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Shahin Shadnia - One of the best experts on this subject based on the ideXlab platform.
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inhibition of glucose 6 phosphate dehydrogenase protects hepatocytes from Aluminum Phosphide induced toxicity
Pesticide Biochemistry and Physiology, 2017Co-Authors: Ahmad Salimi, Nasim Zamani, Shahin Shadnia, Hossein Hassanianmoghaddam, Maryam Paeezi, Bahareh Sadat Yousefsani, Jalal PourahmadAbstract:Aluminum Phosphide (AlP) poisoning is a severe toxicity with 30-70% mortality rate. However, several case reports presented AlP-poisoned patients with glucose-6-phosphate dehydrogenase (G6PD) deficiency and extensive hemolysis who survived the toxicity. This brought to our mind that maybe G6PD deficiency could protect the patients from severe fatal poisoning by this pesticide. In this research, we investigated the protective effect of 6-aminonicotinamide (6-AN)- as a well-established inhibitor of the NADP+- dependent enzyme 6-phosphogluconate dehydrogenase- on isolated rat hepatocytes in AlP poisoning. Hepatocytes were isolated by collagenase perfusion method and incubated into three different flasks: control, AlP, and 6-AN+ALP. Cellar parameters such as cell viability, reactive oxygen species (ROS) formation, mitochondria membrane potential collapse (MMP), lysosomal integrity, content of reduced (GSH) and oxidized glutathione (GSSG) and lipid peroxidation were assayed at intervals. All analyzed cellular parameters significantly decreased in the third group (6-AN+AlP) compared to the second group (AlP), showing the fact that G6PD deficiency induced by 6-AN had a significant protective effect on the hepatocytes. It was concluded that G6PD deficiency significantly reduced the hepatotoxicity of AlP. Future drugs with the power to induce such deficiency may be promising in treatment of AlP poisoning.
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vitamin e as a novel therapy in the treatment of acute Aluminum Phosphide poisoning
Turkish Journal of Medical Sciences, 2017Co-Authors: Zahra Halvaei, Kambiz Soltaninejad, Mohammad Abdollahi, Hiva Tehrani, Shahin ShadniaAbstract:BACKGROUND/AIM Aluminum Phosphide (AlP) is commonly used as a fumigant in developing countries. Induction of oxidative stress is one of the most important mechanisms of its toxicity. In this regard, and considering that there is no specific antidote for its treatment, the aim of this study was to evaluate the effect of vitamin E in the treatment of acute AlP poisoning. MATERIALS AND METHODS This was a clinical trial on acute AlP poisoned patients. All patients received supportive treatment. In addition, the treatment group received vitamin E (400 mg/BD/IM). Level of malondialdehyde (MDA) and total antioxidant capacity of plasma were measured. RESULTS There was no significant difference between the treatment and control groups with regard to demographic, clinical, or paraclinical data or Simplified Acute Physiology Score II (SAPSII) on admission. Systolic blood pressure significantly increased during the first 24 h in the treatment group (P < 0.05). The plasma MDA level significantly decreased in the treatment group (P < 0.05). Vitamin E administration decreased the necessity (30% vs. 62%, P < 0.05) and duration of intubation and mechanical ventilation (P < 0.05). It significantly reduced the mortality rate in the treatment group compared to the control group (15% vs. 50%, respectively, P < 0.05). CONCLUSION Vitamin E along with supportive treatment could have a therapeutic effect in acute AlP poisoning.
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trend of blood lactate level in acute Aluminum Phosphide poisoning
World journal of emergency medicine, 2017Co-Authors: Peyman Erfantalab, Nasim Zamani, Kambiz Soltaninejad, Shahin Shadnia, Hossein Hassanianmoghaddam, Arezou Mahdavinejad, Behrooz Hashemi DamanehAbstract:BACKGROUND: Aluminum Phosphide (AlP) poisoning is common in the developing countries. There is no specific antidote for the treatment of acute AlP poisoning. Early diagnosis of poisoning and outcome predictors may facilitate treatment decisions. The objective of this study was to determine the trend of blood lactate level in acute AlP poisoning to evaluate its role as a prognostic factor. METHODS: This was a prospective study on acute AlP intoxicated patients during one year. Demographic data, clinical and laboratory data on admission, and outcome were recorded in a self-made questionnaire. Blood lactate levels were analyzed every two hours for 24 hours. RESULTS: Thirty-nine (27 male, 12 female) patients were included in the study. The mortality rate was 38.5%. The mean blood pressure, pulse rate, blood pH and serum bicarbonate level were significantly different between the survivors and non-survivors groups. Blood lactate level was significantly higher in the non-survivors group during 8 to 16 hours post ingestion. CONCLUSION: Blood lactate level could be used as an index of severity of acute AlP poisoning.
