The Effects of Sulfur Dioxide Inhalation and Antioxidant Vitamins on Red Blood Cell Lipoperoxidation

Etlik, Özdal; Tomur, Ahmet; Kutman, M.N.; Yörükan, Selma; Duman, Özgün Sarımehmet

doi:10.1006/enrs.1995.1063

Cited by 29 publications

(17 citation statements)

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“…Inhaled SO 2 can be easily hydrated to yield sulfurous acid in the respiratory tract, which subsequently dissociates to form sulfite/bisulfate and hydrogen ions (Gunnison & Benton, 1971). The amount of SO 2 in blood and other tissues increases proportionally with its concentration in the inhalation air (Etlik et al, 1995). Tissue damage and bronchoconstriction have been demonstrated to be induced by SO 2 exposure in both animals and humans.…”

mentioning

confidence: 97%

Effect of Sulfur Dioxide Inhalation on Cytokine Levels in Lungs and Serum of Mice

Meng

Liu

2005

Inhalation Toxicology

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In order to elucidate the immunotoxic mechanism exerted by sulfur dioxide (SO(2)), we investigated the effect of SO(2), a major air pollutant, on the cytokine levels in lungs and serum of male mice. Levels of interlukin-6(IL-6), tumor necrosis factor-alpha (TNF-alpha), and transforming growth factor-beta1 (TGF-beta1) in lungs and serum from male mice exposed to SO(2) at various concentrations were measured by the enzyme-linked immunosorbent assay. Sixty Kunming albino male mice were divided randomly into six equal groups: three groups exposed to SO(2) (14.00 +/- 1.25, 28.00 +/- 1.98, and 56.00 +/- 3.11 mg/m(3), which are 5 +/- 0.45, 10 +/- 0.71, and 20 +/- 1.11 ppm) and their respective control groups. The results were as follows: (1) For lung tissues of male mice, exposure to SO(2) at 14 mg/m(3) (5 ppm) caused statistically significant increase of levels of IL-6 and TNF-alpha (p < .05) compared with the control group; exposure at 28 mg/m(3) (10 ppm) caused a statistically highly significant increase of level of IL-6 (p < .01) and a significant increase of TNF-alpha (p < .05); and exposure at 56 mg/m(3) (20 ppm) caused no any significant increase of levels of IL-6 and TNF-alpha. SO(2) at all concentrations tested could not cause significant change of level of TGF-beta1 in lungs. (2) For serum from male mice, after exposure to SO(2) at 14 mg/m(3) (5 ppm), the level of TNF-a was significantly increased (p < .05) compared with the control group, but the changes of levels of IL-6 and TGF-beta1 were not significant. After exposure to SO(2) at 28 mg/m(3) (10 ppm) and 56 mg/m(3) (20 ppm), levels of IL-6 and TNF-alpha were increased nonsignificantly, but the level of TGF-beta1 was decreased nonsignificantly. These results imply that inflammation reaction could be induced in lung tissue by SO(2) inhalation and the inflammation reaction might relate to these cytokines. And determination of cytokines in lung may be more valuable than in serum when lung injury caused by SO(2).

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confidence: 97%

Effect of Sulfur Dioxide Inhalation on Cytokine Levels in Lungs and Serum of Mice

Meng

Liu

2005

Inhalation Toxicology

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“…GSH has been proposed to play a role in detoxification of SO 2 , and GSH in tissues may be lowered by SO 2 exposure. Some studies indicate that the level of TBARS is an indicator of endogenous lipid peroxidation (Tappel & Zalkin, 1960;Ceballos-Picot et al, 1992;Etlik et al, 1995;Gümüşlü et al, 1998). However, what TBARS reflect is not accurately known.…”

Section: Z Meng Et Almentioning

confidence: 95%

“…Free radical-induced oxidative damage has been implicated in the pathogenesis of a number of injury and diseases states (Freeman & Crapo, 1982;Halliwell, 1987;Max, 1987). Several studies have found that SO 2 inhalation enhances lipid peroxidation in the brains of rats and guinea pigs and in the rat erythrocytes (Haider et al, 1981;Yargicoglu et al, 1999;Etlik et al, 1995). Tyler (1975) also observed the acceleration of mitochondrial lipid peroxidation by sulfite in vitro.…”

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confidence: 87%

“…Several investigations have reported that exposure to SO 2 at 10 ppm (28 mg/m 3 ) may cause increase of lipid peroxidation in brains and erythrocytes of rats (Etlik et al, 1995;Gümüşlü et al, 1998;Yargicoglu et al, 1999). Recently, we have found that SO 2 inhalation may cause changes of oxidative stress and antioxidation status in various organs of mice, including stomachs and intestines (Meng, 2003).…”

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confidence: 96%

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Oxidative Damage of Sulfur Dioxide Inhalation on Stomachs and Intestines of Mice

