In vivo incorporation of3H arachidonic acid and14C linoleic acid into liver lipids from essential fatty acid-deficient rats

Lipids ◽  
1973 ◽  
Vol 8 (3) ◽  
pp. 156-158 ◽  
Author(s):  
Osvaldo Mercuri ◽  
Maria Elena De Tomás







1965 ◽  
Vol 97 (2) ◽  
pp. 485-499 ◽  
Author(s):  
R Ostwald ◽  
P Bouchard ◽  
P Miljanich ◽  
RL Lyman

1. Groups of intact male and female rats and castrated rats injected with oestradiol or testosterone were given a diet containing hydrogenated coconut oil for 9 weeks, and at intervals the amounts and fatty acid compositions of the carcass and liver lipids were determined. 2. Male rats grew faster and larger, and exhibited typical external essential fatty acid deficiency symptoms sooner than did females. Testosterone-treated castrated male rats were similar to males, and oestradiol-injected castrated male rats resembled females. 3. Intact females maintained a higher linoleic acid concentration in their carcass than did males. Total amounts of carcass linoleic acid remained similar for all groups, only 200mg. being removed in 9 weeks regardless of body size. 4. The amounts of total cholesteryl esters were independent of liver size. They were higher in males and testosterone-treated castrated male rats than in females and oestrogen-treated castrated male rats. 5. Phospholipids represented about 80% of the liver lipids. The total amounts of the phospholipid linoleic acid and arachidonic acid were similar for all groups regardless of liver size, and were not affected appreciably by the deficiency. Females and oestrogen-treated castrated male rats maintained a higher proportion of phospholipid arachidonic acid for longer periods than did their male counterparts. Both the total amounts and the proportions of eicosatrienoic acid and palmitic acid were higher in males than in females. 6. Supplementation of the essential fatty acid-deficient diet with linoleic acid caused a rapid loss of eicosatrienoic acid and palmitic acid with a concomitant increase in stearic acid and arachidonic acid. 7. There were no obvious differences in the way that the essential fatty acids were metabolized or mobilized from adipose tissue of male or female rats during essential fatty acid deficiency. 8. The results indicated that the greater growth rate of the male rats caused them to require and synthesize more phospholipids than did the females. In the absence of adequate amounts of arachidonic acid, eicosatrienoic acid was substituted into the additional phospholipid. The earlier symptoms of essential fatty acid deficiency in the male rat could therefore be ascribed to the higher tissue concentrations of this unnatural phospholipid and its inability to perform the normal metabolic functions of phospholipids.



1989 ◽  
Vol 67 (2) ◽  
pp. 811-816 ◽  
Author(s):  
H. A. Ball ◽  
J. A. Cook ◽  
K. M. Spicer ◽  
W. C. Wise ◽  
P. V. Halushka

Because leukotrienes and prostaglandins are inflammatory mediators derived from arachidonic acid, their potential role in oleic acid-induced lung injury was evaluated in control and in essential fatty acid-deficient (EFAD) rats depleted of arachidonic acid substrate. In control rats, oleic acid (0.06 ml/kg iv) increased the pulmonary permeability index (measured by scintigraphy) from -10 +/- 13 x 10(-6) s-1 to 217 +/- 20 x 10(-6) s-1 and 118 +/- 13 x 10(-6) s-1 at 5 and 50 min (P less than 0.05), respectively. It also caused arterial hypoxemia at 30 min (P less than 0.05). Compared with saline controls, oleic acid increased bronchoalveolar lavage fluid levels of immunoreactive (i) LTC4/D4, iLTB4, (P less than 0.01), and 6-ketoprostaglandin F1 alpha (6-keto-PGF1 alpha) (P less than 0.05). In EFAD rats, oleic acid failed to significantly increase the lung permeability index at 5 and 50 min. In contrast to control rats, oleic acid failed to cause hypoxemia in the EFAD rats. Bronchoalveolar lavage levels of iLTB4 and i6-keto-PGF1 alpha after oleic acid in EFAD rats were lower compared with oleic acid controls, whereas iLTC4/D4 in the oleic acid EFAD group was not decreased. Treatment with intraperitoneal ethyl arachidonate (400 mg over 2 wk) reversed the resistance of EFAD rats such that the pulmonary edema (P less than 0.05) was evident after oleic acid. This latter group also manifested a significant (P less than 0.05) rise in the bronchoalveolar lavage levels of iLTB4 and i6-keto-PGF1 alpha. These results suggest that arachidonic acid metabolites contribute to oleic acid-induced pulmonary permeability.



1988 ◽  
Vol 59 (2) ◽  
pp. 273-278 ◽  
Author(s):  
Stephen C. Cunnane

1. Young male rats were fed on diets containing 3·4, 36 or 411 mg zinc/kg for 10 weeks in order to determine whether effects of Zn deficiency on plasma and liver essential fatty acid composition could be distinguished from those of reduced protein and energy intake.2. Fatty acid analysis revealed that a Zn intake of 3·4 mg/kg (plasma Zn 0·80 v. 1·97 mmol/l in controls fed on 36 mg Zn/kg) resulted in a significant increase in the linoleic acid: arachidonic acid ratio in both plasma and liver phospholipids in comparison with rats fed on 36 or 411 mg Zn/kg.3. Zn supplementation (411 mg/kg) decreased the linoleic acid: arachidonic acid ratio in plasma phosphatidylserine compared with that of the controls.4. The previously reported increase in arachidonic acid (mol %) in liver triacylglycerol of Zn-deficient rats was shown to be a function of a reduced liver triacylglycerol pool size; quantitatively, triacylglycerol content of arachidonic acid in the liver was not significantly affected by Zn intake.



Metabolism ◽  
2012 ◽  
Vol 61 (3) ◽  
pp. 395-406 ◽  
Author(s):  
Pei-Ra Ling ◽  
Alpin Malkan ◽  
Hau D. Le ◽  
Mark Puder ◽  
Bruce R. Bistrian


Lipids ◽  
1971 ◽  
Vol 6 (11) ◽  
pp. 787-790 ◽  
Author(s):  
Maria Elena De Tomas ◽  
Osvaldo Mercuri


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