Meng Ziqiang, Liu Yuxiang
Institute of Environmental Medicine and Toxicology, Shanxi University, Taiyuan, China.
Inhal Toxicol. 2007 May;19(6-7):543-51. doi: 10.1080/08958370701271373.
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.
二氧化硫（SO₂）是一种常见的空气污染物，在社区空气中浓度较低，而在一些工作场所浓度较高。我们之前的研究表明，SO₂可对小鼠的多个器官造成氧化应激和DNA损伤。然而，尚无直接证据表明SO₂是否以及如何导致形态学变化。在本研究中，通过电子显微镜观察了吸入浓度为28.00±1.98和56.00±3.11 mg/m³ SO₂的小鼠的肺、肝、脾、睾丸、脑、心脏和肾脏的超微结构形态。我们的结果表明：（1）SO₂暴露组小鼠肺的II型肺泡细胞有明显的病理变化，包括嗜锇性多层小体空泡化、微绒毛含量减少、线粒体固缩或肿胀，以及细胞核和染色质结构的各种变化。同时，II型肺泡细胞的线粒体和核区室也有明显变化。（2）SO₂暴露组肝细胞出现一系列病理变化，如细胞核肿胀、脂滴分散、线粒体退化和粗面内质网扩张。对于暴露于56 mg/m³ SO₂的小鼠，观察到细胞核膜不清或几乎溶解的肝细胞坏死以及细胞器减少。（3）吸入SO₂使暴露于SO₂的小鼠凋亡脾细胞数量呈剂量依赖性增加。（4）在SO₂暴露组中，一些大脑皮层神经元、许多神经胶质细胞和神经纤维受损。（5）发现SO₂暴露导致心脏组织线粒体肿胀、线粒体嵴减少或消失、心肌肌原纤维紊乱、细胞核和染色质的各种变化、闰盘解离以及内皮水肿。此外，在暴露于56 mg/m³ SO₂的组中还观察到其他效应，如肌原纤维断裂和溶解、一些心肌细胞膜破裂以及炎症细胞浸润。（6）SO₂暴露导致肾近端小管衬里细胞出现严重的超微结构损伤；此外，肾小球和远端小管衬里细胞也呈剂量依赖性受损。（7）与对照组相比，SO₂暴露组睾丸的基底膜、各种生精细胞、精子以及支持细胞均呈剂量依赖性改变。总的来说，这些结果得出一个结论，即吸入SO₂可导致小鼠多个器官的细胞超微结构损伤。因此，吸入二氧化硫似乎不仅对呼吸系统有毒，而且也是一种全身性毒素。
