Erucic acid metabolism in rat liver a combined biochemical and radioautographical study

Abstract

Metabolism of erucic acid was studied in rat liver in comparison with oleic acid in relation with diet lipids. Rats were fed for 3 or 60 days a balanced diet containing 30% of the calories of either rapeseed oil rich in erucic acid or sunflower seed oil rich in linoleic acid. They were intravenously injected with tritiated erucic or oleic acid. After 1 or 15 min, the radioactivity recovered in liver lipids was 9 to 26% whatever the diet or the acid injected. One minute after injection of erucic acid a high part of radioactivity was recovered in the free fatty acid fraction and as untransformed erucic acid. After 15 min the major part of radioactivity was recovered in the triacylglycerol fraction which contained a high proportion of labelled oleic acid formed by shortening of erucic acid. The autoradiography did not show any marked difference between the labelling of peroxisomes and mitochondria when tritiated erucic or oleic acid was injected. These data do not bring about arguments for a peroxisomal nor for a mitochondrial location of erucic acid shortening in liver.

Erucic Acid is Differentially Taken up and Metabolized in Rat Liver and Heart

“…infusion of [28]. Similar results are observed following pulse infusion of tritiated 22:1n-9 [26,27]. We did not see such a large difference between heart and liver uptake, this is more than likely because the concentration of labeled 22:1n-9 used in pulse infusion experiments was about 10-fold higher than that used in our experimental paradigm, certainly high enough to alter the normal plasma concentration of 22:1n-9.…”

“…Similar results are reported in isolated organs [22][23][24][25], and in intact animals [26][27][28]. Although 22:1n-9 is poorly oxidized to CO 2 [29,30], it is quickly converted into oleic acid (18:1n-9) in vivo and in isolated tissues and cultured cells [15,18,19,24,[26][27][28][31][32][33][34][35]. This conversion is presumably through peroxisome localized b-oxidation [19,33,36], although a possible mitochondrial pathway for 22:1n-9 oxidation can not be excluded [26,27].…”

“…In cultured cells, 22:1n-9 is rapidly esterified into TAG and to a lesser extent into PL pools [18][19][20][21]. Similar results are reported in isolated organs [22][23][24][25], and in intact animals [26][27][28]. Although 22:1n-9 is poorly oxidized to CO 2 [29,30], it is quickly converted into oleic acid (18:1n-9) in vivo and in isolated tissues and cultured cells [15,18,19,24,[26][27][28][31][32][33][34][35].…”

“…In contrast, constant exposure of the brain to 22:1n-9 alters the pools in which it is found esterified, with minimal impact on 22:1n-9 chain shortening to 18:1n-9 [15]. Pulse infusion studies using labeled 22:1n-9 in vivo also demonstrate an increase in chain shortening even in animals fed with regular diets [26][27][28]. In these studies, the initial concentration of 22:1n-9 is much higher than its normal physiological levels found in plasma.…”

“…Although 22:1n-9 is poorly oxidized to CO 2 [29,30], it is quickly converted into oleic acid (18:1n-9) in vivo and in isolated tissues and cultured cells [15,18,19,24,[26][27][28][31][32][33][34][35]. This conversion is presumably through peroxisome localized b-oxidation [19,33,36], although a possible mitochondrial pathway for 22:1n-9 oxidation can not be excluded [26,27]. Whole liver and liver cells are capable of converting 22:1n-9 into 18:1n-9 more efficiently than other organs and cell types [18,[28][29][30][31][32], leading to the conclusion that liver plays a central role in 22:1n-9 utilization with other organs utilizing 18:1n-9 exported from liver after 22:1n-9 chain shortening [33].…”