Aluminium Phosphide Poisoning and Oxidative Stress

Kariman, Hamid; Heydari, Kamran; Fakhri, Mohammad; Shahrami, Ali; Dolatabadi, Ali Arhami; Mohammadi, Hossein Ali; Gharibi, Morteza

doi:10.1007/s13181-012-0219-1

Cited by 45 publications

(44 citation statements)

References 21 publications

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“…Oxidative degradation of lipids known as lipid peroxidation, and other oxidant mechanisms damage biological macromolecules specially the cell membrane ultimately leading to cell death [29]. This is in agreement with our findings of significant increase in TBARS levels of plasma, liver and kidney of aluminium phosphide treated rats ( Table 1).…”

Section: Discussionsupporting

confidence: 92%

Aluminium Phosphide-induced Hepato-nephrotoxicity and Oxidative Damage in Rats: The Protective Effect of α-lipoic Acid

Yousef¹,

Soliman²,

El‐Demerdash³

2015

TOPROCJ

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The present experiment was carried out to investigate the effectivness of -lipoic acid in allevating the toxicity of aluminium phosphide on biochemical parameters, free radicals and enzyme activities in plasma, liver and kidney of male rats. Animals were orally treated with aluminium phosphide, -lipoic acid and their combination for 30 consecutive days. Treatment with aluminium phosphide led to significant decrease in plasma total protein and glucose and increase in transaminases, phosphatases, urea, creatinine and bilirubin. Treatment with aluminium phosphide significantly decreased glutathione S-transferase (GST), catalase (CAT) and reduced glutathione (GSH) in plasma, liver and kidney. While, thiobarbituric acid reactive substances (TBARS; as an index of lipid peroxidation) and superoxide dismutase (SOD) were increased in plasma, liver and kidney of rats treated with aluminium phosphide. Administration of -lipoic acid in combination with aluminium phosphide minimized and alleviated its toxic effects on most of the measured parameters. In conclusion, lipoic acid has beneficial effects and could be able to attenuate aluminium phosphide toxicity.

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Section: Discussionsupporting

confidence: 92%

Aluminium Phosphide-induced Hepato-nephrotoxicity and Oxidative Damage in Rats: The Protective Effect of α-lipoic Acid

Yousef¹,

Soliman²,

El‐Demerdash³

2015

TOPROCJ

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“…In a previous study, AlP caused huge alterations in the levels of antioxidant enzymes . In other studies, severe reduction in antioxidant capacity was observed . A significant decrease was also shown in thiol group levels .…”

Section: Oxidative Stress: Effect Of Melatonin and Aluminium Phosphidementioning

confidence: 57%

“…The inhibition of respiratory chain complexes by AlP seems to initiate disastrous events resulting in ROS production. Consequently, these free radicals induce lipid peroxidation and DNA damage ending in blemished cycle which eventually leads to more oxidative stress and triggers apoptosis cascade in the cardiomyocytes . In a previous study, AlP caused huge alterations in the levels of antioxidant enzymes .…”

Section: Oxidative Stress: Effect Of Melatonin and Aluminium Phosphidementioning

confidence: 94%

“…Consequently, these free radicals induce lipid peroxidation and DNA damage ending in blemished cycle which eventually leads to more oxidative stress and triggers apoptosis cascade in the cardiomyocytes. [42][43][44] In a previous study, AlP caused huge alterations in the levels of antioxidant enzymes. [13] In other studies, severe reduction in antioxidant capacity was observed.…”

Section: Oxidative Stress: Effect Of Melatonin and Aluminium Phosphidementioning

confidence: 99%

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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. 2016

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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“…Morever, Kariman et al (2012) (30) found that plasma total thiol concentration was lower in patients with acute aluminium phosphide toxicity versus control subjects, while the level of thiobarbituric reactive substance values showed a significant increase in patients compared with healthy controls.…”

Section: Discussionmentioning

confidence: 98%

Evaluation of Potential Oxidative Stress in Egyptian Patients with Acute Zinc Phosphide Poisoning and the Role of Vitamin C

Sagah

Oreby

Elgharabawy³

et al. 2015

IJHS

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Objective: To evaluate potential oxidative stress in patients with acute phosphide poisoning and the effect of vitamin C. Methods:Participants were females and divided into three groups; group I: healthy volunteers group II: healthy volunteers received vitamin C, group III: patients with acute phosphide poisoning received the supportive and symptomatic treatment and group IV: patients with acute phosphide poisoning received the supportive and symptomatic treatment in addition to vitamin C. All the participants were subjected to thorough history, clinical examination, ECG and laboratory investigations were carried on collected blood and gastric lavage samples on admission. Blood samples were divided into two parts, one for measurement of routine investigations and the second part was used for evaluation of malondialdehyde and total thiol levels before and after receiving the treatment regimen.Results: Most of the cases in this study were among the age group of 15-25 years, females, single, secondary school education, from rural areas and suicidal. All vital signs were within normal range and the most common complaint was vomiting and abdominal pain. All cases in this study showed normal routine investigations. The mean MDA levels after receiving treatment decreased significantly in groups II and IV. The mean total thiol levels increased significantly after receiving treatment in groups II and IV. Conclusion:It can be concluded that vitamin C has a potential benefit due to its antioxidant property on zinc phosphide induced-oxidative stress in acute zinc phosphide poisoned patients.

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Aluminium Phosphide Poisoning and Oxidative Stress

Cited by 45 publications

References 21 publications

Aluminium Phosphide-induced Hepato-nephrotoxicity and Oxidative Damage in Rats: The Protective Effect of α-lipoic Acid

Aluminium Phosphide-induced Hepato-nephrotoxicity and Oxidative Damage in Rats: The Protective Effect of α-lipoic Acid

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

Evaluation of Potential Oxidative Stress in Egyptian Patients with Acute Zinc Phosphide Poisoning and the Role of Vitamin C

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