Reaction of ozone with amino acids and proteins

Mudd, J.B.; Leavitt, R. I.; Ongun, Alpaslan; McManus, T.T.

doi:10.1016/0004-6981(69)90024-9

Cited by 244 publications

(113 citation statements)

References 17 publications

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“…Uric acid and ascorbic acid were found to be the major plasma scavengers of 03 (81). Although it is often assumed that lipids are a major target of attack by 03, no evidence of substantial lipid damage by 03 was obtained (81), in keeping with other studies in the literature (82,83). Instead, oxidative protein damage was observed in 03-exposed plasma, as -SH group loss and protein carbonyl formation (84).…”

Section: Causes Of Oxidative Stress: Environmental Air Pollutantssupporting

confidence: 70%

Oxygen-derived species: their relation to human disease and environmental stress.

Halliwell

Cross

1994

Environ Health Perspect

490

276

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Free radicals and other reactive oxygen species (ROS) are constantly formed in the human body, often for useful metabolic purposes. Antioxidant defenses protect against them, but these defenses are not completely adequate, and systems that repair damage by ROS are also necessary. Mild oxidative stress often induces antioxidant defense enzymes, but severe stress can cause oxidative damage to lipids, proteins, and DNA within cells, leading to such events as DNA strand breakage and disruption of calcium ion metabolism. Oxidative stress can result from exposure to toxic agents, and by the process of tissue injury itself. Ozone, oxides of nitrogen, and cigarette smoke can cause oxidative damage; but the molecular targets that they damage may not be the same. -Environ Health Perspect 1 02(Suppl 1 0): 5-12 (1994)

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Section: Causes Of Oxidative Stress: Environmental Air Pollutantssupporting

confidence: 70%

Oxygen-derived species: their relation to human disease and environmental stress.

Halliwell

Cross

1994

Environ Health Perspect

490

276

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“…It can form free radicals and other reactive intermediates by oxidizing the biological molecules. It can cause lipid peroxidation [44] and oxidize different functional groups, for example, amine, alcohol, aldehyde and sulphydryl, present in proteins [45,46] and nucleic acids [47]. It can also cause chromosomal aberrations which may be due to direct attack by O 3 or by the free radicals generated by it [48].…”

Section: Reactive Oxygen Species (Ros) and Reactive Nitrogen Species mentioning

confidence: 99%

Free Radicals: Properties, Sources, Targets, and Their Implication in Various Diseases

2014

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Free radicals and other oxidants have gained importance in the field of biology due to their central role in various physiological conditions as well as their implication in a diverse range of diseases. The free radicals, both the reactive oxygen species (ROS) and reactive nitrogen species (RNS), are derived from both endogenous sources (mitochondria, peroxisomes, endoplasmic reticulum, phagocytic cells etc.) and exogenous sources (pollution, alcohol, tobacco smoke, heavy metals, transition metals,

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“…These are located in the signal peptide region, the collagen-like domain, and the carbohydrate recognition domain (CRD) (9). Given that there is an order of preference (Cys>Trp=Met>Tyr>His) for ozone to react with free amino acid (10) and that certain amino acids in which the SP-A alleles differ may be more susceptible to oxidation, it is possible that certain SP-A alleles are more susceptible to oxidation than others.…”

mentioning

confidence: 99%

The effect of ozone exposure on the ability of human surfactant protein a variants to stimulate cytokine production.

Wang

Umstead

Phelps

et al. 2002

Environ Health Perspect

126

197

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Ozone exposure can cause inflammation and impaired lung function. Human surfactant protein A (SP-A) may play a role in inflammation by modulating cytokine production by macrophages. SP-A is encoded by two genes, SP-A1 and SP-A2, and several allelic variants have been characterized for each gene. These allelic variants differ among themselves in amino acids that may exhibit differential sensitivity to ozone-induced oxidation and this may produce functional differences. We studied the effects of SP-A variants before and after ozone exposure on the production of tumor necrosis factor (TNF)-alpha and interleukin (IL)-8. These are important proinflammatory cytokines and are expressed by the macrophage-like THP-1 cells. Eight variants were expressed in vitro, characterized by gel electrophoresis, and studied. These included six single-gene SP-A alleles and two SP-A variants derived from both genes. Variants were exposed to ozone at 1 ppm for 4 hr at 37 degrees C, and we compared their ability to stimulate cytokine (TNF-alpha and IL-8) production by THP-1 cells to air-exposed and unexposed SP-A variants. We found that a) SP-A2 variants (1A, 1A(0), 1A(1) stimulate significantly more TNF-alpha and IL-8 production than SP-A1 variants (6A, 6A(2), 6A(4); b) coexpressed SP-A variants (1A(0)/6A(2), 1A(1)/6A(4) have significantly higher activity than single gene products; c) after ozone exposure, all SP-A variants showed a decreased ability to stimulate TNF-alpha and IL-8 production, and the level of the decrease varied among SP-A variants (26-48%); and d) human SP-A from patients with alveolar proteinosis exhibited a minimal decrease (18% and 12%, respectively) in its ability to stimulate TNF-alpha and IL-8 after in vitro ozone exposure. We conclude that biochemical and functional differences exist among SP-A variants, that ozone exposure modulates the ability of SP-A variants to stimulate cytokines by THP-1 cells, and that SP-As from bronchoalveolar lavage (BAL) fluid of certain alveolar proteinosis patients may be oxidized in vivo.

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Reaction of ozone with amino acids and proteins

Cited by 244 publications

References 17 publications

Oxygen-derived species: their relation to human disease and environmental stress.

Oxygen-derived species: their relation to human disease and environmental stress.

Free Radicals: Properties, Sources, Targets, and Their Implication in Various Diseases

The effect of ozone exposure on the ability of human surfactant protein a variants to stimulate cytokine production.

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