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Unintentional poisoning by phosphine released from Aluminum Phosphide. Hum Exp Toxicol 2008; 27: 87–89
2016Co-Authors: Shahin Shadnia, O Mehrpour, M AbdollahiAbstract:Aluminum Phosphide as a releaser of phosphine gas is used as a grain preservative. In this case report, we describe an accidental severe poisoning in a 35-year-old woman, her 18-year-old daughter, and 6-year-old son caused by inhalation of phosphine gas released from 20 tablets of Aluminum Phosphide stored in 15 rice bags. The boy died 2 days after exposure before admission to hospital and any special treatment, but the others were admitted 48 h after exposure. They had signs and symp-toms of severe toxicity, and their clinical course included metabolic acidosis, electrocardiographic changes, and hypotension. They were treated by intravenous adminis-tration of sodium bicarbonate, magnesium sulfate, and calcium gluconate. The patients were discharged after 3 days and followed up for 1 week after discharge. Rapid absorption of phosphine by inhalation, induction of hyperglycemia, and surviving of patients are interest-ing issues of this case report. Key words: Aluminum Phosphide; poisoning; survival; unintentiona
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protective effects of n acetylcysteine on Aluminum Phosphide induced oxidative stress in acute human poisoning
Clinical Toxicology, 2013Co-Authors: Hiva Tehrani, Kambiz Soltaninejad, Shahin Shadnia, Zahra Halvaie, Mohammad AbdollahiAbstract:Objective. Aluminum Phosphide is used as a fumigant. It produces phosphine gas (PH3). PH3 is a mitochondrial poison which inhibits cytochrome c oxidase, it leads to generation of reactive oxygen species; so one of the most important suggested mechanisms for its toxicity is induction of oxidative stress. In this regard, it could be proposed that a drug like N-acetylcysteine (NAC) as an antioxidant would improve the tolerance of Aluminum Phosphide-intoxicated cases. The objective of this study was to evaluate the protective effects of NAC on acute Aluminum Phosphide poisoning. Methods. This was a prospective, randomized, controlled open-label trial. All patients received the same supportive treatments. NAC treatment group also received NAC. The blood thiobarbituric acid reactive substances as a marker of lipid peroxidation and total antioxidant capacity of plasma were analyzed. Results. Mean ingested dose of Aluminum Phosphide in NAC treatment and control groups was 4.8 ± 0.9 g vs. 5.4 ± 3.3 g, respectively...
Omid Mehrpour - One of the best experts on this subject based on the ideXlab platform.
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Cardiogenic Shock Due to Aluminum Phosphide Poisoning Treated with Intra-aortic Balloon Pump: A Report of Two Cases
Cardiovascular Toxicology, 2019Co-Authors: Omid Mehrpour, Sadegh Asadi, Mohammad Ali Yaghoubi, Nahid Azdaki, Nastaran Mahmoodabadi, Seyedyoosef JavadmoosaviAbstract:The mortality rate from Aluminum Phosphide (AlP) poisoning is as high as 70–100%, with refractory hypotension and severe metabolic acidosis being the two most common presentations in this poisoning. As this poisoning has no specific antidote, treatments revolve around supportive care. Cardiogenic shock created by toxic myocarditis is considered the main cause of mortality in these patients. Meanwhile, the intra-aortic balloon pump (IABP) has been suggested for the treatment of cardiogenic shock. This article reports the successful treatment of cardiogenic shock caused by AlP poisoning in a 17-year-old man and a 21-year-old woman using the IABP procedure.
