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Abstract Aluminum phosphide (AlP) poisoning had high morbidities and mortalities with absence of a standardized approach for the treatment. The present study investigated the efficiency of GIT decontamination methods and Coenzyme Q10(Co Q10) (Ubiquinone) in improving the outcome of acute AlP poisoning. A total of 90 patients were included and all patients received immediately supportive measures, then they distributed into three equal groups: In group I, gastric lavage was done using KMNO4 solution (1:10 000); group II received 250–500 ml liquid paraffin oil orally; group III received 300 mg of Co Q10 dissolved in liquid paraffin. Co Q10 was continued in a dose of 200 mg/day every 12 h. Follow-up blood pressure, arterial blood gases, serum troponin level and need for intubation revealed that the best improvement was in group III followed by group II. The percentage of survivors was 76.67% in group III and 70% of the patients had no residual effects. In group II, the survivors were 63.33%, and 36.67% of the cases discharged without sequelae. The survivors in group I constituted 26.67% and only 16.67% of the patients had no residual effects. GIT decontamination with aqueous solutions in acute AlP poisoning should be avoided. Rapid oral intake of any available oil as a prehospital treatment or immediately on hospital admission could critically improve the outcome of acute AlP poisoning. Besides, the addition of Co Q10 to the oil further improve patients’ prognosis. HighlightsAcute aluminum phosphide (AlP) poisoning is associated with high mortalities.The appropriate method of GIT decontamination in acute AlP poisoning is controversy.Conventional gastric lavage was associated with poor prognosis in acute AlP poisoning.GIT decontamination using liquid paraffin oil improved outcome of acute AlP poisoning.Coenzyme Q10 ameliorated AlP toxicity with improvement of cardiac functions.

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Occupational exposure to antimony has gained much interest when specific toxic effects were noticed among workers processing antimony. Thus, the aim of the present work was to investigate the potential DNA oxidative damage occurring among Egyptian workers occupationally exposed to antimony trioxide. The study was conducted on 25 subjects exposed to antimony trioxide while working in the polymerization process of polyester in Misrayon and Polyester Fiber Company, KafrEldawwar, Beheira, Egypt. Urinary antimony levels were assessed using inductive coupled plasma-optical emission spectrometry (ICP-OES) and considered as a biological exposure index. DNA damage and total oxidant capacity (TOC) were assessed using ELISA. DNA damage was detected in the form of increased apurinic/apyrimidinic (AP) sites among antimony trioxide-exposed workers compared to control subjects, but it could not be explained by oxidative mechanisms due to lack of significant correlation between DNA damage and measured TOC. Antimony trioxide might have a genotoxic impact on occupationally exposed workers which could not be attributed to oxidative stress in the studied cases.

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