The modification of mammalian membrane polyunsaturated fatty acid composition in relation to membrane fluidity and function

Polyunsaturated Fatty Acid Families and Interrelationships Omega-6 Fatty Acids and Plasma Lipids Plasma Cholesterol Plasma Triglycerlde Plasma LJpoprotelns and Apolipoproteins Hypolipldemic Mechanisms of Linoleic Acid Decrease in Cholesterol Absorption Increase in Fecal Steroid Excretion Reduced Cholesterol Synthesis and the Transfer of Cholesterol to the Tissues Decrease in Cholesterol Content of LJpoproteins Changes in the Rates of Synthesis and Catabolism of LJpoproteins Membrane Fatty Acid Composition and Upoprotein Metabolism

Polyunsaturated fatty acids, hyperlipidemia, and thrombosis.

Cancer a Comprehensive Treatise 2

Crassostrea gigas spat were fed diets of Pavlova lutheri, Dunaliella tertiolecta or Tetraselmis suecica . The D. tertiolecta diet contained no fatty acid longer or more unsaturated than linolenic acid (18:3ω3) and the T. suecica diet was deficient in decosahexaenoic acid (22:6ω3). The algal diets were supplemented with micro-encapsulated triolein, oyster lipid extract or 22:6ω3. Spat were also starved or fed carbohydrate diets.

https://www.cambridge.org/core/services/aop-cambridge-core/content/view/S0025315400047056

The effect of algal and artificial diets on the growth and fatty acid composition of Crassostrea gigas Spat

The composition, metabolism, and significance of fatty acids in insect biology are addressed. Fatty acids enter a number of metabolic pathways not directly related to energy storage and production; the unifying theme is that the fatty acids are not only structurally altered in these pathways, but that the alterations carry them from one area of biological significance into another. This theme is developed by offering a perspective on fatty acids in insects and then reviewing three major areas: 1) fatty acid composition, 2) biosynthesis of fatty acids (including polyunsaturated fatty acids and characteristics of certain biosynthetic enzymes), and 3) the biological significance of fatty acids. This last section includes discussions of the biochemistry of waxes, pheromones, and prostaglandins and the roles of fatty acids as components of defensive secretions. Little is known at the biochemical level about the regulation of fatty acid metabolism, and it is suggested that work in this area represents another frontier in insect biochemistry.

Fatty acids in insects: Composition, metabolism, and biological significance

Publisher Summary This chapter explains structural requirements, metabolism of action, and the role of the essential fatty acids. These acids are metabolized in ways common to other unsaturated fatty acids. In addition, the unsaturated acids possessing the 9, 12 double bond system (C18 acids) or the 11–14 double bond system (C20 acids) possesses special properties that are essential to the animal. Presumably, they function in esterified forms rather than as free fatty acids, and their essential roles may be determined by relative concentrations of phospholipids, glycerides, and sterol esters, which in turn seem to involve hormonal regulation. There is evidence to suggest that they are concerned, via phospholipids, in membrane integrity. This may be related to certain biochemical lesions that have been reported in connection with a deficiency of essential fatty acids in cases where membranes possess recognized biochemical activity, for example, in mitochondria. The essential fatty acids are the precursors of the prostaglandins, but the relationships of the latter to the classical deficiency symptoms is not certain and there is no evidence suggesting a relationship of this hormone family to the reported biochemical lesions of the deficiency.

The essential fatty acids.

Vitamin E deficiency in the rat. IV. Alteration in mitochondrial membrane and its relation to respiratory decline

Liver cytoplasm from either vitamin E-deficient or normal rats has been shown to suppress mitochondrial respiratory decline induced by microsomes in vitro. The present study is an attempt to identify cytoplasmic factor(s) responsible for this suppression. The effect of cytoplasm from both groups of animals could be removed by trichloroacetate precipitation, boiling, and dialysis against 0.3 M mannitol-o.1 mM Tris buffer, pH 7.4, but not by aging or extraction with isooctane. The addition of oxalacetate of alpha-ketoglutarate plus asparate to cytolplasm potentiated the suppressant effect. Dialyzed cytoplasm was not effective in depressing the respiratory decline. However, the addition of NAD, osalacetate, or alpha-ketoglutarate plus aspartate to dialyzed cytoplasm restored its ability to depress the respiratory decline. When oxalacetate or alpha-ketoglutarate plus aspartate was added to fresh cytoplasm, followed by dialysis, the effect of these compounds was not seen. These results suggest that cytoplasmic factor(s) required for suppression of the respiratory decline were enzymes of the malate shuttle and transamination, which are heat labile and trichloroacetate precipitable, plus the dialyzable metabolites that are associated with these enzymes in the generation of NAD in mitochondria.

Vitamin E deficiency in the rat. Cytoplasmic factors required for suppression of mitochondrial respiratory decline.

Liver mitochondria from alphatocopherol deficient rats swell more rapidly, both spontaneously and in the presence of GSH, than those from control animals. The increased swelling of deficient mitochondria induced by GSH was completely eliminated when mitochondria were left longer than two hours at 0 degrees in the suspending medium. GSH-induced swelling of liver mitochondria from alpha-tocopherol deficient rats is reversed by ATP, polyvinyl pyrrolidone (PVP) and by oral administration alpha-tocopherol (2 mg/day per rat). Swelling of mitochondria in the above system was completely inhibited by the respiratory chain inhibitor, cyanide (.001 M), and partially by azide (0.001 M). We suggest that the swelling tendency of liver mitochondria from alpha-tocopherol deficient rats might be associated with an altered respiratory mechanism and/or an alteration in membrane permeability.

Ralph M. Johnson

Papers

The essential fatty acids.

Vitamin E deficiency in the rat. IV. Alteration in mitochondrial membrane and its relation to respiratory decline

Vitamin E deficiency in the rat. Cytoplasmic factors required for suppression of mitochondrial respiratory decline.

Effects of vitamin E deficiency on GSH-induced swelling of rat liver mitochondria.