Vitamin A and lysosomal stability in rats fed an atherogenic diet.
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.
D000818:Animals; D001011:Aorta / Q000201:enzymology / Q000378:metabolism; D001161:Arteriosclerosis / Q000201:enzymology / Q000209:etiology; D002403:Cathepsins / Q000378:metabolism; D002784:Cholesterol / Q000097:blood; D004036:Diet, Atherogenic; D004305:Dose-Response Relationship, Drug; D005966:Glucuronidase / Q000378:metabolism; D008099:Liver / Q000201:enzymology / Q000378:metabolism; D008247:Lysosomes / Q000201:enzymology*; D008297:Male; D010743:Phospholipids / Q000097:blood; D051381:Rats; D014280:Triglycerides / Q000097:blood; D014801:Vitamin A / Q000378:metabolism / Q000494:pharmacology*; D014802:Vitamin A Deficiency / Q000150:complications
D010743:Phospholipids; D014280:Triglycerides; D014801:Vitamin A; D002784:Cholesterol; D005966:Glucuronidase; D002403:Cathepsins