Effects On Ultrastructure And Apoptosis Of Several Mouse Organs Of Sulfur Dioxide And Its Derivatives

SO2 is a common irritant gas all over the world. Many researchers are devoting themselves on studying its toxicity.In the present study, we studied the apoptotic induction on mouse lung and spleen and their pathological structural changes of short-term sulfur dioxide inhalation. We also investigated the pathological changes of mouse liver, thymus and cerebrum cortex challenged by SO2 inhalation by in vivo tests. We studied the apoptotic induction on mouse spleen cells and cytotoxicity of human embryo lung fibroblasts of SO2 derivatives by in vitro tests.In vivo tests of sulfur dioxide inhalation showed:(1) Effects on mouse lung of SO2 challenge: We found no significant apoptotic changes induced by SO2 inhalation but obvious pathological changes of lung with vacuolating of osmiophilic multilamellar bodies which maybe related with the decrease of surfacant and decrease of microvillus of type II alveolar cells; We also found thickening of part of basement lamina between type I alveolar cells and capillary endothelium cells which may inhibit the dispersion of oxygen and contribute to lung dysfunction.(2) Effects on mouse spleen of SO2 challenge: We found significant apoptotic changes of mouse spleen through TEM observation and DNA electrophoresis analysis and flow cytometric analysis. We found condensed, marginating, half-moon like apoptotic lymphocytes both in white pulp and red pulp; We found significant DNA degradation with DNA ladders from the DNA electrophoresis analysis in the 168 mg/m3 SO2 treated group; We also found marked increase of apoptotic rate between 168 mg/m3 SO2 treated group and control group from the flow cytometric analysis. These suggested that SO2 may affect body immunity to a certain degree.(3) Effects on mouse thymus of SO2 challenge : HE staining showed no obvious structure changes of thymus in all treatment groups compaired with the control group; The ultrastructure of thymus can be seen injured in SO2 treated groups from TEM observation. We found nuclear deformation lymphocytes with increased heterochromatin and impaired thymus epithelium cells with increased lysosomes and deformation of mitochondrias.(4) Effects on mouse liver of SO2 challenge: SO2 can cause significant liver injury. HEstaining showed several kinds of necrosis of liver including spot necrosis, focal necrosis and submassive necrosis infiltrated with lymphocytes, monocytes, few neutrophils and eosinophils;TEM observation showed fatty degeneration with dispersion of fatty droplets and dilation of rough endoplasmic reticulums, acid degeneration with significant hyperplasia of mitochondrias, necrosis of hepatocytes with karyorrhexis and other organelles losing their normal structure.(5) Effects on mouse cerebrum cortex of SO2 challenge: we found no pathological changes of mouse cerebrum cortex challenged by SO2 by HE staining and TEM observation,In vitro tests of SO2 derivatives challenge showed that:(1) SO2 derivatives has significant toxicity on mouse spleen cells, the LC50 of 4h and 24h exposure is 1.1293 mmol/L and 1.3777mmol/L respectively. It has marked apoptotic induction on mouse spleen cells tested by DNA agarose gel electrophoresis analysis and flow cytometric assay in certain degree. It also can decrease the activity of lactate dehydrogenase(LDH) outside of mouse the spleen cells and increase the quantity of reduced GSH inside the mouse spleen cells.(2) SO2 derivatives has significant toxicity on human embryo lung fibroblasts, the LC50 of 4h and 24h exposure is 1. 1133 and 2. 0070mmol/L respectively. It also cause signigicant decrease of LDH activity both inside and outside of the human embryo lung fibroblasts.In conclusion, SO2 can not only affect respiratory system, but also other organs such as spleen, liver, thymus on their histological structures and every organ performs very differently under SO2 exposure. SO2 derivatives has cytotoxicity both on mouse spleen cells and human embryo lung fibroblasts. SO2 may injure other...