Physiopathology of multiple organ dysfunctions in severely monocrotophos-poisoned rabbits

Abstract

Objective: Acute organophosphorus pesticides poisoning has a serious threat on people's health. This study aimed to investigate the pathogenesis and molecular mechanism of multiple organ dysfunction syndrome (MODS) in severely monocrotophos-poisoned rabbits.

Methods: Chinchilla rabbits were used to build the monocrotophos-poisoned animal model via subcutaneous abdominal injection. Acetylcholinesterase activity was determined using the dithiobisnitrobenzoic acid enzyme kinetics method, and the free organophosphorus (FOP) toxic substances content was analyzed using the enzyme inhibition method. The contents of tumor necrosis factor (TNF-α), interleukin 1-β (IL-β) and thromboxane B₂ (TXB₂) in the plasma and tissue homogenates were determined via radioimmunoassay.

Results: Twenty-four hours after exposure, in comparison to the plasma, blood cells and homogenates of various tissues, the bile had a significantly different FOP content (P < 0.05). In different phases, HE staining results confirmed that several degrees of pathological lesions (such as hemorrhage, edema, degeneration and necrosis) were detected in FOP poisoned rabbits. The TXB₂ and TNF contents in plasma were significantly higher than those of the control (P < 0.05). Except for the intercostal muscle, all of the tissues had significantly higher TXB₂ contents than the control. The TNF contents of the liver and lung and the IL-1β contents of the liver and kidney were significantly higher than those of the control (P < 0.05).

Conclusion: FOP stored in the gallbladder may play important role in enterohepatic circulation. In MODS rabbits, caused by OP poisoning, the TXB₂ and TNF-α may play important role in inflammatory response and complement and coagulation systems respectively.

Keywords: Molecular damage; Monocrotophos poisoning; Multiple organ dysfunction; Pathological injury.