Pathophysiological effects of Androctonus australis hector scorpion venom: tissue damages and inflammatory response

Sonia Adi-Bessalem1, Djelila Hammoudi-Triki, Fatima Laraba-Djebari

  • 1Faculté des Sciences Biologiques, Université des Sciences et de la Technologie Houari Boumédienne Bab Ezzouar, 16111, BP 63, El Alia, Alger, Algeria.

Insights

Androctonus australis hector venom causes severe heart and lung damage in mice by triggering rapid cytokine and complement system responses. These responses lead to inflammation and tissue damage, highlighting key mechanisms in scorpion envenomation.

Area of Science:

  • Toxicology
  • Immunology
  • Pathology

Background:

  • Androctonus australis hector (Aah) envenomation poses a significant health risk.
  • Understanding the pathophysiological mechanisms of Aah venom is crucial for effective treatment.

Purpose of the Study:

  • To investigate the effects of sublethal Aah venom dose on NMRI mice.
  • To analyze enzymatic activities, histopathological changes, complement system lytic activity, and cytokine profiles.

Main Methods:

  • Mice were envenomed with a sublethal dose of Aah venom.
  • Enzymatic activities (creatine phospho-kinase, lactate dehydrogenase) were measured.
  • Histopathological analysis of heart and lungs was performed.
  • Complement system lytic activity, plasma cytokine levels, and peripheral blood cell infiltration were assessed.

Main Results:

  • Severe myocardial edema, hemorrhages, necroses, and acute bronchopneumonia were observed.
  • Elevated serum lactate dehydrogenase and creatine kinase levels correlated with tissue damage.
  • Rapid production of pro-inflammatory (IL-1β, IL-6, TNF-α) and anti-inflammatory (IL-4, IL-10) cytokines occurred within 30 minutes.
  • Increased complement system lytic activity and leukocytosis with mononuclear and neutrophil cell predominance were noted.

Conclusions:

  • Aah envenomation induces significant cardiac and pulmonary histopathological damage.
  • Cytokines and the complement system play a sequential or simultaneous role in Aah envenomation pathophysiology.
  • Leukocyte activation by these systems contributes to tissue damage.

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