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Stereospecific degradation and combined gas chromatographic--mass spectrometric (gc/ms) analysis were employed in a detailed investigation of the triacylglycerol structure of mustard seed oil and of the triacylglycerols transiently accumulating in the hearts of young rats receiving the oil in their diet. It was shown that feeding of mustard seed oil at 40% of the daily caloric requirement resulted in a deposition of cardiac triacylglycerols containing a high proportion of enantiomers of a positional distribution and molecular association of fatty acids which were closely similar to those found in the dietary oil. Complete structures were derived for a total of 88 species representing 75 to 85% of the triacylglycerols. About 90% of the accumulated triacylglycerol contained at least one long-chain (C20--C22) monounsaturated fatty acid per molecule. The long-chain acids were confined mainly to the primary positions and preferentially to the sn-3-position of the glycerol molecule. The dietary lipidosis, is, therefore, accompanied by little or no accumulation of the normal rat tissue triacylglycerols containing C16 and C18 fatty acids. It is suggested that the deposition and eventual clearance of the enantiomeric long-chain triacylglycerols in the rat heart during mustard seed oil feeding may be largely a result of a gradual change in specificity of the cardiac lipases.

Rats of weaning age were feed for a period of 1 or 3 weeks either a low fat diet (laboratory stock diet) or a semi-synthetic diet containing 20% by weight of either corn oil (2/3 of the total fatty acids consisted of linoleic acid) or mustard seed oil (1/3 of the total fatty acids were comprised of erucic acid). Feeding of a diet rich in erucic acid for 1 week increased by twofold the cholesterol ester content of the aorta. However, the concentrations of unesterified cholesterol and individual phospholipids in the aorta were uninfluenced by hyperlipemia induced by this diet. Fatty acid analyses indicated that erucic (22:1) and eicosenoic (20:1) acids are found in the triglyceride and cholesterol esters of the aorta in the proportion similar to that found in the plasma triglyceride and cholesterol esters. Our results demonstrated further that a significantly greater quantity of 14C-labelled erucate than labelled palmitate, oleate or linoleate was incorporated into the cholesterol ester fraction of the control aorta. The incorporation rates of erucate and linoleate into phosphatidic acid were more rapid, while the rates of erucate into phosphatidylcholine, phosphatidylethanolamine, phosphatidylserine, phosphatidylinositol and lysophosphatidylcholine were significantly slower than those of other fatty acids.

When male weaning rats were fed a high fat-high erucic acid and diet (mustard seed oil) for 1 week, there were increases in the triglyceride and erucic acid contents in the myocardium, and an increase in the rate of incorporation of [1-14C]palmitic acid into triglyceride in the perfused heart, in comparison to rats that had consumed a high fat-high linoleic acid diet (corn oil) or a low fat diet (laboratory chow). However, continuation of the mustard seed oil diet (3-6 weeks) tended to normalize these biochemical parameters. The size of the papillary muscle isolated from the mustard seed oil-fed rats was greater than that of the muscle of the chow-fed rats, and its developed isometric tension was lower. Electron microscopic examination revealed that, in the hearts of rats having eaten the mustard seed oil diet, there were isolated foci where the number and size of mitochondria appeared to be increased.