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is cytochrome oxidase inhibition the primary mechanism in Aluminum Phosphide poisoning
Expert Opinion on Drug Metabolism & Toxicology, 2019Co-Authors: Omid Mehrpour, Natalie R NeumannAbstract:Aluminum Phosphide (AlP) has common applications as rodenticides and grain fumigants in Asian countries. It has a very high mortality rate [1–3]. Overall mortality related to AlP reported from 30% ...
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oxidative stress and hyperglycemia in Aluminum Phosphide poisoning
Journal of Research in Medical Sciences, 2014Co-Authors: Omid Mehrpour, Mohammad Abdollahi, Mohammad SharifiAbstract:Aluminum Phosphide (AlP) poisoning via rice tablet ingestion can be fatal, as there is no effective antidote. The exact AlP’ mechanism of action remains poorly understood, although appears to induce oxidative stress and increase extramitochondrial release of free oxygen radicals resulting in lipid peroxidation and protein denaturation of cellular membranes in various organs.[1] Meanwhile, hyperglycemia has been a known prognostic factor in severe AlP poisoning cases.[2] In our previous study, patients admitted to emergency room (ER) with glucose levels above 140 mg/dL had an increased risk of death, suggesting involvement of other mechanisms such as impaired mitochondrial respiratory function or insulin resistance and β-cell dysfunction.[3] Moreover, oxidative stress is a common finding in AlP poisoning and reportedly there has been a significant increase in lipid peroxidation in AlP intoxication patients along with a reduction in total antioxidant capacity and total thiol molecules.[4] However, it is unknown whether hyperglycemia induces oxidative stress or hyperglycemia is a result of oxidative stress in AlP poisoning. Some consequences oxidative stress in AlP poisoning include the development of insulin resistance, pancreatic β-cell dysfunction, glucose tolerance impairment, and mitochondrial dysfunction, which all end up with hyperglycemic state. Animal and human studies have shown an inverse association between insulin sensitivity and levels of reactive oxygen species.[5] Moreover, oxidative stress can activate a series of pathways involving a family of serine/threonine kinases, which in turn have a negative effect on insulin signaling.[5] On the other hand, hyperglycemia causes increased oxidative stress through several pathways, of which a main mechanism seems to be overproduction of superoxide (O2−) through mitochondrial electron transport chain.[6] Thus, oxidative stress can be possibly ameliorated by management of hyperglycemia and changes or disruptions in these mechanisms may reduce the risk of insulin resistance and the development of hyperglycemia and, furthermore, may have a potential role in its treatment. Meanwhile, the use of antioxidants may present a useful role in the treatment of oxidative stress and hyperglycemia. The purpose of this communication was to alert toxicologists to these related mechanisms of AlP-induced toxicity and to propose further studies to elucidate other factors involved in such.
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intravascular haemolysis due to glucose 6 phosphate dehydrogenase deficiency in a patient with Aluminum Phosphide poisoning
Journal of Forensic Medicine, 2013Co-Authors: Fariba Farnaghi, Nasim Zamani, Shahin Shadnia, Hossein Hassanianmoghaddam, Hamid Owliaey, Nader Momtazmanesh, Omid MehrpourAbstract:Aluminum Phosphide (AlP) poisoning and glucose?6?phosphate dehydrogenase (G6PD) deficiency are two common clinical problems in Iran. However, hemolysis associated with AlP poisoning is extremely rare. We report a 24-year-old G6PD deficient patient with AlP poisoning presenting with intravascular hemolysis.
