ELIMINATION OF EXCESS SMOOTH ENDOPLASMIC-RETICULUM AFTER PHENOBARBITAL ADMINISTRATION
ELIMINATION OF EXCESS SMOOTH ENDOPLASMIC-RETICULUM AFTER PHENOBARBITAL ADMINISTRATION
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DOI：
10.1177/28.9.7410819
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发表时间：
1980-01-01
影响因子：
3.2
通讯作者：
BECKER, J
中科院分区：
文献类型：
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作者：
FELDMAN, D;SWARM, RL;BECKER, J
对查尔斯河大鼠在苯巴比妥治疗过程中和治疗后的肝脏进行了研究，以探讨参与消除过度的平滑内质网的可能机制。在复合给药过程中，最明显的结构变化是平滑内质网的增殖；糖原的耗竭和脂质沉积的增加也被观察到。终止治疗后，这些变化被逆转。大量自噬空泡和溶酶体的出现以及酸性磷酸酶反应产物在这些小体中的定位表明，自噬可能是消除过度的平滑内质网的机制。血窦内可见胞质小泡和充满光滑内质网的碎片。这些片段周围的Kupffer细胞质延伸和Kupffer细胞包涵体内酸性磷酸酶反应产物的存在表明，异噬作用是参与去除多余的平滑内质网的另一种过程。
Livers from Charles River rats during and after treatment with phenobarbital were studied in order to investigate possible mechanisms involved in the elimination of excess smooth endoplasmic reticulum. The most pronounced structural change during compound administration was proliferation of smooth endoplasmic reticulum; depletion of glycogen and an increase in lipid deposits were also observed. After termination of treatment, these changes were reversed. The appearance of an increased number of autophage vacuoles and lysosomes plus the localization of acid phosphatase reaction product in these bodies suggests autophagy as 1 possible mechanism for the elimination of excess smooth endoplasmic reticulum. Cytoplasmic blebs and fragments replete with smooth endoplasmic reticulum were observed within the sinusoids. The presence of Kupffer cell cytoplasmic extensions surrounding these fragments and acid phosphatase reaction product within Kupffer cell inclusions suggests heterophagy as another process participating in the removal of excess smooth endoplasmic reticulum.