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Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)
 
 
 
 
 

Pulmonary oxygen toxicity in rats: prevention by pyrogenic diphosphoryl lipid A and potentiation by nontoxic monophosphoryl lipid A and lipid X.

Pretreatment with gram-negative bacterial endotoxin protects rats from the lethal intrathoracic edema produced by continuous exposure to greater than 95% O2 for 3 days. To help elucidate structure-activity relationships of endotoxin, we administered lipid part-structures of endotoxin intraperitoneally (at dosages up to 5.0 mg/kg) to male Sprague-Dawley rats prior to exposure to greater than 99% O2 (at 760 mm Hg) for 72 hr. We found that Salmonella minnesota mutant Re595 diphosphoryl lipid A protected rats from O2 toxicity as effectively as the parent S. minnesota endotoxin molecule at equimolar concentration. Diphosphoryl lipid A exhibited less acute toxicity (2 hr post-treatment hypothermia) than did endotoxin, although both produced prolonged fevers (greater than 24 hr) and similar patterns of protection in O2. In contrast, nontoxic lipid X (2,3-diacylglucosamine 1-phosphate) and monophosphoryl (1-dephospho) lipid A potentiated pulmonary O2 toxicity. We conclude that within the range of dosages investigated, diphosphoryl lipid A is the minimal essential structure responsible for the protection of rats from O2 toxicity by endotoxin.[1]

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