Cardiotoxicity of Aluminum Phosphide Poisoning; Biochemical and Electrophysiological Studies and the Utility of Tropinin and CKmb as Early Biomarkers
Cardiotoxicity of Aluminum Phosphide Poisoning; Biochemical and Electrophysiological Studies and the Utility of Tropinin and CKmb as Early Biomarkers
Aluminum phosphide (AlP) or rice tablet is a cheap pesticide. When it comes in contact with acid (gastric acid) or moisture, it releases phosphine (PH3) gas. The heart,lungs, liver are the main targets in acute Aluminum phosphide (AlP) poisoning. Most deaths occur due to cardiovascular toxicity.
Aluminium phosphide is a potent respiratory chain enzyme inhibitor. Its most important effect is the inhibition of cytochrome c oxidase. The inhibition of cytochrome c oxidase and other enzymes leads to the generation of superoxide radicals and cellular peroxides , and subsequent cellular injury through lipid peroxidation and other oxidant mechanisms. It stimulates the production of hydrogen peroxide and reactive oxygen species, malonyldialdehyde (MAD), increases superoxide dismutase and inhibits catalase, peroxidase and glutathione . Oxidative stress is one of the main mechanisms of action of aluminium phosphide toxicity
Inclusion Criteria: ALP poisoned cases
Exclusion Criteria:
concomitant ingesion of other drugs or toxins
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