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Metabolism and disposition of diphacinone in rats and mice.

14C-diphacinone (0.2-1.5 mg/kg) was orally administered to rats and mice. Residue distribution in various tissues and radiocarbon elimination in feces and urine were determined. More than 60% of the administered radiocarbon was eliminated in feces and about 10% in urine in 4 days from mice and in 8 days from rats. The greatest amount of radioactivity in tissues of both rats and mice appeared in liver. Brain, muscle, blood, and fat had the lowest residue levels. Metabolites in feces and liver were chromatographically isolated and identified by mass spectrometry. In addition to unchanged diphacinone, four hydroxylated metabolites were identified in feces and liver. Hydroxylation occurred on either or both the indandione or phenyl rings. The positions of the hydroxy groups on the rings were not established.

Animals↗
PubMed1984

Potentiation of alpha-naphthyl thiourea-induced lung injury by prostaglandin E1 and platelet depletion.

alpha-Naphthyl thiourea ( ANTU ) produces pulmonary endothelial injury, pulmonary edema, and pleural effusions in rats in a dose-dependent manner. Since prostaglandins of the E series have been shown to modulate inflammatory responses in vivo and neutrophil and platelet function in vitro we investigated the effects of prostaglandin E1 (PGE1) on ANTU -induced lung injury. Systemic administration of 15-(S)-15-methyl-PGE1 (15-M-PGE1), a stable analog of PGE1, potentiated lung injury induced by ANTU in a dose- and time-dependent manner. 15-M-PGE1 (1 mg/kg, subcutaneously) administered 1 hour prior to ANTU treatment (1 mg/kg, intraperitoneally) resulted in a 164% increase (p less than 0.001) in pleural effusion formation and a 42% increase (p less than 0.02) in wet lung weight at 4 hours after ANTU administration. This was associated with increased pulmonary endothelial cell blebbing and gap formation with a decrease in the number of platelet thrombi in 15-M-PGE1-treated animals compared with controls. 15-(S)-15-methyl-prostaglandin F2 alpha, was less effective than 15-M-PGE1 in potentiating ANTU -induced lung injury. Platelet depletion, but not neutrophil depletion, also potentiated ANTU -induced lung injury, suggesting a protective role for platelets. Platelets isolated from 15-M-PGE1-treated animals demonstrated an approximately 50% decreased aggregation response to adenosine diphosphate. 15-M-PGE1 (1 mg/kg) treatment combined with platelet depletion resulted in a 1.7-fold increase (p less than 0.01) in pleural effusions in ANTU -treated (1 mg/kg) animals compared with platelet depletion alone. These studies indicate that systemic treatment of rats with 15-M-PGE1 will potentiate ANTU -induced lung injury. This injury may be in part secondary to the ability of 15-M-PGE1 to inhibit platelet function. However, platelet depletion studies suggest that 15-M-PGE1 has additional effects, possibly on endothelial cells and/or vascular smooth muscle cells that contribute to the potentiation of ANTU -induced lung injury.

Alprostadil↗
PubMed1983

The pharmacology and therapeutics of vitamin K.

Much has been learned in the past 10 years about the mechanism of action of coumarin anticoagulants and the role of vitamin K in the production of functional clotting factors. This paper reviews the mechanism for post-ribosomal modification of precursor proteins into functional clotting factors, the therapeutic uses of vitamin K, pharmacologic and therapeutic uses of vitamin K antagonists, and the current means of testing for vitamin K antagonism. In addition, information concerning newly discovered vitamin K-dependent proteins in other tissues and pathologic processing is discussed.

1-Carboxyglutamic Acid↗