In vitro conversion of erucic acid by microsomes and mitochondria from liver, kidneys and heart of rats

Abstract

Microsomes and mitochondria of liver, kidneys, and heart were incubated with [14-(14)C] erucic acid in three assay media: one favorable for chain elongation (NADPH + KCN), another favorable for beta-oxidation and the last one for shortening (NADP + KCN). Elongating reactions occurred mainly in microsomes, those of kidneys being very active; the mitochondria also showed some activity, heart mitochondria being, however, more active than the microsomes, when considering the amount of erucic acid activated. In the medium for beta-oxidation, practically no shortened fatty acids were found. On the contrary, when beta-oxidation was inhibited, and in the presence of NADP, the formation of shorter monoenes, probably in the outer membrane of the mitochondria, was observed, namely eicosenoic acid in high amount, oleic acid and hexadecenoic acid. Mitochondria from liver were very active as were those of heart, when compared with the quantity of activated erucic acid. In heart, the mitochondria shortened erucic acid into oleic acid and hexadecenoic acid, which were then probably used as energy substrates. With carnitine and without NADP, shortened fatty acids were formed in the mitochondria of liver, probably by the first reactions of beta-oxidation. In this case, the proportions of oleic acid and hexadecenoic acid were higher than with NADP alone. In the presence of carnitine and NADP, the level of the chain-shortening reaction did not differ from that observed with NADP alone. It appears, therefore, that the activated erucic acid is mainly directed towards shortening reactions and not towards transfer reactions across the mitochondrial membranes.

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

“…4). These results confirm previous reports showing that 22:1n-9 is quickly converted into 18:1n-9 in all models studied [15,18,19,24,26,27,[31][32][33][34][35]. Presumably, this conversion is through peroxisome localized b-oxidation [33,36,68].…”

“…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].…”

“…We [15] and others have shown that 22:1n-9 is readily converted into 18:1n-9 through chain shortening pathway in various organs and cell types [18,19,24,[26][27][28][31][32][33][34][35], however none of these studies have addressed conversion of 22:1n-9 to other fatty acids under steady-state-like conditions or its conversion into saturated fatty acids (SFA). Previously we found that [91% of the infused tracer was recovered as plasma 22:1n-9, with 6.5% of the tracer found in plasma found as 18:0 under steady-statelike conditions [15].…”

“…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].…”

Erucic acid metabolism in rat heart. A combined biochemical and radioautographical study

“…On the other hand ingestion of rapeseed oil (CLOUET et ul., 1976) or marine oil (CHRISTIANSEN et al, 1981) increases the amount of mitochondria in heart. Since mitochondria can also shorten erucic acid (CLOUET & BEZARD, 1979;CLOUET et al, 1982) and since oxidative activity in liver mitochondria is much more elevated than in peroxisomes even when peroxisomal proliferation is induced (MANNAERTS et al, 1979), the question raises whether mitochondria could also participate to shortening of erucic acid when heart adapts itself to rapeseed oil ingestion.…”