Involvement of lipoxygenase and cyclo-oxygenase pathways in hypoxia and metabolic alkalosis produced by canatoxin in rats.
This paper reports on the metabolic alkalosis produced in rats by canatoxin, a neurotoxic principle extracted from Canavalia ensiformis seeds. Rats receiving canatoxin showed increased blood bicarbonate concentration with alkaline pH and no change in pCO2. A fall in pO2 was also seen. A dose-dependent relationship between pO2 decrease and bicarbonate increase was also observed with the toxin, suggesting that hypoxia may result from respiratory compensation. Canatoxin-induced hypoxia was both lipoxygenase and cyclo-oxygenase dependent but metabolic alkalosis was only blocked with cyclo-oxygenase inhibitors. Canatoxin activates the lipoxygenase pathway and probably increases leukotriene (LT) production. Since LT may release cyclo-oxygenase products, this may explain the metabolic alkalosis observed with canatoxin.
D000136:Acid-Base Equilibrium; D000471:Alkalosis / Q000139:chemically induced* / Q000378:metabolism; D000818:Animals; D001639:Bicarbonates / Q000097:blood; D006863:Hydrogen-Ion Concentration; D000860:Hypoxia / Q000378:metabolism*; D037102:Lectins; D008084:Lipoxygenase / Q000378:metabolism*; D008297:Male; D010940:Plant Proteins; D011451:Prostaglandin-Endoperoxide Synthases / Q000378:metabolism*; D051381:Rats; D011919:Rats, Inbred Strains; D014118:Toxins, Biological
D001639:Bicarbonates; D037102:Lectins; D010940:Plant Proteins; D014118:Toxins, Biological; C032815:canatoxin; D008084:Lipoxygenase; D011451:Prostaglandin-Endoperoxide Synthases