Citation

Anand R, Sharma DR, Verma D, Bhalla A, Gill KD, Singh S. Hum. Exp. Toxicol. 2013; 32(8): 807-816.

Affiliation

Department of Biochemistry, Postgraduate Institute of Medical Education and Research, Chandigarh, India.

Copyright

(Copyright © 2013, SAGE Publishing)

DOI

10.1177/0960327112468909

PMID

23821638

Abstract

Aluminum phosphide (ALP), a widely used fumigant and rodenticide, leads to high mortality if ingested. Its toxicity is due to phosphine that is liberated when it comes in contact with moisture. The exact site or mechanism of action of phosphine is not known, although it is widely believed that it affects mitochondrial oxidative phosphorylation. Basic serum biochemical parameters, activity of mitochondrial complexes, antioxidant enzymes and parameters of oxidative stress were estimated in the platelets of 21 patients who developed severe poisoning following ALP ingestion. These parameters were compared with 32 healthy controls and with 22 patients with shock due to other causes (cardiogenic shock (11), septic shock (9) and hemorrhagic shock (2)). The serum levels of creatine kinase-muscle brain and lactate dehydrogenase were higher in patients poisoned with ALP, whereas a significant decrease was observed in the activities of mitochondrial complexes I, II and IV. The activity of catalase was lower but the activities of superoxide dismutase and glutathione peroxidase were unaffected in them. A significant increase in lipid peroxidation and protein carbonylation was observed, whereas total blood thiol levels were lower. In patients severely poisoned with ALP, not only cytochrome c oxidase but also other complexes are involved in mitochondrial electron transport, and enzymes are also inhibited.

Language: en