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comment on an update on toxicology of Aluminum Phosphide
DARU, 2012Co-Authors: Omid MehrpourAbstract:Sir I read with interest the recent published article by Dr Moghadamnia titled “An update on toxicology of Aluminum Phosphide” [1]. Since Aluminum Phosphide (AlP) poisoning is an important medical concern in Iran, I have had the opportunities to work and publish many papers in this regard [2-11]. I would like to comment on that paper as follows: The author stated that" Leukopenia indicates severe AlP toxicity" and also mentioned that "Increased serum glutamic oxaloacetic transaminase (SGOT) or serum glutamic pyruvic transaminase (SGPT) and induced metabolic acidosis indicate moderate to severe AlP overdose". Leukopenia and hepatotoxicity due to AlP poisoning is reported in the literature, but according to my knowledge there is no study supported that they are good indicators of severity of AlP poisoning [2,3]. Even some studies indicated that leukosytosis is known as a prognostic factor in AlP poisoning [3]. Shadnia et al. in a study found that the prognostic factors in AlP poisoning are Simplified Acute Physiology Score II (SAPSII), low GCS, hypotension, hyperglycemia, acidosis, hemoconcentration, leukocytosis, hyperuremia and ECG abnormalities [3]. Moreover the author stated that" The serum level of cortisol is usually decreased in severe AlP poisoning". Very few studies have published about blood cortisol level changes in AlP poisoning. Generally in clinical situations such as stress, hypotension, shock or critically ill patients, there is evidence of increasing in plasma cortisol level. In addition, some surveys showed that AlP poisoning has been postulated to stimulate cortisol, glucagon, and adrenaline secretion, or inhibit insulin synthesis [6,12]. Moreover Chugh, et al. (1989) reported findings in thirty cases that showed a significant rise in plasma cortisol (greater than 1048 nmol/L) in 20 cases
Kambiz Soltaninejad - One of the best experts on this subject based on the ideXlab platform.
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vitamin e as a novel therapy in the treatment of acute Aluminum Phosphide poisoning
Turkish Journal of Medical Sciences, 2017Co-Authors: Zahra Halvaei, Kambiz Soltaninejad, Mohammad Abdollahi, Hiva Tehrani, Shahin ShadniaAbstract:BACKGROUND/AIM Aluminum Phosphide (AlP) is commonly used as a fumigant in developing countries. Induction of oxidative stress is one of the most important mechanisms of its toxicity. In this regard, and considering that there is no specific antidote for its treatment, the aim of this study was to evaluate the effect of vitamin E in the treatment of acute AlP poisoning. MATERIALS AND METHODS This was a clinical trial on acute AlP poisoned patients. All patients received supportive treatment. In addition, the treatment group received vitamin E (400 mg/BD/IM). Level of malondialdehyde (MDA) and total antioxidant capacity of plasma were measured. RESULTS There was no significant difference between the treatment and control groups with regard to demographic, clinical, or paraclinical data or Simplified Acute Physiology Score II (SAPSII) on admission. Systolic blood pressure significantly increased during the first 24 h in the treatment group (P < 0.05). The plasma MDA level significantly decreased in the treatment group (P < 0.05). Vitamin E administration decreased the necessity (30% vs. 62%, P < 0.05) and duration of intubation and mechanical ventilation (P < 0.05). It significantly reduced the mortality rate in the treatment group compared to the control group (15% vs. 50%, respectively, P < 0.05). CONCLUSION Vitamin E along with supportive treatment could have a therapeutic effect in acute AlP poisoning.
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trend of blood lactate level in acute Aluminum Phosphide poisoning
World journal of emergency medicine, 2017Co-Authors: Peyman Erfantalab, Nasim Zamani, Kambiz Soltaninejad, Shahin Shadnia, Hossein Hassanianmoghaddam, Arezou Mahdavinejad, Behrooz Hashemi DamanehAbstract:BACKGROUND: Aluminum Phosphide (AlP) poisoning is common in the developing countries. There is no specific antidote for the treatment of acute AlP poisoning. Early diagnosis of poisoning and outcome predictors may facilitate treatment decisions. The objective of this study was to determine the trend of blood lactate level in acute AlP poisoning to evaluate its role as a prognostic factor. METHODS: This was a prospective study on acute AlP intoxicated patients during one year. Demographic data, clinical and laboratory data on admission, and outcome were recorded in a self-made questionnaire. Blood lactate levels were analyzed every two hours for 24 hours. RESULTS: Thirty-nine (27 male, 12 female) patients were included in the study. The mortality rate was 38.5%. The mean blood pressure, pulse rate, blood pH and serum bicarbonate level were significantly different between the survivors and non-survivors groups. Blood lactate level was significantly higher in the non-survivors group during 8 to 16 hours post ingestion. CONCLUSION: Blood lactate level could be used as an index of severity of acute AlP poisoning.
