氯化镉致小鼠胸腺病理及酶组织化学改变

CHANGES IN HISTOPATHOLOGY AND ENZYME HISTOCHEMISTRY OF THYMUS IN CADMIUM EXPOSURE MICE

作者用昆明种雄鼠单次腹腔染镉,通过一般组织病理学和酶组织化学方法,观察了镉致胸腺损伤的形态及酶活性改变。结果:亚致死剂量镉(3mg/kg)单次染毒可导致胸腺急性萎缩,其发生机理是氯化镉抑制毛细血管内皮细胞酶活性,从而造成毛细血管损伤,致皮质淋巴细胞缺氧,大片坏死。单次染镉致胸腺急性萎缩后胸腺有较强的再生能力。

The changes in histopathology and en-zyme histochemistry of thymus induced bya single intraperitoneal injection of suble-thal doses of cadmium chloride into Kun-ming male mice were examined .The swollenendothelium of capillaries was observed,with an obviously decreased activity ofICDH, LDH and ATPase, which seemed tobe due to direct inhibition by cadmium atthe 4th hour. The necroses of the cortexthymocytes were found at the 8th hour af-ter injection and reached an extreme at the16-24th hour, while few necroses of thelymphocytes in the medulla. Beginning 4thto 8th hour after exposure, the activity ofenzymes was located in mitochondria of thecortex thycytes, i.e., SDH, ICDH, CCOand ATPase, was decreased gradually. Itsuggested that thymic cortex had a markedimpairment of blood supply and anoxia.Within 2 days after a single injection thecortex of the gland was mainly populatedby epithelial reticular cells except a fewlymphocytes. It was noted that there weresome bigger cells which were characterizedby their large size, basophilic cytoplasma.rough chromatin and high mitotic abilityand activity of MDH, LDH, G-6-PDincreased in these cells. From above observation the author con-cluded that the cause of cadmium-inducedacute thymic atrophy was lymphocyte ne-croses within thymic cortex. The mechanismof the cortex thymocytes necrosis was pos-sibly secondary to an anoxia of cortex re-sulting from capillary damage in the cortex.The ability of thymic regeneration is strongafter being damaged. The regenerate cellspossessed characteristics of morphology andenzyme histochemistry of immature cells,which probably came from the bone marrow.