Meng

Zhang

Bai

et al. 2003

Inhalation Toxicology

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Effects of exposure to sulfur dioxide (SO(2)) on levels of thiobarbituric acid-reactive substances (TBARS), levels of reduced glutathione (GSH), and the activities of Cu,Zn-superoxide dismutase (SOD), glutathione peroxidase (GPx), and catalase (CAT) were investigated in stomachs and intestines of Kunming albino mice of both sexes. SO(2) exposure at different concentrations (22, 56, and 112 mg/m(3)) was administered to the animals of SO(2) groups in the exposure chambers for 6 h/day for 7 days, while control groups were exposed to filtered air under the same condition. Our results show that SO(2) caused lipid peroxidation and changes of antioxidative status in stomachs and intestines of mice. Exposure to SO(2) at all concentrations tested caused significantly the increase of TBARS levels in stomachs and intestines of mice. For the stomachs, activities of these antioxidant enzymes and levels of GSH were significantly unaltered by SO(2) at low concentrations, except significant increase of SOD activity in the stomachs of male mice. However, higher SO(2) caused the significant increases of CAT activities and the significant decreases of GSH levels and activities of SOD and GPx. For intestines, SO(2) at all concentrations tested decreased significantly activities of SOD relative to control animals; SO(2) caused the decreases of GPx activities, but only the decreases of GPx activities caused by SO(2) exposures at higher concentrations (56 and 112 mg/m(3)) were statistically significant. SO(2) at all concentrations tested tended to increase the CAT activities in a dose-dependent manner, but the decreases of CAT activities caused by higher SO(2) were significant. SO(2) at all concentrations tested decreased significantly levels of GSH in intestines of both sexual mice. These results lead to conclusion that SO(2) exposure can caused oxidative damage to stomachs and intestines of mice, and SO(2) is a toxic agent to stomachs and intestines of mammals, not only to respiratory system. Further work is required to understand toxicological role of SO(2) on multiple or even all organs in human and animal.

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“…The overproduction of superoxide and other ROS probably causes further cell damage and mutations of mtDNA finally resulting in cell death (Esposito et al, 1999). Several studies have found that SO 2 inhalation enhances lipid peroxidation in the brains of rats and guinea pigs and in the rat erythroctes and nine organs of mice (Haider et al, 1981;Etlik et al, 1995;Gumuslu et al, 1998;Yargicoglu et al, 1999;Meng, 2003). Mitochondrial swelling and decrease in oxidative phosphorylation (Utsumi et al, 1965), release of hydrolytic enzymes from lysosomes (Wills and Wilkinson, 1966), and change in endoplasmic reticulum (Bidlack and Tappel, 1974) all have been described as biochemical distortions following lipid peroxidation.…”

Section: Electron Transportmentioning

confidence: 98%

Alterations of gene expression profiles induced by sulfur dioxide in rat lungs

et al. 2007

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Sulfur dioxide (SO 2 ) is a ubiquitous air pollutant, presents in low concentrations in urban air and in higher concentrations in working environment. Few data are available on the effects of being exposed to this pollutant on the molecular mechanism, although some biochemical changes in lipid metabolism, intermediary metabolism and oxidative stress have been detected. The present investigation aimed at analyzing the gene expression profiles of the lungs of Wistar rats short-term (20 ppm, 6 h/day, for seven days) and longterm (5 ppm, 1 h/day, for 30 days) exposed to SO 2 by Affymetrix GeneChip (RAE230A) analysis. It was found that 31 genes, containing 18 known genes and 13 novel genes, were up-regulated, and 31 genes, containing 20 known genes and 11 novel genes, were down-regulated in rats short-term exposed to SO 2 compared with control rats. While there were 176 genes, containing 82 known genes and 94 novel genes, were up-regulated, and 85 genes, containing 46 known genes and 39 novel genes, were down-regulated in rats long-term exposed to SO 2 compared with control rats. It is suggested that: (1) SO 2 exerts its effects by different mechanisms in vivo at high-dose short-term inhalation and at low-dose long-term inhalation; (2) a notable feature of the gene expression profile was the decreased expression of genes related to oxidative phosphorylation in lungs of rats short-term exposed to SO 2 , which shows high-dose short-term exposed to SO 2 may cause the deterioration of mitochondrial functions; (3) discriminating genes in lungs of rats long-term exposed to SO 2 included those involved in fatty acid metabolism, immune, inflammatory, oxidative stress, oncogene, tumor suppresser and extracellular matrix. The mechanism of low-dose long-term exposed to SO 2 is more complex.

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The Effects of Sulfur Dioxide Inhalation and Antioxidant Vitamins on Red Blood Cell Lipoperoxidation

Cited by 29 publications

References 0 publications

Effect of Sulfur Dioxide Inhalation on Cytokine Levels in Lungs and Serum of Mice

Effect of Sulfur Dioxide Inhalation on Cytokine Levels in Lungs and Serum of Mice

Oxidative Damage of Sulfur Dioxide Inhalation on Stomachs and Intestines of Mice

Alterations of gene expression profiles induced by sulfur dioxide in rat lungs

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