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protective effects of n acetylcysteine on Aluminum Phosphide induced oxidative stress in acute human poisoning
Clinical Toxicology, 2013Co-Authors: Hiva Tehrani, Kambiz Soltaninejad, Shahin Shadnia, Zahra Halvaie, Mohammad AbdollahiAbstract:Objective. Aluminum Phosphide is used as a fumigant. It produces phosphine gas (PH3). PH3 is a mitochondrial poison which inhibits cytochrome c oxidase, it leads to generation of reactive oxygen species; so one of the most important suggested mechanisms for its toxicity is induction of oxidative stress. In this regard, it could be proposed that a drug like N-acetylcysteine (NAC) as an antioxidant would improve the tolerance of Aluminum Phosphide-intoxicated cases. The objective of this study was to evaluate the protective effects of NAC on acute Aluminum Phosphide poisoning. Methods. This was a prospective, randomized, controlled open-label trial. All patients received the same supportive treatments. NAC treatment group also received NAC. The blood thiobarbituric acid reactive substances as a marker of lipid peroxidation and total antioxidant capacity of plasma were analyzed. Results. Mean ingested dose of Aluminum Phosphide in NAC treatment and control groups was 4.8 ± 0.9 g vs. 5.4 ± 3.3 g, respectively...
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fatal Aluminum Phosphide poisoning in tehran iran from 2007 to 20100
Indian Journal of Medical Sciences, 2012Co-Authors: Kambiz Soltaninejad, Lewis S Nelson, Seyed Ali Bahreini, Shahin ShadniaAbstract:Background: Aluminum Phosphide (AlP) is also known as "rice tablet" in Iran. Due to the high incidence of acute AlP poisoning and its associated mortality in Iran, the authorities banned AlP-containing tablets in 2007. The aim of this study is to evaluate the trend of acute fatal AlP poisoning subsequent to this restriction. 0Materials and Methods: 0 This is a retrospective chart review of patients with acute "rice tablet" poisoning who were admitted to Loghman Hakim Hospital Poison Center, Tehran, Iran, from 2007 to 2010. Collected information included gender, age, type of poisoning, marital status, duration of hospitalization, and outcome. Results: There were 956 cases with a mortality rate of 24.06%. The incidence of fatal AlP poisoning was 2.1 and 5.81 per one million populations of Tehran in 2007 and 2010, respectively. In 223 of the fatal cases (97%) and 697 of the non-fatal cases (96%), the poisoning was intentional. The male to female ratio in the fatal and non-fatal cases was 1.04:1 and 1:1.3, respectively. Most of the fatal cases (n = 122, 53%) were unmarried. The mean age was 27.32 ± 11.31 and 24.5 ± 8.19 years in fatal and non-fatal cases, respectively. In 196 (85.2%) of the fatal cases and in 577 (79%) of non-fatal cases, the duration of hospitalization was less than 24 hours and between 48-72 hours, respectively. Conclusion: The results of this study showed the incidence of "rice tablet" poisoning, and its mortality increased since 2007 in spite of the ban. It seems that legislative means alone without other interventions, such as suicide prevention and public education, will not always be able to control or prevent acute intentional poisonings. Language: en
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unusual complication of Aluminum Phosphide poisoning development of hemolysis and methemoglobinemia and its successful treatment
Indian Journal of Critical Care Medicine, 2011Co-Authors: Kambiz Soltaninejad, Leiws S Nelson, Nastaran Khodakarim, Zohreh Dadvar, Shahin ShadniaAbstract:Methemoglobinemia and hemolysis are rare findings following phosphine poisoning. In this paper, a case of Aluminum Phosphide (AlP) poisoning complicated by methemoglobinemia and hemolysis with a successful treatment is reported. A 28-year-old male patient presented following intentional ingestion of an AlP tablet. In this case, hematuria, hemolysis and methemoglobinemia were significant events. A methemoglobin level of 46% was detected by CO-oximetry. The patient was treated with ascorbic acid and methylene blue and he also received supportive care. Two weeks after admission, the patient was discharged from the hospital. Hemolysis and methemoglobinemia may complicate the course of phosphine poisoning.
Ahmad Salimi - One of the best experts on this subject based on the ideXlab platform.
