피마자(Ricinus communis)의 씨로부터 추출한 ricin 100ng/1ml PBS(pH7.0)/mouse를 ICR계 mouse에 주사하여 간, 비장, 흉선, 폐 및 심장에 대한 시간 경과에 따른 손상정도를 광학현미경과 전자현미경으로 관찰하였다. 간에서는 ricin투여 6시간군부터 간세포의 ...
피마자(Ricinus communis)의 씨로부터 추출한 ricin 100ng/1ml PBS(pH7.0)/mouse를 ICR계 mouse에 주사하여 간, 비장, 흉선, 폐 및 심장에 대한 시간 경과에 따른 손상정도를 광학현미경과 전자현미경으로 관찰하였다. 간에서는 ricin투여 6시간군부터 간세포의 핵막이 거치상으로 변했고, 조면소포체의 내강이 좁아지면서 미토콘드리아를 둘러싸고, 활면소포체가 감소하는 현상이 48시간군까지 지속되었다. Kupffer cell은 24시간군부터 apoptosis를 일으켜 핵이 응축되어 있었고, 내피세포도 24시간군부터 괴사되어 있었다. 비장의 경우, 적수에서는 ricin 투여 6시간군부터, 백비수에서는 12시간군부터 임파구와 대식세포들이 apoptosis를 일으키기 시작하여 48시간군에서는 거의 모든 임파구가 사멸되었다. 그러나 간상세포와 세망내피세포는 그 상해가 늦어져 48시간군에서 핵막부근의 염색질이 응축되거나 세포막이 붕괴되어 있었다. 흉선에서도 ricin 투여 6시간군부터 흉선 임파구와 대식세포가 apoptosis를 일으키기 시작하였고, 시간이 경과함에 따라 이러한 현상은 더욱 현저하였다. 혈관 내피세포와 흉선상피세포는 24시간군부터 핵막 부근 염색질의 응축현상을 나타내었으며, 48시간군에서는 거의 모든 세포가 사멸되어 있었다. 폐에서는 ricin 투여 6시간군부터 폐포벽에 대식세포와 혈관이 증가하여 폐포벽이 두꺼워지는 부종현상이 관찰되었다. 24시간군에서는 부종이 최고조에 달했으며, 폐포대식세포에서는 핵질이 응축되고, 폐포상피세포들에서는 핵막 주변의 핵질이 응축되었으며, 혈관내피세포는 세포질이 파괴되어 괴사 현상을 보였다. 48시간군에서는 거의 모든 세포들이 사멸되었고 확대된 혈관내에는 응집된 적혈구로 가득 채워져 있었다. 심장에서는 ricin 투여 24시간군부터 혈관 내강이 확장되어, 혈관 내에 apoptosis를 일으킨 대식세포가 소수 나타났으며, 이때 심근섬유의 핵막이 평활하게 변형되고, mitochondria 등의 세포내 소기관이 손상 되었으며, 근원섬유의 해리, 심근섬유들의 분리 등도 관찰되었다. 48시간군에서는 이러한 현상이 더욱 현저하였다. 결론적으로, ricin에 의해서 가장 민감하게 상해를 받은 조직은 면역계 조직(비장과 흉선)이었다. 각 조직별로는 면역계 세포, 혈관내피세포, 실질 조직세포들의 순으로 상해정도가 커서 이들 세포들의 순으로 ricin에 대한 민감도가 크다는 것이 시사되었다. 또한, 각 세포들의 종류에 따라 ricin에 의한 조직학적 변화가 달라, 면역계 세포는 apoptosis를, 나머지 세포들은 necrosis를 일으키고 있음이 밝혀졌다.
