Sudhakaran P R, Kurup P A
Atherosclerosis. 1976 Jul-Aug;24(1-2):281-91. doi: 10.1016/0021-9150(76)90083-6.
The relation between vitamin A status and lysosomal stability was studied in rats fed a high fat-cholesterol diet. Increase in the total activity of lysosomal enzymes as well as that in the nuclear fraction, intact lysosomal fraction and free activity (activity present in the 15,000 X g supernatant) in the liver was observed in rats fed an atherogenic diet with adequate vit. A. Vitamin A deficiency and hypervitaminosis (10,000 IU) augmented this increase in the total enzyme activity as well as the activity in the subcellular fractions except in the case of intact lysosomes where the activity was not significantly altered. At 2,000 IU, there was no significant alteration in either the total activity or the activity of the subcellular fractions. An analysis of the ratio of soluble activity (released from the lysosomes) to the activity present in the intact lysosomes, showed that hepatic lysosomal stability was decreased in the rats fed an atherogenic diet with normal dose of vit. A. Vitamin A deficiency as well as hypervitaminosis decreased the lysosomal stability still further. At a dose of 2,000 IU, lysosomal stability increased as compared to the rats fed an adequate dose of vit. A, while total lysosomal activity remained not significantly altered. Studies on the rate of release of enzymes from the lysosomes revealed that there was significantly more release of the enzyme between 30 and 45 min in the liver and aorta in the rats fed a high fat-cholesterol diet with adequate vit. A This release was still more in the rats fed a low dose of vit. A. At 2,000 IU, there was no significant difference in the enzyme release. But the pattern of change in the liver and aorta in the hypervitaminotic group was different. In the case of hepatic lysosomes, there was an increase in the enzymes released while in the aorta there was significant decrease. This has been attributed to the fact that lytic concentration of the vitamin A is not attained in the aorta.
在喂食高脂肪高胆固醇饮食的大鼠中研究了维生素A状态与溶酶体稳定性之间的关系。在喂食含充足维生素A的致动脉粥样化饮食的大鼠中,观察到肝脏中溶酶体酶的总活性以及核部分、完整溶酶体部分和游离活性(存在于15,000×g上清液中的活性)均增加。维生素A缺乏和维生素过多症(10,000国际单位)增强了总酶活性以及亚细胞部分中的活性增加,但完整溶酶体的情况除外,其活性没有显著改变。在2,000国际单位时,总活性或亚细胞部分的活性均无显著变化。对可溶性活性(从溶酶体释放)与完整溶酶体中存在的活性之比的分析表明,喂食含正常剂量维生素A的致动脉粥样化饮食的大鼠肝脏溶酶体稳定性降低。维生素A缺乏以及维生素过多症进一步降低了溶酶体稳定性。在2,000国际单位的剂量下,与喂食充足剂量维生素A的大鼠相比,溶酶体稳定性增加,而溶酶体总活性仍无显著变化。对溶酶体酶释放速率的研究表明,在喂食含充足维生素A的高脂肪高胆固醇饮食的大鼠肝脏和主动脉中,在30至45分钟之间酶的释放明显更多。在喂食低剂量维生素A的大鼠中,这种释放更多。在2,000国际单位时,酶释放没有显著差异。但维生素过多症组肝脏和主动脉中的变化模式不同。对于肝脏溶酶体,释放的酶增加,而在主动脉中则显著减少。这归因于主动脉中未达到维生素A的裂解浓度这一事实。