Effect of acute aluminum phosphide exposure on rats—A biochemical and histological correlation

Anand, Rajeev; Kumari, Priyanka; Kaushal, Alka; Bal, Amanjit; Wani, Willayat Yousuf; Sunkaria, Aditya; Dua, Raina; Singh, Surjit; Bhalla, Ashish; Gill, Kiran Dip

doi:10.1016/j.toxlet.2012.09.020

Cited by 57 publications

(42 citation statements)

References 38 publications

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“…Previous studies demonstrated that phosphine can trigger apoptosis pathways in several tissues such as heart, kidney and liver . It was shown that AlP affects mitochondrial membrane fluidity leading to mitochondrial swelling and outer membrane rupture, thus resulting in the release of pro‐apoptotic factors which in turn activates caspases to induce cell death . The recent studies also confirmed the AlP‐induced cardiomyocyte death through several pathways.…”

Section: Melatonin and Aluminium Phosphide‐induced Apoptosismentioning

confidence: 77%

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A review of the protective role of melatonin during phosphine-induced cardiotoxicity: focus on mitochondrial dysfunction, oxidative stress and apoptosis

Asghari

Abdollahi

Oliveira

et al. 2017

Journal of Pharmacy and Pharmacology

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Objectives Acute poisoning with aluminium phosphide (AlP) is a major cause of mortality in developing countries. AlP mortality is due to cardiac dysfunction leading to cardiomyocyte death. The main mechanism is an inhibition of cytochrome c oxidase in the cardiomyocyte mitochondria, resulting in a decreased ATP production and oxidative stress. Unfortunately, the administration of exogenous drugs does not meet the desired requirements of an effective therapy. Melatonin is an amphiphilic molecule and can easily pass through all cellular compartments with the highest concentration recorded in mitochondria. It is known as a vigorous antioxidant, acting as a potent reactive oxygen species (ROS) scavenger. Our aim is to summarize the mechanisms by which melatonin may modulate the deteriorating effects of AlP poisoning on cardiac mitochondria. Key findings Melatonin not only mitigates the inhibition of respiratory chain complexes, but also increases ATP generation. Moreover, it can directly inhibit the mitochondrial permeability transition pore (mPTP) opening, thus preventing apoptosis. In addition, melatonin inhibits the release of cytochrome c from mitochondria to hinder caspase activation leading to cell survival. Summary Based on the promising effects of melatonin on mitochondria, melatonin may mitigate AlP-induced cardiotoxicity and might be potentially suggested as cardioprotective in AlP-intoxicated patients.

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Section: Melatonin and Aluminium Phosphide‐induced Apoptosismentioning

confidence: 77%

“…It is demonstrated that AlP‐induced cardiotoxicity is due to the generation of free radicals . On the other hand, the heart is highly susceptible to oxidative damage.…”

Section: Oxidative Stress: Effect Of Melatonin and Aluminium Phosphidementioning

confidence: 99%

A review of the protective role of melatonin during phosphine-induced cardiotoxicity: focus on mitochondrial dysfunction, oxidative stress and apoptosis

Asghari

Abdollahi

Oliveira

et al. 2017

Journal of Pharmacy and Pharmacology

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“…Myocardial damage can be traced by the many folds of CPK-MB and LDH elevations in AlP poisoning (Shah et al 2009; Anand et al 2012) though elevation of CPK levels without any changes in CPK-MB fraction was reported by Duenas et al (1999). Contrary to our finding, CPK levels and CPK/CPK-MB ratio were not found to be reliable cardiac injury markers in AlP poisoning by Soltaninejad et al (2012).…”

Section: Discussionmentioning

confidence: 99%

The effect of N-acetyl cysteine (NAC) on aluminum phosphide poisoning inducing cardiovascular toxicity: a case–control study

et al. 2016

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Background Aluminum phosphide (AlP) is a very effective indoor and outdoor pesticide. We investigated the effects of N-acetyl cysteine (NAC) on the survival time, hemodynamics, and cardiac biochemical parameters at various time intervals in some cases of AlP poisoning.MethodsThis research was a case–control study to evaluate 63 AlP poisoned patients during 2010–2012. Patients with cardiovascular complications of AlP to be treated with intravenous NAC plus conventional treatment were considered as the case group and compared with patients who did not receive NAC. NAC infusion was administered to the case group at 300 mg/kg for 20 h. The data gathered included age, sex, heart rate, Systolic blood pressure (SBP), creatine phosphokinase (CPK), creatine kinase MB (CK-MB), and ECG at the admission time and 12, 18, and 24 h after admission. Analysis of repeated measures was performed to check the variability of parameters over time.ResultsThe mean ages in the case and control groups were 26.65 ± 1.06 (19–37 years) and 28.39 ± 1.11 (18–37 years), respectively (P = 0.266). Most of the patients were female (56.5%). CK-MB means were significantly different between the two groups, but no differences between the other variables were observed. Also, CK-MB, CPK, heart rate, and systolic blood pressure means became significantly different over time (0, 12, 18, and 24 h) in both groups (P < 0.001). NAC prevented sharp heart rate fluctuations in AlP patients in the case group. Regarding the outcomes, 17 patients died (10 patients in the control and 7 patients in the case groups). No side-effects of NAC were observed.ConclusionOur patients could be managed by the positive role of NAC as the biochemical index of cardiotoxicity was found to elevate in both the case and control groups. Therefore, for the management protocol optimization, NAC evaluation should be done in further cases.

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“…Phosphine gas released as a result of AlP reaction with water, moisture or hydrochloric acid of the stomach, mediates the cardiotoxic effect of AlP. Ample evidences suggest that mitochondrial impairment and oxidative stress are two crucial modulators of AlP induced cell loss and contractile dysfunction in myocardium [41,4].…”

Section: Accepted Manuscriptmentioning

confidence: 99%

Molecular and biochemical evidences on the protective effects of triiodothyronine against phosphine-induced cardiac and mitochondrial toxicity

et al. 2015

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Effect of acute aluminum phosphide exposure on rats—A biochemical and histological correlation

Cited by 57 publications

References 38 publications

A review of the protective role of melatonin during phosphine-induced cardiotoxicity: focus on mitochondrial dysfunction, oxidative stress and apoptosis

A review of the protective role of melatonin during phosphine-induced cardiotoxicity: focus on mitochondrial dysfunction, oxidative stress and apoptosis

The effect of N-acetyl cysteine (NAC) on aluminum phosphide poisoning inducing cardiovascular toxicity: a case–control study

Molecular and biochemical evidences on the protective effects of triiodothyronine against phosphine-induced cardiac and mitochondrial toxicity

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