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COPPER DEFICIENCY IN THE RAT EFFECT ON SYNTHESIS OF PHOSPHOLIPIDS
Author(s) -
Gallagher CH,
Reeve Vivienne E
Publication year - 1971
Publication title -
australian journal of experimental biology and medical science
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.999
H-Index - 104
eISSN - 1440-1711
pISSN - 0004-945X
DOI - 10.1038/icb.1971.3
Subject(s) - mitochondrion , microsome , phospholipid , biochemistry , cytochrome c oxidase , oxidase test , carnitine , chemistry , biology , enzyme , membrane
Summary Copper deficiency depresses phospholipid synthesis by liver mitochondria, but not by liver microsomes. The effect of copper deficiency on mitochondrial phospholipid synthesis is eliminated by adding 1 mM ATP. Phospholipid synthesis by liver mitochondria from normal rats is inhibited by 0·1–1 mM CN − and restored to normal by 1mM ATP. Mitochondria do not synthesise phospholipids significantly under anaerobic conditions with or without added electron transfer systems unless ATP is added. There appears to be a direct causal relationship between the two major biochemical disturbances in copper deficiency. One, the loss of cytochrome oxidase activity, leading to the other, depressed synthesis of phospholipids by liver mitochondria, by interfering with the provision of endogenous ATP to maintain an optimal rate of synthesis under the experimental conditions. Copper deficiency does not deplete acyl‐CoA:L‐glycerol‐3‐phosphate acyltransferase (E.C.2.3.1.15.) from either microsomes or mitochondria. The activies of palmitoyl‐CoA hydrolase (E.C.3.1.2.2.) in liver microsomes or liver mitochondria and of palmitoyl‐CoA:carnitine palmitoyl‐transferase in liver mitochondria are not affected by copper deficiency.