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Biomedical subjects

J H Lipton

Publications and source records attributed to J H Lipton.

61 records · Page 4Linked to original sources
PubMed1978

Release of cryptic monoamine oxidase activity by growth of BHK-21 cells in D-chloramphenicol.

The activity of monoamine oxidase, a marker enzyme of the outer mitochondrial membrane, is stimulated in BHK cells grown in the presence of 100 microgram ml-1 D-chloramphenicol. The observed stimulation can be reversed by removal of the antibiotic. Addition of the non-ionic detergent Triton X-100, to cell homogenates results in an elevation of the enzyme activity similar to that produced by D-chloramphenicol treatment. The activation by chloramphenicol is apparently related to a release of cryptic monoamine oxidase activity.

Cells, Cultured↗
PubMed1977

Mitochondrial biogenesis in cultured animal cells. I. Effect of chloramphenicol on morphology and mitochondrial respiratory enzymes.

The effects of chloramphenicol on the morphology and respiratory enzymes of BHK-21 cells in spinner culture have been examined with time. Cells treated with chloramphenicol double twice before growth ceases; these cells have increased size as measured by several techniques. Mitochondria are enlarged and appear to degenerate with prolonged treatment. Cytochrome c oxidase and succinate cytochrome c reductase activities are reduced while there is no decrease in the activities of monoamine oxidase, glutamate dehydrogenase or NADPH-cytochrome c reductase. Cytochromes aa3 and b disappear on treatment while cytochromes c + c1 appears to be unaffected. All these effects are reversible if chloramphenicol is removed within a limited period of time.

Cell Division↗
PubMed1977

Mitochondrial biogenesis in cultured mammalian cells. II. Mitochondrial protein and phospholipid synthesis in chloramphenicol-treated BHK-21 cells.

The effect of growth of BHK-21 cells in chloramphenicol on the synthesis of cellular proteins and phospholipids has been examined. The incorporation of leucine into total cellular proteins, or into the proteins of specific subcellular fractions are not significantly reduced by cell culture in the presence of chloramphenicol. In cells treated with cycloheximide, a small amount of chloramphenicol-sensitive labelling of protein was detected within the first hour of exposure to the drug. Chloramphenicol inhibits the incorporation of delta-amino-levulinic acid into hemoproteins, only if it is present during both the 48-h culturing and 4-h labelling period. De novo synthesis of cellular lipids as measured by pulse labelling with 32Pi or [3H]glycerol, is decreased in chloramphenicol-treated cells. This decrease is observed in all sub-cellular fractions, although the mitochondrial fraction is most affected. All phospholipids are affected, with diphosphatidylglycerol labelling reduced to the greatest extent. Although fatty acid synthesis is inhibited, the labelling of diphosphatidylglycerol with fatty acids is stimulated on chloramphenicol treatment.

Acetates↗
PubMed1977

Mitochondrial biogenesis in cultured mammalian cells. III. Synthesis of mitochondrial phospholipids by subcellular fractions isolated from normal and chloramphenicol-treated BHK-21 cells.

The capacity of subcellular fractions isolated from chloramphenicol-treated BHK-21 cells to synthesize various mitochondrial phospholipids in vitro and examined. Both mitochondria and microsomes showed the capacity to acylate sn-glycerol 3-phosphate and dihydroxyacetone phosphate to lysophosphatidic acid and acyldihydroxyacetone phosphate and subsequently to phosphatidic acid. Both processes are inhibited in mitochondria from chloramphenicol-treated cells. The synthesis of CDPdiacylglycerol in mitochondria or microsomes, and the synthesis of phosphatidylinositol and of phosphatidylcholine in microsomes were stimulated in treated cells. A slight stimulation was also observed in the synthesis of phosphatidylglycerol and diphosphatidylglycerol when the labelled precursor was sn-glycerol 3-phosphate in treated cells, although the process was inhibited with labelled glycerol as the precursor. Conversion of phosphatidylglycerol phosphate to phosphatidylglycerol by mitochondria was rate limiting unless the post-microsomal supernatant fraction was added. These results are discussed in regard to the observed inhibition of phospholipid synthesis in BHK-21 cells in culture by chloramphenicol.

Cell Line↗