Factors involved in the fatal susceptibility to submicrogram doses of endotoxin in cycloheximide-treated mice.
Analysis of fatal sensitivity to 0.2 microgram of S. enteritidis lipopolysaccharide in cycloheximide-treated mice identified two independent lethal elements. First, an absolute requirement for steroid supplementation to ensure survival suggests a crucial role for cycloheximide-mediated inhibition of steroidogenesis. The second factor is the development of virtually total bilateral renal cortical necrosis, itself a consequence of glomerular capillary occlusion with fibrin-like material. The survival of cycloheximide and endotoxin-challenged mice requires both hydrocortisone treatment and defibrination with ancrod. Cycloheximide and a smaller dose of endotoxin (0.1 microgram per mouse) is also fatal, but here steroid deficiency is not a crucial factor, protection being conferred by ancrod defibrination alone.
Parry
E W
EW
Department of Human Anatomy and Cell Biology, University of Liverpool, U.K.
D000721:Ancrod / Q000494:pharmacology; D000818:Animals; D003513:Cycloheximide / Q000633:toxicity*; D004731:Endotoxins / Q000633:toxicity*; D006854:Hydrocortisone / Q000494:pharmacology; D007673:Kidney Cortex Necrosis / Q000139:chemically induced* / Q000473:pathology; D008070:Lipopolysaccharides / Q000633:toxicity*; D008297:Male; D051379:Mice; D008808:Mice, Inbred CBA; D012477:Salmonella enteritidis
D004731:Endotoxins; D008070:Lipopolysaccharides; D003513:Cycloheximide; D000721:Ancrod; D006854:Hydrocortisone