Effects of chloroquine and 4,4'-bis(diethylaminoethoxy)α,β-diethyldiphenylethane on the incorporation of [3H]glycerol into the phospholipids of rat liver lysosomes and other subcellular fractions, in vivo
Identifieur interne : 003822 ( Main/Exploration ); précédent : 003821; suivant : 003823Effects of chloroquine and 4,4'-bis(diethylaminoethoxy)α,β-diethyldiphenylethane on the incorporation of [3H]glycerol into the phospholipids of rat liver lysosomes and other subcellular fractions, in vivo
Auteurs : Matsuzawa Yuji [États-Unis] ; Karl Y. Hostetler [États-Unis]Source :
- Biochimica et Biophysica Acta (BBA) - Lipids and Lipid Metabolism [ 0005-2760 ] ; 1980.
English descriptors
- Teeft :
- Acid phosphatase, Amphiphilic, Biol, Cationic, Chem, Chloroquine, Glycerol, Glycerol incorporation, Incorporation, Lipid, Lipidosis, Liver microsomes, Lysosomal, Lysosomal fractions, Lysosome, Marker enzymes, Matsuzawa, Microsomal, Microsomal contamination, Microsomal fraction, Microsome, Mitochondrial, Mitochondrial fraction, Mitochondrion, Phosphatase, Phosphatidate phosphohydrolase, Phosphatidylcholine, Phosphatidylethanolamine, Phosphatidylglycerol, Phosphatidylinositol, Phosphoglycerides, Phospholipid, Phospholipid content, Reductase, Respective lysosomal fractions, Subcellular, Succinate dehydrogenase, Triton.
Abstract
Abstract: Oral treatment of rats with 100 mg/kg chloroquine or 4,4'-bis(diethylaminoethoxy)α,β-diethyldiphenylethane for one week causes phospholipid storage in liver and other tissues. The mechanism of this drug-induced lipidosis is not fully understood although several hypotheses have been advanced.In these studies [1,3-3H]glycerol was injected intravenously into control rats and into chloroquine and 4,4'-bis(diethylaminoethoxy)α,β-diethyldiphenylethane-treated rats. The [3H]glycerol was incorporated into phospholipids by de novo synthesis in liver microsomes and transferred to other intracellular membranes which lack the capacity for de novo synthesis of phospholipids. Liver microsomes, mitochondria and lysosomes were isolated and the incorporation of [3H]glycerol into phosphoglycerides was determined as a function of time. Treatment with chloroquine or 4,4'-bis(diethylaminoethoxy)α,β-diethyldiphenylethane results in greatly enhanced incorporation of [3H]glycerol into lysosomal phospholipids in spite of the fact that the incorporation of [3H]glycerol into microsomal phosphatidylcholine, phosphatidylethanolamine and phosphatidylinositol by de novo synthesis is reduced.Phosphatidylglycerol, a precursor of lysosomal bis(monoacylglycerol)phosphate, is labeled at a greatly increased rate, especially in liver microsomes from chloroquine- or 4,4'-bis(diethylaminoethoxy)α,β-diethyldiphenylethane-treated rats, while the incorporation of [3H]glycerol into phosphatidylinositol in microsomes is reduced. Since both phosphatidylinositol and phosphatidylglycerol are formed from CDP-diacylglycerol, the enhanced incorporation of [3H]-glycerol into phosphatidylglycerol cannot be due only to inhibition of phosphatidate phosphohydrolase by these two cationic amphiphilic agents suggesting the possibility of a specific effect of these drugs on phosphatidylglycerol metabolism in liver. [3H]Glycerol incorporation into bis(monoacylglycero)phosphate is found only in lysosomes in agreement with our earlier observations.The results suggest increased transfer of newly-synthesized microsomal phospholipids to lysosomes and/or decreased lysosomal catabolism of phospholipids in chloroquine- and 4,4'-bis(diethylaminoethoxy)α,β-diethyldiphenylethane-treated rat liver. Incorporation of newly-formed 3H-labeled phosphatidylcholine, phosphatidylethanolamine and phosphatidylinositol into mitochondria is not increased, indicating that a non-specific increase in intracellular phospholipid exchange is not responsible for our observations.
