Literature DB >> 17497532

Cell morphological ultrastructural changes in various organs from mice exposed by inhalation to sulfur dioxide.

Ziqiang Meng1, Yuxiang Liu.   

Abstract

Sulfur dioxide (SO2) is a common air pollutant, present in low concentrations in the community air as well as in higher concentrations in some workplaces. Our previous studies demonstrated that SO2 can cause oxidative stress and DNA damage to multiple organs of mice. However, there was no direct proof if and how the morphological changes are caused by SO2. In this study, the ultrastructural morphologies of lungs, livers, spleens, testis, brains, hearts, and kidneys from mice exposed by inhalation to SO2 at 28.00 +/- 1.98 and 56.00 +/- 3.11 mg/m3 were observed with electron microscopy. Our results show that (1) type II alveolar cells of lungs in SO2-exposure groups had obvious pathological changes including vacuolation of osmiophilic multilamellar bodies, a decrease in microvilli content and mitochondrial pyknosis or swelling, as well as various changes in the structure of the nucleus and chromatin. Meanwhile obvious changes in the mitochondrial and nuclear compartments, in type II alveolar cells were also observed. (2) A series of pathological changes was discovered in hepatic cells in SO2-exposure groups, such as swelling of the nucleus, dispersion of lipid droplets, degenerated mitochondria, and dilatation of rough endoplasmic reticulum. For mice exposed to SO2 at 56 mg/m3, necrosis of hepatocytes with unclear karyotheca or nearly dissolved karyotheca and decreases in organelles were observed. (3) The numbers of apoptotic splenocytes from mice exposed to SO2 were increased by SO2 inhalation in a dose-dependent manner. (4) In SO2-exposure groups, some of the cerebral cortex neurons, many glial cells and nerve fibers were damaged. (5) Mitochondrial swelling, decrease or disappearance of mitochondria crista, myocardial myofibril disorder, various changes of nucleus and chromatin, intercalated discs dissociation, and endothelium edema caused by SO2 exposure in heart tissues were found. In addition, other effects, such as myofibrillar fragmentation and dissolution, some myocardial cell membranes breach, and inflammatory cell infiltration, were observed in groups exposed to SO2 at 56 mg/m3. (6) SO2 exposure induced serious ultrastructural lesions in renal proximal tubular lining cells; moreover glomeruli and distal tubular lining cells were damaged in a dose-dependent manner. (7) Compared with the control group, the basement membranes, various seminiferous cells, as well as spermatozoa, and Sertoli cells of testes were altered in the SO2-exposure groups in a dose-dependent manner. In the aggregate, these results lead to a conclusion that inhalation of SO2 can cause the ultrastructure cellular damage of multiple organs in mice. Thus, inhalation of sulfur dioxide appears to be not only toxic to the respiratory system, but also a systemic toxin as well.

Entities:  

Mesh:

Substances:

Year:  2007        PMID: 17497532     DOI: 10.1080/08958370701271373

Source DB:  PubMed          Journal:  Inhal Toxicol        ISSN: 0895-8378            Impact factor:   2.724


  8 in total

1.  Sulfur dioxide induces apoptosis via reactive oxygen species generation in rat cardiomyocytes.

Authors:  Shuyue Li; Zhifang Xu; Jin Xia; Guohua Qin; Nan Sang
Journal:  Environ Sci Pollut Res Int       Date:  2019-02-02       Impact factor: 4.223

2.  Sulfur dioxide inhibits expression of mitochondrial oxidative phosphorylation genes encoded by both nuclear DNA and mitochondrial DNA in rat lungs.

Authors:  Guohua Qin; Jiaoxia Wang; Nan Sang
Journal:  Environ Sci Pollut Res Int       Date:  2016-11-08       Impact factor: 4.223

3.  Environmental car exhaust pollution damages human sperm chromatin and DNA.

Authors:  A E Calogero; S La Vignera; R A Condorelli; A Perdichizzi; D Valenti; P Asero; U Carbone; B Boggia; N De Rosa; G Lombardi; R D'Agata; L O Vicari; E Vicari; M De Rosa
Journal:  J Endocrinol Invest       Date:  2010-10-15       Impact factor: 4.256

4.  Association between gaseous air pollutants and idiopathic nephrotic syndrome in children: a 12-year population-based cohort study.

Authors:  Chieh Wang; Jeng-Dau Tsai; Lei Wan; Cheng-Li Lin; Chang-Ching Wei
Journal:  Ital J Pediatr       Date:  2022-05-12       Impact factor: 3.288

5.  The PI3K/Akt, p38MAPK, and JAK2/STAT3 signaling pathways mediate the protection of SO2 against acute lung injury induced by limb ischemia/reperfusion in rats.

Authors:  Yan-Rui Zhao; Dong Wang; Yang Liu; Lei Shan; Jun-Lin Zhou
Journal:  J Physiol Sci       Date:  2015-11-05       Impact factor: 2.781

6.  Inhaled matters of the heart.

Authors:  Ahmed Zaky; Aftab Ahmad; Louis J Dell'Italia; Leila Jahromi; Lee Ann Reisenberg; Sadis Matalon; Shama Ahmad
Journal:  Cardiovasc Regen Med       Date:  2015-09-20

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

Authors:  Hui-Jie Ma; Xin-Li Huang; Yan Liu; Ya-Min Fan
Journal:  Acta Pharmacol Sin       Date:  2012-07-16       Impact factor: 6.150

8.  Sulfur dioxide reduces lipopolysaccharide-induced acute lung injury in rats.

Authors:  Yu Zhai; Xin-Li Huang; Hui-Jie Ma; Xiao-Hong Zhou; Jun-Lin Zhou; Ya-Min Fan
Journal:  Cent Eur J Immunol       Date:  2019-09-30       Impact factor: 2.085

  8 in total

北京卡尤迪生物科技股份有限公司 © 2022-2023.