Resistance to endotoxin in essential fatty acid-deficient (EFAD) rats is associated with reduced synthesis of certain arachidonic acid metabolites. It was hypothesized that EFAD rats would manifest decreased vascular permeability changes during endotoxemia as a consequence of reduced arachidonic acid
The Journal of biological chemistry, 256(18), 9573-9578 (1981-09-25)
[5,6,8,9,11,12-3H6]Leukotriene C3 was converted to polar metabolites which ere excreted in feces and urine for 4-5 days after subcutaneous administration to guinea pigs. Lung homogenates converted leukotriene C3 to leukotriene D3. Liver and kidney homogenates did not catabolize leukotriene C3
Advances in prostaglandin, thromboxane, and leukotriene research, 16, 383-396 (1986-01-01)
In vitro and in vivo experiments have demonstrated that a major pathway of metabolism of the glutathione containing leukotrienes involves modifications of the tripeptide substituent. The metabolic alterations are initiated by elimination of the N-terminal gamma-glutamyl residue, catalyzed by the
The Journal of biological chemistry, 257(1), 531-535 (1982-01-10)
The distribution of [5,6,8,9,11,12-3H6]leukotriene C3 in mice was determined by whole body autoradiography of sagittal sections. Tritium was rapidly eliminated from the circulation by uptake in liver and excretion in bile as well as by renal uptake and excretion in
European journal of pharmacology, 86(2), 207-215 (1982-12-24)
Eight biosynthetically formed cysteine-containing leukotrienes dose dependently (0.01-100 nM) contracted parenchymal strips of guinea-pig lung. The response to the leukotrienes was slow in onset, remarkably long-lasting and often tachyphylactic upon repeated administration. All the leukotrienes (LTC3, 8,9-LTC3, LTC4, 11-trans-LTC4, LTC5
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