Adjuvant potential of selegiline in treating acute toxicity of aluminium phosphide in rats.

Aluminium phosphide (AlP) is a highly toxic substance with a high mortality rate and no effective antidote. Once exposed to the moisture and acidic conditions of the stomach, AlP releases toxic phosphine (PH3 ) gas, which results in severe toxicity in poisoned subjects. Selegiline is a monoamine oxidase inhibitor with antioxidant and anti-apoptotic properties, which is mostly prescribed for the treatment of mood disorders and Parkinson's disease. Since AlP has detrimental effects on cardiac physiology and mitochondrial function, we tested the protective effects of acute selegiline treatment on cardiac mitochondrial function, redox status and electrocardiographic parameters in rats after AlP poisoning. To do this, AlP was given to rats by gavage to induce toxicity. Selegiline was injected intraperitoneally in the treatment groups 1 hour after AlP poisoning. Selegiline treatment after AlP intoxication was not associated with a significant difference in the mortality rate of animals. However, selegiline reduced oxidative stress (decreased the reactive oxygen species and malondialdehyde) and increased glutathione in the cardiac tissue of rats exposed to AlP. Further, the mitochondrial membrane potential (ΔΨm) collapse reversed after treatment with selegiline. Selegiline also improved the electrocardiographic (ECG) parameters and enhanced heart rate. The histopathological evaluation revealed that selegiline eliminated the inflammation and injuries induced by AlP in the stomach and duodenum, as well as cardiac tissue. In conclusion, selegiline treatment can ameliorate the AlP-induced cardiac and gastrointestinal injuries in rats via boosting redox status and mitochondrial function with no significant effect on survival. We suggest that using selegiline, apart from other clinical treatments, may improve the quality of treatment process for AlP toxicity.

Hydroxyethyl Starch Could Save a Patient With Acute Aluminum Phosphide Poisoning.

A 40-year-old male patient with suicidal ingestion of one tablet of aluminium phosphide was referred to the department of toxicology emergency of Baharloo Hospital, Tehran, Iran. The garlic odor was smelled from the patient and abdominal pain and continuous vomiting as well as agitation and heartburn were the first signs and symptoms. Systolic and diastolic blood pressures at the arrival time were 95 and 67 mmHg, respectively. Gastric lavage with potassium permanganate (1:10,000), and 2 vials of sodium bicarbonate through a nasogastric tube was started for the patient and the management was continued with free intravenous infusion of 1 liter of NaCl 0.9% serum plus NaHCO3, hydrocortisone acetate (200 mg), calcium gluconate (1 g) and magnesium sulfate (1 g). Regarding the large intravenous fluid therapy and vasoconstrictor administering (norepinephrine started by 5 µg/min and continued till 15 µg/min), there were no signs of response and the systolic blood pressure was 49 mmHg. At this time, hydroxyethyl starch (HES) (6% hetastarch 600/0.75 in 0.9% sodium chloride) with a dose of 600 cc in 6 hours was started for the patient. At the end of therapy with HES, the patient was stable with systolic and diastolic blood pressure of 110 and 77 mmHg, respectively. He was discharged on the 6th day after the psychological consultation, with normal clinical and paraclinical examinations. This is the first report of using HES in the management of AlP poisoning and its benefit to survive the patient.

Successful treatment of acute aluminium phosphide poisoning: possible benefit of coconut oil.

Aluminium phosphide is used to control rodents and pests in grain storage facilities. It produces phosphine gas, which is a mitochondrial poison. Unfortunately, there is no known antidote for aluminium phosphide intoxication, but our recent experience with a case showed that rapid prevention of absorption by coconut oil might be helpful. In the present case, we used the same protocol in a 28-year-old man who had ingested a lethal amount (12 g) of aluminium phosphide with suicidal intent and was admitted to hospital approximately 6 hours postingestion. The patient had signs and symptoms of severe toxicity, and his clinical course included metabolic acidosis and liver dysfunction. Treatment consisted of gastric lavage with potassium permanganate solution, oral administration of charcoal and sorbitol suspension, intravenous administration of sodium bicarbonate, magnesium sulphate and calcium gluconate, and oral administration of sodium bicarbonate and coconut oil. Conservative and supportive therapy in the Intensive Care Unit was also provided. The patient survived following rapid treatment and supportive care. It is concluded that coconut oil has a positive clinical significance and can be added to the treatment protocol of acute aluminium phosphide poisoning in humans.

Fatal aluminum phosphide poisoning.

A 39-year-old man committed suicide by ingestion of aluminum phosphide, a potent mole pesticide, which was available at the victim's workplace. The judicial authority ordered an autopsy, which ruled out any other cause of death. The victim was discovered 10 days after the ingestion of the pesticide. When aluminum phosphide comes into contact with humidity, it releases large quantities of hydrogen phosphine (PH3), a very toxic gas. Macroscopic examination during the autopsy revealed a very important asphyxia syndrome with major visceral congestion. Blood, urine, liver, kidney, adrenal, and heart samples were analyzed. Phosphine gas was absent in the blood and urine but present in the brain (94 mL/g), the liver (24 mL/g), and the kidneys (41 mL/g). High levels of phosphorus were found in the blood (76.3 mg/L) and liver (8.22 mg/g). Aluminum concentrations were very high in the blood (1.54 mg/L), brain (36 microg/g), and liver (75 microg/g) compared to the usual published values. Microscopic examination revealed congestion of all the organs studied and obvious asphyxia lesions in the pulmonary parenchyma. All these results confirmed a diagnosis of poisoning by aluminum phosphide. This report points out that this type of poisoning is rare and that hydrogen phosphine is very toxic. The phosphorus and aluminum concentrations observed and their distribution in the different viscera are discussed in relation to data in the literature.

Serum & tissue magnesium content in patients of aluminium phosphide poisoning and critical evaluation of high dose magnesium sulphate therapy in reducing mortality.

Role of high dose magnesium sulphate therapy was evaluated in 50 patients of Aluminium Phosphide (AIP) poisoning. Simultaneously serum and RBC magnesium levels were studied in these patients at six different points within first 24 hours. In non-survivors magnesium content of various tissues (brain, stomach, kidneys, liver, lungs and heart) was also estimated. Magnesium estimation (tissue as well as serum) was done using atomic absorption spectrophotometer. No significant difference was found in dose related mortality rates in patients treated with and without magnesium sulphate. The immediate causes of death in these patients included intractable shock, shock coupled with arrhythmias and adult respiratory distress syndrome (ARDS). Serum as well as RBC magnesium content was within normal range at all the six points (0, 1, 3, 6, 12 and 24 hours after arrival in hospital). Tissue magnesium content of various organs (in non-survivors) was more (p < 0.01) compared to that of corresponding organs in controls (accidental deaths). No significant alterations were seen in other serum electrolytes (Na, K, Ca, PO4). The data confirmed that neither there was any evidence of hypomagnesemia in these patients nor magnesium sulphate therapy improved survival. Survival can be improved (to some extent) with continuous cardiac monitoring and use of appropriate anti-arrhythmic agents. However, imposition of stringent restrictions on the free supply of AIP and caging of tablets in plastic packs with holes and spikes may yield better results in preventing AIP poisoning rather than treating these patients.