HYPOXIC PROTECTION IN PARAQUAT POISONING

  • 1 January 1976
    • journal article
    • research article
    • Vol. 35  (5) , 496-500
Abstract
Ingestion or injection of the herbicide paraquat (1,1''-dimethyl-4,4''-dipyridylium dichloride) has caused more than 120 deaths in humans. Most were due to respiratory failure caused by pulmonary edema, hemorrhage and atelectasis, or subsequent pulmonary fibrosis. Paraquat is concentrated in lung tissue and is believed to cause superoxide radical formation in the presence of O2 and suitable electron donors. Exposure to increased concentrations of O2 was reported to accelerate the toxicity of paraquat. The therapeutic efficacy of a reduced O2 environment was investigated by exposing paraquat-poisoned mice to 10% O2 after stepwise drops from 14% O2. Mice (61) were given i.p. injections of 27 mg/kg of paraquat. The 25 mice in hypoxia for 7 days had a 32% mortality rate vs. a 78% mortality rate for the remainder of the mice in room air, P < 0.01. After a dose of 20 mg/kg of paraquat administered i.p., 24 mice in hypoxia had a 25% mortality rate vs. 51% for 35 animals in room air. Brief exposures of the hypoxia group to normoxia (room air) led to pulmonary edema and death. The continuous exposure of paraquat-poisoned animals to hypoxic environments was protective. This approach may be useful in other oxidant lung injuries.

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