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chrysin ameliorates Aluminum Phosphide induced oxidative stress and mitochondrial damages in rat cardiomyocytes and isolated mitochondria
Environmental Toxicology, 2020Co-Authors: Saleh Khezri, Asal Jahedsani, Towhid Sabzalipour, Sepideh Azizian, Saman Atashbar, Ahmad SalimiAbstract:Apart from the anticancer, antioxidant, anti-inflammatory effects, and inhibition of aromatase, chrysin is involved in the protection of cardiovascular disorders. Cardiovascular complications are the main cause of death induced by Aluminum Phosphide (AlP) which is related to oxidative stress and mitochondrial damages. For this purpose, we investigated the effect of chrysin as an antioxidant and mitochondrial protective agent against AlP-induced toxicity in isolated cardiomyocytes and mitochondria obtained from rat heart ventricular. Using by biochemical and flow cytometry, cell viability, reactive oxygen species (ROS) formation, mitochondria membrane potential (MMP), lysosomal membrane integrity, malondialdehyde (MDA) content, and glutathione (GSH) and oxidized glutathione (GSSG) content were measured in isolated cardiomyocytes. Also, mitochondrial toxicity parameters such as mitochondrial NADH/succinate dehydrogenase activity, mitochondrial swelling, ROS formation, MMP collapse, and lipid peroxidation were analyzed in isolated mitochondria. Our results showed that the administration of chrysin (up to 10 μM) efficiently decreased (P < 0.05) cytotoxicity, oxidative, lysosomal, and mitochondrial damages induced by AlP, in isolated cardiomyocytes. Also, our finding in isolated mitochondria showed that chrysin (up to 10 μM) significantly (P < 0.05) decreased AlP-induced mitochondrial toxicity. These findings demonstrated that chrysin as an antioxidant and mitochondrial protective agent exert protective effect in wild-type cardiomyocyte treated with AlP. It was concluded that chrysin significantly reduced the toxicity of AlP in isolated cardiomyocytes and mitochondria. Due to the very low toxicity of chrysin for humans, it could be a promising agent in treatment of AlP poisoning.
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apigenin attenuates Aluminum Phosphide induced cytotoxicity via reducing mitochondrial lysosomal damages and oxidative stress in rat cardiomyocytes
Pesticide Biochemistry and Physiology, 2020Co-Authors: Asal Jahedsani, Saleh Khezri, Mahsa Ahangari, Saba Bakhshii, Ahmad SalimiAbstract:Abstract Apigenin, is a natural compound that found in high amounts in vegetables and fruits. This natural flavone has shown strong cardioprotective effects in animal and clinical studies. Due to cardioprotective effects of apigenin in previous studies, we hypothesized that apigenin protects isolated cardiomyocytes from Aluminum Phosphide(AlP)-induced toxicity as the most common disturbances after exposure with this agent. By using of biochemical and flowcytometry techniques; cell viability, reactive oxygen species (ROS) generation, mitochondria membrane potential (MMP), lysosomal membrane integrity, malondialdehyde (MDA) and oxidized/reduced glutathione (GSH/GSSG) content were measured in rat heart isolated cardiomyocytes. Our results showed that the administration of apigenin (5–100 μM) efficiently decreased (P
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inhibition of glucose 6 phosphate dehydrogenase protects hepatocytes from Aluminum Phosphide induced toxicity
Pesticide Biochemistry and Physiology, 2017Co-Authors: Ahmad Salimi, Nasim Zamani, Shahin Shadnia, Hossein Hassanianmoghaddam, Maryam Paeezi, Bahareh Sadat Yousefsani, Jalal PourahmadAbstract:Aluminum Phosphide (AlP) poisoning is a severe toxicity with 30-70% mortality rate. However, several case reports presented AlP-poisoned patients with glucose-6-phosphate dehydrogenase (G6PD) deficiency and extensive hemolysis who survived the toxicity. This brought to our mind that maybe G6PD deficiency could protect the patients from severe fatal poisoning by this pesticide. In this research, we investigated the protective effect of 6-aminonicotinamide (6-AN)- as a well-established inhibitor of the NADP+- dependent enzyme 6-phosphogluconate dehydrogenase- on isolated rat hepatocytes in AlP poisoning. Hepatocytes were isolated by collagenase perfusion method and incubated into three different flasks: control, AlP, and 6-AN+ALP. Cellar parameters such as cell viability, reactive oxygen species (ROS) formation, mitochondria membrane potential collapse (MMP), lysosomal integrity, content of reduced (GSH) and oxidized glutathione (GSSG) and lipid peroxidation were assayed at intervals. All analyzed cellular parameters significantly decreased in the third group (6-AN+AlP) compared to the second group (AlP), showing the fact that G6PD deficiency induced by 6-AN had a significant protective effect on the hepatocytes. It was concluded that G6PD deficiency significantly reduced the hepatotoxicity of AlP. Future drugs with the power to induce such deficiency may be promising in treatment of AlP poisoning.
