The major sterols of the seeds ofBenincasa cerifera, Cucumis sativus, Cucurbita maxima, C. pepo andTrichosanthes japonica and of the mature plant tissues (leaves and stems) ofCitrullus battich, Cucumis sativus andGynostemma pentaphyllum of the family Cucurbitaceae were 24-ethyl-Δ(7)-sterols which were accompanied by small amounts of saturated and Δ(5)-and Δ(8)-sterols. The 24-ethyl-Δ(7,22),Δ(7,25(27)) and Δ(7,22,25(27))-sterols constituted the predominant sterols for the seed materials, whereas the 24-ethyl-Δ(7) and Δ(7,22)-sterols were the major ones for the mature plant tissues. The configurations of C-24 of the alkylsterols were examined by high resolution(1)H NMR and(13)C NMR spectroscopy. Most of the 24-methyl- and 24-ethylsterols examined which lack a Δ(25(27))-bond (i.e., 24-methyl-, 24-methyl-Δ(22)-, 24-ethyl- and 24-ethyl-Δ(22) sterols) were shown to occur as the C-24 epimeric mixtures in which the 24α-epimers predominated in most cases. The 24-ethylsterols which possess a Δ(25(27)) (i.e., 24-ethyl-Δ(25(27))-and 24-ethyl-Δ(7,22,25(27))-sterols) were, on the other hand, composed of only 24β-epimers. The Δ(8)-sterols identified and characterized were four 24-ethyl-sterols: 24α-and 24β-ethyl-5α-cholesta-8,22-dien-3β-ol, 24β-ethyl-5α-cholesta-8,25(27)-dien-3β-ol and 24β-ethyl-5α-cholesta-8,22,25(27)-trien-3β-ol. This seems to be the first case of the detection of Δ(8)-sterols lacking a 4-methyl group in higher plants, and among the four Δ(8)-sterols the latter two are considered to be new sterols. The probable biogenetic role of the Δ(8)-sterols and the possible biosynthetic pathways leading to the 24α- and 24β-alkylsterols in Cucurbitaceae are discussed.

Forty weanling male Sprague rats were randomly assigned to two dietary treatments, copper-deficient (9.0 mumol/kg diet) and copper-adequate (102.2 mumol/kg diet). After 7 wk of treatment, reductions in body weight and hematocrit, and an increase in relative heart weight, were observed in the copper-deficient rats. Plasma VLDL, LDL and HDL were isolated by ultracentrifugation and Sepharose column chromatography. In copper-deficient rats, the percent composition of protein was reduced by one-half, and triglyceride was increased by 1.6- and 2.7-fold in LDL and VLDL fractions, respectively. In VLDL, the marked increase in triglyceride was compensated by at least a 75% decrease in percent composition of cholesterol and phospholipids as a result of copper deficiency. No treatment difference in percent composition of HDL components was detected. When the data were expressed as the amount present in the vascular pool corrected for body weight, the plasma pool size of protein, triglyceride, phospholipid and cholesterol of LDL and HDL were increased twofold or more by copper deficiency. In VLDL, a sixfold increase in triglyceride, a 36% reduction in cholesterol, and no change in phospholipid and protein pool size were observed in copper-deficient rats. These data suggest that copper deficiency may enlarge the particle size but not particle number of VLDL, increase both particle size and number of LDL, and elevate particle number but not size of HDL.

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This study examined the influence of dietary copper status on the in vivo hepatic fatty acid synthesis and the incorporation of nascent fatty acids into various hepatic lipid classes. Fifty weanling male Sprague-Dawley rats were assigned to two dietary treatments, copper deficient (5.4 nmol/g of diet) and copper adequate (102 nmol/g of diet). After 7 weeks of treatment, rats were injected with 0.111 MBq of [1-14C] acetate (1.85 GBq/mM)/100 g body wt through the femoral vein. Five rats from each treatment were sacrificed at 3, 6, 9, 12, and 24 min after injection. Radioactivities of nascent fatty acid samples were used to determine relative rates of fatty acid synthesis and their assembly into triacylglycerols and phospholipids. Linear increases were observed up to 12 min after injection for total hepatic fatty acid synthesis and their assembly into triacylglycerols and phospholipids for both treatments. In addition, 46% and 30% of total fatty acid synthesized were assembled into triacylglycerols and phospholipids, respectively, for both groups. Furthermore, hepatic fatty acid synthesis and assembly into triacylglycerols and phospholipids were enhanced more than 2-fold by copper deficiency when the data were expressed as per liver per 100 g body weight.

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