Evaluation of Oleic Acid, Arachidonic Acid, and Various Drugs as Competitors for Serum Binding of Thyroxine

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.

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Fatty acid stimulation of membrane phosphatidylinositol hydrolysis by brain phosphatidylinositol phosphodiesterase

Biochemical Journal ◽

10.1042/bj1780497 ◽

1979 ◽

Vol 178 (2) ◽

pp. 497-500 ◽

Cited By ~ 83

Author(s):

R F Irvine ◽

A J Letcher ◽

R M Dawson

Keyword(s):

Arachidonic Acid ◽

Oleic Acid ◽

Fatty Acid ◽

Acid Content ◽

Microsomal Fraction ◽

Fatty Acid Content ◽

Membrane Bound ◽

Liver Microsomal Fraction ◽

Hydrolysis Of ◽

Stimulation Of

The hydrolysis of membrane-bound phosphatidylinositol in rat liver microsomal fraction by the soluble phosphatidylinositol phosphodiesterase from rat brain was markedly stimulated by oleic acid or arachidonic acid. The stimulation did not require added calcium, although it was abolished by EDTA. Lysophosphatidylcholine also totally suppressed the stimulation. A possible role for the fatty acid content of a membrane in controlling phosphatidylinositol turnover is suggested.

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Fatty Acid-mediated Gastroprotection Does Not Correlate with Prostaglandin Elevation in Rats Exposed to Various Chemical Insults

Veterinary Pathology ◽

10.1177/030098589403100608 ◽

1994 ◽

Vol 31 (6) ◽

pp. 679-688 ◽

Cited By ~ 2

Author(s):

K. G. Mandel ◽

T. A. Bertram ◽

M. K. Eichhold ◽

S. C. Pepple ◽

M. J. Doyle

Keyword(s):

Fatty Acids ◽

Arachidonic Acid ◽

Oleic Acid ◽

Fatty Acid ◽

Gastric Mucosa ◽

Linolenic Acid ◽

Mucosal Damage ◽

Taurocholic Acid ◽

Gastric Mucosal Damage ◽

Gastric Mucosal Lesions

This study involved a comparison of activity of several long-chain fatty acids (arachidonic acid, dihomo-[γ]-linolenic acid, linoleic acid, and oleic acid) for protection against gastric mucosal damage elicited by taurocholic acid, acidified aspirin, and ethanol in rats. Each damaging agent induced gastric mucosal lesions in the corpus. Mucosal damage was induced by all agents, and all fatty acids protected the gastric mucosa; however, ethanol and arachidonic acid were the most potent damaging and protecting agents, respectively. Maximally protective doses for prevention of taurocholic acid-induced damage by arachidonic, dihomo-[γ]-linolenic, linoleic, and oleic acids were 50, 200, 100, and 200 mg/kg, respectively; however, 10 mg/kg arachidonic acid reduced lesion length by >50%, whereas minimally effective doses of the other fatty acids were ≥50 mg/kg. Similar potency differences were observed for fatty acid protection against acidified aspirin-induced gastric damage. Although all the fatty acids reduced macroscopic damage, histologic studies showed they did not totally eliminate surface mucosal damage. Microscopic analysis showed that treatment with dihomo-[γ]-linolenic acid or oleic acid attenuated depletion of neutral and acidic glycoproteins from the mucus neck cells of the gastric mucosa in response to exposure to taurocholic acid. Despite having similar gastroprotective activity, arachidonic, dihomo-[γ]-linolenic, linoleic, and oleic acids had very dissimilar abilities to elevate gastric mucosal E-series prostaglandins. Both arachidonic and dihomo-[γ]-linolenic acids elevated E-series prostaglandins, but arachidonic acid had 2–5-fold greater gastroprotective potency. Furthermore, oleic and linoleic acids, which had protective potency similar to that dihomo-[γ]-linolenic acid, did not significantly elevate prostaglandins. These studies failed to demonstrate an absolute correlation between prostaglandin elevation and gastroprotection. The results of this investigation suggest that prostaglandin elevation, although associated with gastroprotection, does not appear to be the sole mechanism for fatty acid-mediated protection of rat gastric mucosa.

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Magnesium influences incorporation of [3H]arachidonic acid in perfused rabbits hearts

AJP Heart and Circulatory Physiology ◽

10.1152/ajpheart.1993.265.1.h83 ◽

1993 ◽

Vol 265 (1) ◽

pp. H83-H90

Author(s):

M. T. Weis

Keyword(s):

Arachidonic Acid ◽

Oleic Acid ◽

Time Points ◽

Tissue Lipids ◽

Perfused Hearts ◽

Total Tissue

Ca(2+)-free perfusion of rabbit hearts produces a 50% loss of tissue Ca2+ and Mg2+ and results in reduced incorporation of arachidonic acid into tissue lipids. This work was undertaken to determine whether the reduced incorporation was specific for arachidonic acid and whether it was correlated to the loss of either (or both) cation(s). Single 170-pmol bolus doses of [3H]arachidonic or [3H]oleic acid were given to perfused hearts with or without Ca2+ in the perfusate. The experiment was terminated, and the lipids were extracted 1-15 min after administration of label. At all time points, significantly less arachidonate was incorporated into total tissue lipids in the absence of than in the presence of Ca2+. The presence or absence of Ca2+ had no effect on the incorporation of oleate. When [3H]arachidonate was administered to hearts perfused with buffer containing 104 mM Li+ and 35 mM Na+ (which reduces tissue Mg2+ by approximately 25% and increases tissue Ca2+ by approximately 35%), the incorporation into lipids was reduced from 0.882 +/- 0.0739 to 0.598 +/- 0.0722 pmol/mg lipid (P < 0.05; n = 6). The incorporation of [3H]oleate during 104 mM Li+ and 35 mM Na+ was not different from control. These data suggest that the incorporation of arachidonic, but not oleic, acid into tissue lipids is dependent on the tissue Mg2+ content.

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