피마자(Ricinus communis)의 씨로부터 추출한 ricin 100ng/1ml PBS(pH7.0)/mouse를 ICR계 mouse에 주사하여 간, 비장, 흉선, 폐 및 심장에 대한 시간 경과에 따른 손상정도를 광학현미경과 전자현미경으로 관찰하였다. 간에서는 ricin투여 6시간군부터 간세포의 핵막이 거치상으로 변했고, 조면소포체의 내강이 좁아지면서 미토콘드리아를 둘러싸고, 활면소포체가 감소하는 현상이 48시간군까지 지속되었다. Kupffer cell은 24시간군부터 apoptosis를 일으켜 핵이 응축되어 있었고, 내피세포도 24시간군부터 괴사되어 있었다. 비장의 경우, 적수에서는 ricin 투여 6시간군부터, 백비수에서는 12시간군부터 임파구와 대식세포들이 apoptosis를 일으키기 시작하여 48시간군에서는 거의 모든 임파구가 사멸되었다. 그러나 간상세포와 세망내피세포는 그 상해가 늦어져 48시간군에서 핵막부근의 염색질이 응축되거나 세포막이 붕괴되어 있었다. 흉선에서도 ricin 투여 6시간군부터 흉선 임파구와 대식세포가 apoptosis를 일으키기 시작하였고, 시간이 경과함에 따라 이러한 현상은 더욱 현저하였다. 혈관 내피세포와 흉선상피세포는 24시간군부터 핵막 부근 염색질의 응축현상을 나타내었으며, 48시간군에서는 거의 모든 세포가 사멸되어 있었다. 폐에서는 ricin 투여 6시간군부터 폐포벽에 대식세포와 혈관이 증가하여 폐포벽이 두꺼워지는 부종현상이 관찰되었다. 24시간군에서는 부종이 최고조에 달했으며, 폐포대식세포에서는 핵질이 응축되고, 폐포상피세포들에서는 핵막 주변의 핵질이 응축되었으며, 혈관내피세포는 세포질이 파괴되어 괴사 현상을 보였다. 48시간군에서는 거의 모든 세포들이 사멸되었고 확대된 혈관내에는 응집된 적혈구로 가득 채워져 있었다. 심장에서는 ricin 투여 24시간군부터 혈관 내강이 확장되어, 혈관 내에 apoptosis를 일으킨 대식세포가 소수 나타났으며, 이때 심근섬유의 핵막이 평활하게 변형되고, mitochondria 등의 세포내 소기관이 손상 되었으며, 근원섬유의 해리, 심근섬유들의 분리 등도 관찰되었다. 48시간군에서는 이러한 현상이 더욱 현저하였다. 결론적으로, ricin에 의해서 가장 민감하게 상해를 받은 조직은 면역계 조직(비장과 흉선)이었다. 각 조직별로는 면역계 세포, 혈관내피세포, 실질 조직세포들의 순으로 상해정도가 커서 이들 세포들의 순으로 ricin에 대한 민감도가 크다는 것이 시사되었다. 또한, 각 세포들의 종류에 따라 ricin에 의한 조직학적 변화가 달라, 면역계 세포는 apoptosis를, 나머지 세포들은 necrosis를 일으키고 있음이 밝혀졌다.
The pathological aspects of toxicity of purified ricin from the seeds of the castor oil plant, Ricinus communis, were examined, using light and transmission electron microscopy. Mice were exposed to ricin by peritoneal injection with 100ng/1ml PBS(pH7.0)/mouse at intervals up to 48h after exposure. ...
The pathological aspects of toxicity of purified ricin from the seeds of the castor oil plant, Ricinus communis, were examined, using light and transmission electron microscopy. Mice were exposed to ricin by peritoneal injection with 100ng/1ml PBS(pH7.0)/mouse at intervals up to 48h after exposure. In the liver, the first sign of change in ultrastructure was seen at 6h after exposure in hepatocytes: the nuclear membrane became crenated, rER with narrowed lumen surrounded mitochondria, and sER decreased in number. Further change of these aspects continued by 48h after exposure. From 24h after exposure onwards, sinusoidal Kupffer cells with condensed nucleoplasm and capillary endothelial cells with impaired cytoplasm took the form of apoptotic and necrotic changes, respectively. In the spleen, both lymphocytes and macrophages underwent the progressive apoptotic degradation from 6h and 12h after exposure onward in the red and white pulps, respectively. Meanwhile, little change was noted both in the rod cells and the reticular epithelial cells prior to 48h. At 48h after exposure, heterochromatin condensation at the nuclear periphery and degradation of the cell membranes were shown in these cells. In case of the thymus, apoptotic changes were first observed also in lymphocytes and macrophages from 6h after exposure, and further destruction of these cells were progressed with the lapse of time. Both the capillary endothelial cells and thymic epithelial cells had undergone heterochromatin condensation in the nuclear periphery from 24h after exposure. At 48h after exposure, no intact cell was found in the sections observed. There were increase of alveolar macrophages and capillaries in the lung from 6h after exposure and culminating in intra-alveolar edema at 24h after exposure. From 24h after exposure onwards, macrophages with condensed heterochromatin in the whole nuclear, alveolar epithelial cells with condensed heterochromatin in the nuclear periphery, and the necrotic capillary endothelial cells were found. At 48h after exposure, intact cells were hardly seen, and a number of erythrocytes were influxed into the enlarged blood vessels due to degeneration of capillary endotherium. In the heart, from 24h after exposure onwards, macrophages which had undergone apoptosis were found in the enlarged capillaries. Concurrent with these changes, cardiac muscle fibers also were damaged. The crenated nuclear membrane became smooth in outline, myoplasmic organelles such as mitochondria were