Cell morphological ultrastructural changes in various organs from mice exposed by inhalation to sulfur dioxide.
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.
Meng
Ziqiang
Z
Institute of Environmental Medicine and Toxicology, Shanxi University, Taiyuan, China. zqmeng@sxu.edu.cn
Liu
Yuxiang
Y
D000393:Air Pollutants / Q000633:toxicity; D000818:Animals; D001921:Brain / Q000187:drug effects / Q000648:ultrastructure; D002462:Cell Membrane / Q000187:drug effects* / Q000648:ultrastructure*; D019570:Inhalation Exposure / Q000009:adverse effects*; D008297:Male; D051379:Mice; D009928:Organ Specificity / Q000187:drug effects / Q000502:physiology; D011650:Pulmonary Alveoli / Q000187:drug effects / Q000648:ultrastructure*; D013458:Sulfur Dioxide / Q000008:administration & dosage* / Q000633:toxicity; D013737:Testis / Q000187:drug effects / Q000648:ultrastructure
D000393:Air Pollutants; D013458:Sulfur Dioxide