ArticleThe Indian journal of medical research2016
Prevention of phosphine-induced cytotoxicity by nutrients in HepG2 cells.
Article in The Indian journal of medical research, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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Who cites it
4 citing papers in PubMed, 10 citations in OpenAlex.
- Intravenous Dihydroxyacetone as Adjunctive Therapy in Aluminum Phosphide Poisoning: A Case Series.Clinical case reports · 2026Article
- The therapeutic effect of a novel parenteral formulation of dihydroxyacetone in aluminum phosphide-intoxicated patients.Heliyon · 2023Article
- Thin Degradable Coatings for Optimization of Osteointegration Associated with Simultaneous Infection Prophylaxis.Materials (Basel, Switzerland) · 2019Article
- Glycyrrhizic Acid Ameliorates Mitochondrial Function and Biogenesis Against Aluminum Toxicity in PC12 Cells.Neurotoxicity research · 2019Article
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
BACKGROUND &
objectivesPhosphides used as an insecticide and rodenticide, produce phosphine (PH3) which causes accidental and intentional poisoning cases and deaths. There is no specific treatment or antidote available for PH3poisoning. It is suggested that PH3-induced toxicity is associated with adenosine triphosphate (ATP) depletion; therefore, in this study the effect of some nutrients was evaluated on PH3cytotoxicity in a cell culture model.
methodsPH3was generated from reaction of zinc phosphide (10 mM) with water in the closed culture medium of HepG2 cells, and cytotoxicity was measured after one and three hours of incubation. ATP, glutathione (GSH) and lipid peroxidation were also assessed at one or three hours post-incubation. ATP suppliers including dihydroxyacetone, glyceraldehyde and fructose were added to the culture medium 10 min before PH3generation to prevent or reduce phosphine-induced cytotoxicity.
resultsPhosphine caused about 30 and 66 per cent cell death at one and three hours of incubation, respectively. ATP content of the cells was depleted to 14.7 per cent of control at one hour of incubation. ATP suppliers were able to prevent cytotoxicity and ATP depletion induced by PH3. Dihydroxyacetone, α-ketoglutarate, fructose and mannitol restored the ATP content of the cells from 14.7 per cent to about 40 , 34 , 32 and 30 per cent, respectively. Lipid peroxidation and GSH depletion were not significantly induced by zinc phosphide in this study. INTERPRETATION &
conclusionsThe results supported the hypothesis that phosphine-induced cytotoxicity was due to decrease of ATP levels. ATP suppliers could prevent its toxicity by generating ATP through glycolysis. α-keto compounds such as dihydroxyacetone and α-ketoglutarate may bind to phosphine and restore mitochondrial respiration.
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