Action of vitamin P like compounds on lysosomal fragility in hypercholesterolemia: implication of ascorbic acid and its metabolites.
Possible mechanisms responsible for hepatic lysosomal fragility in hypercholesterolemic rats have been investigated. It was found that certain factor(s) present in the intracellular environment of liver were required for the release of lysosomal enzymes. Elevated hepatic dehydroascorbic acid content in hypercholesterolemic rats is thought to render the lysosomes fragile in this pathological state, since this compound was found to labilise the lysosomes in vitro. Quercetin and hesperidin were found to be responsible for lysosomal stability, probably by reducing the content of dehydroascorbic acid to a normal level in the hypercholesterolemic condition.
D000818:Animals; D001205:Ascorbic Acid / Q000378:metabolism*; D003683:Dehydroascorbic Acid / Q000378:metabolism; D005419:Flavonoids / Q000494:pharmacology*; D006569:Hesperidin / Q000494:pharmacology; D006937:Hypercholesterolemia / Q000378:metabolism*; D008099:Liver / Q000378:metabolism; D008247:Lysosomes / Q000187:drug effects*; D008297:Male; D011794:Quercetin / Q000494:pharmacology; D051381:Rats
D005419:Flavonoids; D011794:Quercetin; D006569:Hesperidin; D001205:Ascorbic Acid; D003683:Dehydroascorbic Acid