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Acute Aluminum phosphide (AlP) poisoning poses a serious global issue, yet the exact mechanisms behind AlP-induced cardiotoxicity are still not well understood. Moreover, there is no specific antidote available for AlP toxicity. Nevertheless, Quercetin (QE) has emerged as a promising therapeutic candidate in various contexts. Accordingly, our study aimed to evaluate the QE potential therapeutic effects against AlP-induced cardiotoxicity and the mechanisms underlying such effects. Rats were assigned into four groups: Group I (control group) , Group II (vehicle (corn oil) group), Group III (AlP group) received a single dose of AlP (10 mg/kg body weight) dissolved in corn oil by oral gavage, and Group IV (AlP + QE group) received a single dose of QE (400 mg/kg body weight) dissolved in saline, one hour after AlP administration. AlP-induced cardiotoxicity was evidenced by the increase in cardiac troponin I (cTnI) as well as the hemodynamic, ECG, and histopathological abnormalities. The AlP group denoted a decrease of the antioxidant enzymes; catalase and SOD and an increase of the lipid peroxidation marker; MDA. This was associated with a notable increase in inflammatory cytokines (TNFα, IL-6, and IL1β), in addition to a significant upregulation of the expression of NOX4, FOXO1, ERK1/2, and NF-κB. Moreover, Caspase3, and BAX showed strong immunopositive expression, while Bcl-2 showed mild immunoexpression. On the other hand, treatment with QE showed an improvement in the cardiotoxic effects of AlP, as indicated by significant enhancements in biomarkers, functional assessments, and histopathological findings. These results suggest that QE may be a promising candidate for treating AlP-induced cardiotoxicity, attributed to its antioxidant, anti-inflammatory, and anti-apoptotic properties, particularly emphasizing the roles of NOX4, FOXO1, ERK1/2, and NF-κB. [Display omitted] • Quercetin (QE) significantly improved the cardiotoxic changes induced by AlP. • QE mitigates the oxidative stress, inflammation, and apoptosis induced by AlP. • NOX4, FoxO1, ERK1/2, NF-κB increased expression induced by AlP was reduced by QE. • QE may have a promising therapeutic action against AlP-induced cardiotoxicity. [ABSTRACT FROM AUTHOR]

• Exposure to AlP can lead to human poisoning by severely damaging mitochondrial DNA.. • Mitochondria shield cells from stress and stimulate the immune system by releasing damage-associated molecular patterns. • Mitochondrial imbalance can trigger excessive immune response, causing organ dysfunction. • Mitochondrial dysfunction is closely linked to the activation of NLRP3. • Targeting the NLRP3 inflammasome could be a promising strategy for developing antidotes for AlP poisoning. Aluminum phosphide (AlP) is a fumigant used to control pests. However, human exposure to this substance can lead to poisoning. AlP reacts with gastric acid and water to release phosphine (PH3). This toxic gas affects the mitochondria and quickly enters the bloodstream. This gas impairs the mitochondria's ability to generate ATP, leading to oxidative stress, mitochondrial dysfunction, and damage to mitochondrial DNA (mt-DNA). Mitochondria release damage-associated molecular patterns (DAMPs) to shield cells from stress and stimulate the innate immune system. Nonetheless, if mitochondrial homeostasis is disrupted, an excessive immune response can occur, causing organ dysfunction. Mitochondrial reactive oxygen species (mt-ROS) and mt-DNA act as DAMPs. Upon recognition of DAMPs, the inflammasome is activated, causing inflammation. The nucleotide-binding domain, leucine-rich-containing family, and pyrin domain-containing-3 (NLRP3) gene on chromosome 1's extended arm encodes a protein that triggers the human inflammasome. NLRP3 is the most extensively researched inflammasome subfamily. It is essential to recognize that the pathophysiology of mitochondrial dysfunction and NLRP3 activation is complex and multifactorial, and a comprehensive approach may be needed to address both the underlying causes and downstream inflammatory responses effectively. The cGAS-STING pathway is essential for immune responses, and targeting specific nodes can be beneficial. Therapeutic approaches include small molecule drugs, biologics, vaccines, and combination therapies. Since there is a significant relationship between mitochondrial events and NLRP3 activation, targeting this inflammasome could be a promising strategy for developing antidotes for AlP poisoning. [ABSTRACT FROM AUTHOR]

Abstract: The chemisorption of CO on aluminum phosphide (AlP) n (n =1–12) clusters are studied with density functional theory. Among various possible CO adsorption sites, the on-top site is identified to be the most favorable chemisorption sit. The Al-top sites are the preferred one in the most cases for one CO adsorption in (AlP) n (n =3–12) clusters, irrespective of the charge state of the clusters. The Al–P bond lengths decrease generally as the size of the cluster increases. There is a slight increase in the mean Al–P bond lengths after CO adsorption on the lowest-energy sites of the most AlP clusters. In general, adsorption energies of CO are found to decrease with an increase in the cluster size for both neutral and ionic clusters. The adsorption energies of CO on the cationic (AlP) n CO+ (n =2–12) clusters are greater than those on the neutral and anionic complexes. The result shows that large adsorption energies of CO on neutral and ionic AlP clusters and large highest occupied and lowest unoccupied molecular-orbital gaps for (AlP)CO, (AlP)CO+ and (AlP)CO− make these species behaving like magic clusters. The CO vibrational frequencies ν CO in all the cationic complexes are always larger than the corresponding quantities in the neutral and anionic clusters. All of them are smaller than those in the free CO molecule. [ABSTRACT FROM AUTHOR]