Url:
DOI: 10.1016/0005-2760(80)90151-4
Affiliations:
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Le document en format XML
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<term>Cationic</term>
<term>Chem</term>
<term>Chloroquine</term>
<term>Glycerol</term>
<term>Glycerol incorporation</term>
<term>Incorporation</term>
<term>Lipid</term>
<term>Lipidosis</term>
<term>Liver microsomes</term>
<term>Lysosomal</term>
<term>Lysosomal fractions</term>
<term>Lysosome</term>
<term>Marker enzymes</term>
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<term>Mitochondrial</term>
<term>Mitochondrial fraction</term>
<term>Mitochondrion</term>
<term>Phosphatase</term>
<term>Phosphatidate phosphohydrolase</term>
<term>Phosphatidylcholine</term>
<term>Phosphatidylethanolamine</term>
<term>Phosphatidylglycerol</term>
<term>Phosphatidylinositol</term>
<term>Phosphoglycerides</term>
<term>Phospholipid</term>
<term>Phospholipid content</term>
<term>Reductase</term>
<term>Respective lysosomal fractions</term>
<term>Subcellular</term>
<term>Succinate dehydrogenase</term>
<term>Triton</term>
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<front><div type="abstract" xml:lang="en">Abstract: Oral treatment of rats with 100 mg/kg chloroquine or 4,4'-bis(diethylaminoethoxy)α,β-diethyldiphenylethane for one week causes phospholipid storage in liver and other tissues. The mechanism of this drug-induced lipidosis is not fully understood although several hypotheses have been advanced.In these studies [1,3-3H]glycerol was injected intravenously into control rats and into chloroquine and 4,4'-bis(diethylaminoethoxy)α,β-diethyldiphenylethane-treated rats. The [3H]glycerol was incorporated into phospholipids by de novo synthesis in liver microsomes and transferred to other intracellular membranes which lack the capacity for de novo synthesis of phospholipids. Liver microsomes, mitochondria and lysosomes were isolated and the incorporation of [3H]glycerol into phosphoglycerides was determined as a function of time. Treatment with chloroquine or 4,4'-bis(diethylaminoethoxy)α,β-diethyldiphenylethane results in greatly enhanced incorporation of [3H]glycerol into lysosomal phospholipids in spite of the fact that the incorporation of [3H]glycerol into microsomal phosphatidylcholine, phosphatidylethanolamine and phosphatidylinositol by de novo synthesis is reduced.Phosphatidylglycerol, a precursor of lysosomal bis(monoacylglycerol)phosphate, is labeled at a greatly increased rate, especially in liver microsomes from chloroquine- or 4,4'-bis(diethylaminoethoxy)α,β-diethyldiphenylethane-treated rats, while the incorporation of [3H]glycerol into phosphatidylinositol in microsomes is reduced. Since both phosphatidylinositol and phosphatidylglycerol are formed from CDP-diacylglycerol, the enhanced incorporation of [3H]-glycerol into phosphatidylglycerol cannot be due only to inhibition of phosphatidate phosphohydrolase by these two cationic amphiphilic agents suggesting the possibility of a specific effect of these drugs on phosphatidylglycerol metabolism in liver. [3H]Glycerol incorporation into bis(monoacylglycero)phosphate is found only in lysosomes in agreement with our earlier observations.The results suggest increased transfer of newly-synthesized microsomal phospholipids to lysosomes and/or decreased lysosomal catabolism of phospholipids in chloroquine- and 4,4'-bis(diethylaminoethoxy)α,β-diethyldiphenylethane-treated rat liver. Incorporation of newly-formed 3H-labeled phosphatidylcholine, phosphatidylethanolamine and phosphatidylinositol into mitochondria is not increased, indicating that a non-specific increase in intracellular phospholipid exchange is not responsible for our observations.</div>
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