balchum, 1967;Goldstein etal, 1969;Balchum etal., 1971;Mudd and Freeman, 1977;Pryor et al, 1976;Leikauf et al, 1993). These primary reaction products then relay the effects of ozone to deeper tissue strata (Pryor, 1993;Goldstein and Balchum, 1967;Pryor et al, 1995b;Leikauf et al, 1995;Wright etal., 1994b).…”

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confidence: 99%

“…3 First, unsaturated fatty acids in lung lipids have long been considered to be a primary target for ozone (Pryor and Church, 1991;Pryor et al, 1991a;Goldstein and Balchum, 1967;Goldstein et al, 1969;Balchum et al, 1971;Mudd and Freeman, 1977). The epithelial cell-lining fluids (ELF) in the lung, including mucus and surfactant, contain from 20 to 40% unsaturated fatty acid-containing lipids (Harwood et al, 1975;Shelley et al, 1984;King, 1974;Sahu et al, 1976).…”

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confidence: 99%