Abstract: The objective of this study was to assess, using a capture-recapture program, the effectiveness of aluminum phosphide tablets for control of Richardson’s ground squirrels (Spermophilus richardsonii) in southern Saskatchewan grasslands, from April to July 2007–2009. Aluminum phosphide tablets were tested in study plots in moist or dry soil conditions, where burrow openings had either been marked with a flag (to ensure that all openings would be found and treated) before treatment or left unmarked. In five study plots with moist soil conditions and flagged burrow openings, the mean control level was 80.9 (SD = 6.3) %. In two study plots with dry soil conditions and flagged burrow openings, and one study with moist soil conditions and unflagged burrow openings, control levels were < 60%. It is recommended that aluminum phosphide tablets be used to control Richardson’s ground squirrels in relatively small areas (i.e., < 5 ha) with moist soil conditions and flagged burrow openings, or in specific sites where there are still high concentrations of ground squirrels after an initial treatment with poison food baits. [Copyright &y& Elsevier]

Abstract: Density functional theory (DFT) calculations were performed to investigate the properties of boron-doped (B-doped) models of representative (4,4) armchair and (6,0) zigzag aluminum phosphide nanotubes (AlPNTs). Chemical shielding (CS) parameters were also calculated for the optimized structures. The results indicated that the bond distances and tip diameters do not detect the effects of dopant whereas band gap energies and dipole moments detect notable effects. CS parameters also indicated that the replacement of P atom by B atom in the zigzag AlPNT yields the most significant changes in properties of nanotube among all B-doped AlPNTs. [ABSTRACT FROM AUTHOR]

[Display omitted] • Theoretical calculations are applied to study the interaction between CaO nanocage and AP molecule. • Structural and electronic properties of CaO nanocage after AP molecule adsorption was reported. • Using Bader charge transfer and adsorption energy, the adsorption of AP molecule on CaO nanocage is studied. • The results suggest that CaO nanocage is a prominent sensing material for AP molecule. In this paper, the reactivity and sensitivity of a pristine calcium oxide (CaO) nanocge are scrutinized towards aluminum phosphide (AP) molecule through calculations based on density functional theory (DFT). The AP molecule is strongly adsorbed onto the CaO nanocage through its P atom with an adsorption energy of approximately −39.75 kcal/mol. Band gap (E g) of the CaO nanocage decreases from 4.67 to 3.39 eV following the adsorption of the AP molecule, which increased the electrical conductivity. Moreover, the work function of the CaO nanocage is impacted to a great extent, which causes a change in the field electron emission. Finally, it is anticipated that the recovery time will be approximately 573 m s for desorption of the AP molecule from the CaO nanocage surface. The results indicate that the CaO nanocage might be employed as an encouraging sensor in detecting the AP molecule. [ABSTRACT FROM AUTHOR]

Aluminum phosphide, which is known as rice tablet in Iran, is being used in an increasing number of cases of self-poisoning, and such cases have a high mortality rate. This poisoning has become an important problem in various developing countries. There is no specific antidote, and supportive care usually fails to restore cardiac systolic function and to resolve the patient's severe hypotension. The main mechanism of action of aluminum phosphide is believed to be an inhibition of cytochrome c oxidase in mitochondria followed by a stoppage of cellular metabolism. Currently, scientific attention is exploring modifying the functioning of mitochondria using various novel therapeutic agents. One such agent is coenzyme Q10, which has an important role in the mitochondrial electron transport chain. It is hydrophobic in nature acting as an antioxidant with the ability to scavenge oxygen-derived free radicals. As a result of these properties, coenzyme Q10 has a crucial role to play in reducing cellular oxidative stress. Moreover, there is evidence suggesting that coenzyme Q10 is able to enhance cardiac systolic function in heart failure patients. Based on the above, we propose that treating patients suffering from aluminum phosphide poisoning with coenzyme Q10 may be able to mitigate mitochondrial dysfunction and improve heart contractility. This novel therapeutic intervention enables this by removing oxygen-derived free radicals from the mitochondria and modifying mitochondrial functioning. We believe that this treatment has potential as an effective adjunct to supportive care in cases of aluminum phosphide poisoning and should also help to alleviate tissue injury. [ABSTRACT FROM AUTHOR]

Abstract: Acute aluminum phosphide poisoning is a serious toxicity and results in high mortality rate despite the progress of critical care. After ingestion, phosphine gas is released and absorbed quickly, causing systemic poisoning and cell hypoxia. Excessive thirst, severe hypotension, arrhythmias, tachypnea, and severe metabolic acidosis are the common clinical manifestations. We think acute metabolic response which characteristically occurs in severe injury also happens in aluminum phosphide poisoning. Necropsy examinations indicate congestion in almost all vital organs because of leakage of fluids from intravascular to extravascular space. The most favorable type of fluid for intravascular volume resuscitation persists and is disputed. Colloids remain in the intravascular space rather than crystalloids, and provide more rapid hemodynamic stabilization. Furthermore, hydroxyethyl starch solution may have other benefits e.g. it can reduce the extra vascular leak of albumin and fluids from an endothelial injury site. As refractory hypotension and cardiovascular collapse, because leakage of fluids from intravascular to extravascular space are common cause of death in this toxicity, we propose that hydroxyethyl starch can dominate this refractory hypotension and consequently acute metabolic response. [Copyright &y& Elsevier]