Micronuclei Induced by Sulfur Dioxide Inhalation in Mouse Bone-Marrow Cells in Vivo

Meng, Ziqiang; Zhang, Bo; Ruan, Aidong; Sang, Nan; Zhang, Jianbiao

doi:10.1080/08958370252809077

Cited by 30 publications

(27 citation statements)

References 17 publications

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“…SO 2 and its derivatives were previously considered systemic www.nature.com/aps Ma HJ et al Acta Pharmacologica Sinica npg toxic agents that can cause many types of toxic effects, such as chromosomal aberrations, micronuclei, sister-chromatid exchanges [19,[26][27][28][29] , gene mutations [30] , lipid peroxidative damage [31] , DNA damage [32,33] , and changes in some enzyme activities [34] in multiple organs in mice and rats. Studies have also indicated that SO 2 inhalation can also cause gene expression changes and alter cytokine levels in the rat lung [35] .…”

Section: Discussionmentioning

confidence: 99%

Sulfur dioxide attenuates LPS-induced acute lung injury via enhancing polymorphonuclear neutrophil apoptosis

Huang

Liu

et al. 2012

Acta Pharmacol Sin

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Section: Discussionmentioning

confidence: 99%

Sulfur dioxide attenuates LPS-induced acute lung injury via enhancing polymorphonuclear neutrophil apoptosis

Huang

Liu

et al. 2012

Acta Pharmacol Sin

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“…Though according to the International Agency for Research on Cancer SO 2 is not classifiable as to its carcinogenicity (IARC, 1992), some studies have associated this gas with DNA damage. Meng et al (2002Meng et al ( , 2005 have reported that inhaled SO 2 damaged the DNA of multiple organs of mice (in addition to the lung) and suggested that the damages could result in mutation, cancer, and other diseases related to DNA damage. Some studies have shown that occupational exposure to SO 2 increases DNA damage in peripheral blood lymphocytes of workers (Yadav and Kaushik, 1996), and epidemiological evidence has linked SO 2 exposure with lung cancer (Lee et al, 2002;Pope et al, 1995).…”

Section: Discussionmentioning

confidence: 99%

Evidence of DNA damage in humans inhabiting a volcanically active environment: A useful tool for biomonitoring

Rodrigues¹,

Arruda

Garcia

2012

Environment International

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This article appeared in a journal published by Elsevier. The attached copy is furnished to the author for internal non-commercial research and education use, including for instruction at the authors institution and sharing with colleagues.Other uses, including reproduction and distribution, or selling or licensing copies, or posting to personal, institutional or third party websites are prohibited. The present study was designed to evaluate whether chronic exposure to a volcanically active environment might result in genotoxic and cytotoxic effects in human oral epithelial cells. A study group of 120 individuals inhabiting a volcanically active environment (exposed group; Furnas village) and a reference group of 122 individuals inhabiting a village without manifestations of volcanic activity (Santo António village) were examined in this study. Individuals from Furnas village inhabit a volcanically active environment marked by several degassing manifestations, including fumarolic fields, thermal and cold CO 2 springs and soil diffuse degassing areas. For each individual, 1000 buccal epithelial cells were analyzed for the frequency of micronucleated cells (MNC) and the frequency of cells with other nuclear anomalies (ONA: pyknosis, karyolysis and karyorrhexis), by using the micronucleus assay. Information on life-style factors and an informed consent were obtained from each participant. The frequencies of MNC and of ONA per 1000 cells in the exposed group (4.3‰ and 23.5‰, respectively) were significantly higher than in the reference group (1.7‰ and 7.7‰, respectively). The risk of having a high frequency of MNC or ONA was 2.4 and 3.1-fold higher in exposed individuals compared to reference group. The analyzed confounding factors (age, gender, smoking status, alcohol consumption, and mouthwash use) did not show any significant association with the frequency of MNC or ONA. The higher risk of DNA damage in individuals inhabiting a volcanically active environment is for the first time clearly highlighted with this biomonitoring study. Given that MNC in oral epithelia are recognized as a predictive biomarker of cancer risk within a population of healthy subjects, these findings could contribute to explain the high incidence rates of lip, oral cavity and pharynx cancers previously referred for Furnas village inhabitants.

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“…In vivo studies Meng et al (2002) investigated the induction of micronuclei in bone marrow cells of male and female Kunming mice following inhalation exposure to sulfur dioxide. Concentrations of 0, 14, 28, 56 and 84 mg SO 2 /m 3 were administered to groups of five male and five female mice for 4h/day for 7 days.…”

Section: Sulfur Dioxidementioning

confidence: 99%

Scientific Opinion on the re‐evaluation of sulfur dioxide (E 220), sodium sulfite (E 221), sodium bisulfite (E 222), sodium metabisulfite (E 223), potassium metabisulfite (E 224), calcium sulfite (E 226), calcium bisulfite (E 227) and potassium bisulfite (E 228) as food additives

Reculusa

Arbault

2016

EFS2

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The EFSA Panel on Food Additives and Nutrient Sources added to Food (ANS) was asked to deliver a scientific opinion re‐evaluating sulfur dioxide (E 220), sodium sulfite (E 221), sodium bisulfite (E 222), sodium metabisulfite (E 223), potassium metabisulfite (E 224), calcium sulfite (E 226), calcium bisulfite (E 227) and potassium bisulfite (E 228) when used as food additives. The Panel noted that sulfur dioxide, bisulfite and sulfite ions existed in a series of equilibria and that these would favour bisulfite ions at the pH of the stomach and sulfite ions at physiological pHs. Therefore, it was considered that once ingested, based on their capacity to form sulfite ions, read across between the different sulfite sources is possible; however, the Panel noted the uncertainties about the reactivity of sulfites in different foods and the resulting reaction products. The overall limited database did not indicate any concern for genotoxicity and did not report any effect in the available chronic, carcinogenicity and reprotoxicity studies after oral exposure in the diet, by gavage, or in the drinking water. A no observed adverse effect level (NOAEL) of 70 mg SO2 equivalent/kg body weight (bw) per day was identified from a long‐term toxicity study in rats. However, the Panel noted several uncertainties and limitations in the database and concluded that the current group acceptable daily intake (ADI) of 0.7 mg SO2 equivalent/kg bw per day (derived using a default uncertainty factor) would remain adequate but should be considered temporary while the database was improved. The Panel recommended that the database and the temporary group ADI should be re‐evaluated and noted that the recommended studies could require 5 years for completion. The Panel further concluded that exposure estimates to sulfur dioxide and sulfites were higher than the group ADI of 0.7 mg SO2 equivalent/kg bw per day for all population groups.

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Micronuclei Induced by Sulfur Dioxide Inhalation in Mouse Bone-Marrow Cells in Vivo

Cited by 30 publications

References 17 publications

Sulfur dioxide attenuates LPS-induced acute lung injury via enhancing polymorphonuclear neutrophil apoptosis

Sulfur dioxide attenuates LPS-induced acute lung injury via enhancing polymorphonuclear neutrophil apoptosis

Evidence of DNA damage in humans inhabiting a volcanically active environment: A useful tool for biomonitoring

Scientific Opinion on the re‐evaluation of sulfur dioxide (E 220), sodium sulfite (E 221), sodium bisulfite (E 222), sodium metabisulfite (E 223), potassium metabisulfite (E 224), calcium sulfite (E 226), calcium bisulfite (E 227) and potassium bisulfite (E 228) as food additives

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