collapsed, myofibrils were dissociated, and the muscle fibers were isolated from each other owing to damaged cell membrane. Such aspects were more significant at 48h after exposure. Collectively, immune organs such as the spleen and the thymus appeared most sensitive to the toxicity following exposure to ricin. In each organ, the damaged induced by ricin was significant in the order of immunocytes(macrophages and lymphocytes), endothelial cells and parenchymal cells(hepatocytes, reticular epithelial cells, alveolar epithelial cells and cardiac muscle fibers), suggesting that the sensitivity to ricin is high in the above order. Moreover, histological changes due to ricin toxicity appeared to be apoptotic in the immunocytes, but necrotic both in the endothelial and parenchymal cells.
The pathological aspects of toxicity of purified ricin from the seeds of the castor oil plant, Ricinus communis, were examined, using light and transmission electron microscopy. Mice were exposed to ricin by peritoneal injection with 100ng/1ml PBS(pH7.0)/mouse at intervals up to 48h after exposure. In the liver, the first sign of change in ultrastructure was seen at 6h after exposure in hepatocytes: the nuclear membrane became crenated, rER with narrowed lumen surrounded mitochondria, and sER decreased in number. Further change of these aspects continued by 48h after exposure. From 24h after exposure onwards, sinusoidal Kupffer cells with condensed nucleoplasm and capillary endothelial cells with impaired cytoplasm took the form of apoptotic and necrotic changes, respectively. In the spleen, both lymphocytes and macrophages underwent the progressive apoptotic degradation from 6h and 12h after exposure onward in the red and white pulps, respectively. Meanwhile, little change was noted both in the rod cells and the reticular epithelial cells prior to 48h. At 48h after exposure, heterochromatin condensation at the nuclear periphery and degradation of the cell membranes were shown in these cells. In case of the thymus, apoptotic changes were first observed also in lymphocytes and macrophages from 6h after exposure, and further destruction of these cells were progressed with the lapse of time. Both the capillary endothelial cells and thymic epithelial cells had undergone heterochromatin condensation in the nuclear periphery from 24h after exposure. At 48h after exposure, no intact cell was found in the sections observed. There were increase of alveolar macrophages and capillaries in the lung from 6h after exposure and culminating in intra-alveolar edema at 24h after exposure. From 24h after exposure onwards, macrophages with condensed heterochromatin in the whole nuclear, alveolar epithelial cells with condensed heterochromatin in the nuclear periphery, and the necrotic capillary endothelial cells were found. At 48h after exposure, intact cells were hardly seen, and a number of erythrocytes were influxed into the enlarged blood vessels due to degeneration of capillary endotherium. In the heart, from 24h after exposure onwards, macrophages which had undergone apoptosis were found in the enlarged capillaries. Concurrent with these changes, cardiac muscle fibers also were damaged. The crenated nuclear membrane became smooth in outline, myoplasmic organelles such as mitochondria were collapsed, myofibrils were dissociated, and the muscle fibers were isolated from each other owing to damaged cell membrane. Such aspects were more significant at 48h after exposure. Collectively, immune organs such as the spleen and the thymus appeared most sensitive to the toxicity following exposure to ricin. In each organ, the damaged induced by ricin was significant in the order of immunocytes(macrophages and lymphocytes), endothelial cells and parenchymal cells(hepatocytes, reticular epithelial cells, alveolar epithelial cells and cardiac muscle fibers), suggesting that the sensitivity to ricin is high in the above order. Moreover, histological changes due to ricin toxicity appeared to be apoptotic in the immunocytes, but necrotic both in the endothelial and parenchymal cells.
AI-Helper
※ AI-Helper는 부적절한 답변을 할 수 있습니다.