A method is described for the separation of neutral lipid, free fatty acid and polar lipid classes using small (600 mg), prepacked silica Sep-Pak columns. Combinations of hexane and methyltertiarybutylether were used to progressively elute cholesteryl ester first then triglyceride from the column. After column acidification, fatty acids were eluted followed by cholesterol. Recoveries of these lipids were 96% or greater. Polar lipids were eluted from the column using combinations of methyltertiarybutylether, methanol and ammonium acetate. Phospholipid classes could not be separated completely from each other. Phosphatidylethanolamine and phosphatidylinositol eluted together, whereas the more polar phosphatidylcholine, sphingomyelin and lysophosphatidylcholine were eluted as a second fraction. Recoveries of each phospholipid was greater than 98%.

Time-resolved and steady-state luminescence and transient resonance Raman measurements have been carried out on the complex [Ru(phen) 2 dppz] 2+ (1) in the presence of single-stranded (ss) DNA that is either covalently attached to or mixed in 1:1 ratio with the complex. The well-known enhancement of luminescence (the "lightswitch" effect) exhibited by (1) when intercalated to double-stranded DNA is also observed in the presence of the single-stranded material, under conditions of covalent attachment or simple mixing. The evidence from both the luminescence and the transient Raman studies suggests that the enhancement need not necessarily reflect deep intercalation of the dppz ligand between the bases of the ss material.

The purpose of these investigations was to ascertain the effect of (−)‐hydroxycitrate on the accumulation of lipid in the meal fed rat by examining the rates of lipogenesis after acute and chronic treatment. Oral administration of (−)‐hydroxycitrate depressed significantly the in vivo lipogenic rates in a dose‐dependent manner in the liver, adipose tissue, and small intestine. The hepatic inhibition was significant for the 8 hr period, when control animals demonstrated elevated rates of lipid synthesis. The kinetics of this reduction of in vivo hepatic lipogenesis were identical after acute or chronic administration of (−)‐hydroxycitrate. However, in vitro rates of lipogenesis were elevated after chronic administration of (−)‐hydroxycitrate for 30 days. Rats receiving (−)‐hydroxycitrate consumed less food than the untreated controls; however, this decreased caloric intake was not responsible for the drug induced depression of hepatic lipogenesis, as shown by studies using pair fed rats.

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