Influence of lipids on gap-junction-mediated intercellular communication between Chinese hamster cells in vitro.

The influence of lipids on gap-junction-mediated intercellular communication (i.e., metabolic cooperation) between Chinese hamster V79 cells was investigated. Unsaturated free fatty acids (oleate, linoleate, linolenate, palmitoleate, myristoleate, and arachidonate) inhibited metabolic cooperation between 6-thioguanine-resistant, hypoxanthine guanine phosphoribosyltransferase-deficient and 6-thioguanine-sensitive, hypoxanthine guanine phosphoribosyltransferase-proficient V79 cells. Saturated fatty acids (stearate, palmitate, myristate, and arachidate) had no effect. Further characterization of the effects of fatty acids on metabolic cooperation is summarized as follows: a relationship between the degree of unsaturation and the ability of unsaturated fatty acids to inhibit metabolic cooperation could not be established (i.e., inhibition of metabolic cooperation by 18:1 greater than 18:2 = 18:3); longer carbon chain monounsaturated fatty acids are more effective in inhibiting metabolic cooperation (i.e., inhibition of metabolic cooperation by 18:1 greater than 16:1 greater than or equal to 14:1); geometric isomerism is of some importance in determining the efficacy of monounsaturated fatty acids to inhibit metabolic cooperation (i.e., inhibition of metabolic cooperation by cis 18:1 greater than trans 18:1 and cis 16:1 greater than trans 16:1); and the position of the double bond(s) is relatively unimportant (i.e., inhibition of metabolic cooperation by 18:3 = gamma 18:3). Unsaturated diacylglycerol compounds (diolein, dilinolein, and 1-oleoyl-2-acetyl glycerol) inhibit metabolic cooperation; a saturated diacylglycerol compound (distearin) had no effect. The position of the unsaturated fatty acid groups is not of importance in the inhibition of metabolic cooperation by diacylglycerols containing unsaturated fatty acid moieties (i.e., 1,2-diolein and 1,3-diolein are equally efficacious in inhibiting metabolic cooperation; relative inhibition of metabolic cooperation by 18:1 greater than 1-oleoyl-2-acetyl glycerol greater than 1,2-diolein). Alterations of membrane biophysical properties and protein kinase C involvement are discussed as possible mechanisms involved in the inhibition of metabolic cooperation by unsaturated lipid.