Surjit Singh - One of the best experts on this subject based on the ideXlab platform.
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antioxidant therapy in patients with severe Aluminum Phosphide poisoning a pilot study
Indian Journal of Critical Care Medicine, 2017Co-Authors: Ashish Bhalla, P Jyothinath, Surjit SinghAbstract:Background: N-acetyl cysteine (NAC) is a powerful antioxidant and has been used extensively in the treatment of paracetamol overdose with great success. Aluminum Phosphide (ALP) ingestion results in significant oxidative stress. In this study, we evaluated the effects of NAC on mortality in patients with severe ALP poisoning. Subjects and Methods: This prospective intervention study was carried out in the emergency medical unit attached to the Nehru Hospital at PGIMER, Chandigarh, over a period of 1 year. All the patients presenting with severe ALP poisoning were randomized into two group. The treatment group received NAC in the dose of 150 mg/kg intravenous over 1 h, followed by 50 mg/kg over 4 h, followed by 100 mg/kg 16 h in 5% dextrose. The placebo group received 5% dextrose. The primary end point was mortality. Results: A total of 50 patients were recruited. The baseline parameters were comparable in both groups. The survivors in the treatment group received 19 g of NAC, but the nonsurvivors received only 12.15 g of NAC. The overall mortality in the study group was 88% with 87.5% mortality in the treatment group and 88.5% in the placebo group. Conclusions: Antioxidant therapy in the form of NAC in severe ALP poisoning did not confer any survival benefit.
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Aluminum Phosphide poisoning
Journal of Mahatma Gandhi Institute of Medical Sciences, 2015Co-Authors: Surjit Singh, Ashish BhallaAbstract:Over the last three decades, Aluminum Phosphide has emerged as an important pesticide agent being sued for self-harm in India is well as other countries. High mortality is due to severe mitochondrial dysfunction leading to disruption of cellular respiration leading to tissue hypoxia and organ dysfunction. In spite of a lot of research, no definitive anbtidote is available, and the treatment remains largely supportive.
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effect of acute Aluminum Phosphide exposure on rats a biochemical and histological correlation
Toxicology Letters, 2012Co-Authors: R Anand, Surjit Singh, Ashish Bhalla, Priyanka Kumari, Alka Kaushal, Amanjit Bal, Willayat Yousuf Wani, Aditya Sunkaria, Raina Dua, Kiran Dip GillAbstract:Aluminum Phosphide (AlP), a widely used fumigant and rodenticide leads to high mortality if ingested. Its toxicity is due to phosphine liberated when it comes in contact with moisture. The exact mechanism of action of phosphine is not known. In this study male Wistar rats were used. The animals received a single dose (20mg AlP/kg body weight i.g.) orally. Basic serum biochemical parameters, activity of mitochondrial complexes, antioxidant enzymes and parameters of oxidative stress, individual mitochondrial cytochrome levels were measured along with tissue histopathology and immunostaining for cytochrome c and compared with controls. The serum levels of creatinine kinase-MB, lactate dehydrogenase, magnesium and cortisol were higher (p<0.01); the activities of mitochondrial complexes I, II, IV were observed to be significantly decreased in liver tissue in treated rats (p<0.01). The activity of catalase was lower (p<0.05) with a significant increase in lipid peroxidation (p<0.05) whereas superoxide dismutase and glutathione peroxidase were unaffected in them. There was a significant decrease in all the cytochromes in brain and liver tissues (p<0.05) with the exception of cytochrome b in brain, the levels of which remained same. Histopathology revealed congestion in most organs with centrizonal hemorrhagic necrosis in liver. Ultra structural changes indicating mitochondrial injury was observed in heart, liver and kidney tissues. There was also a marked reduction in the cytochrome-c immunostaining compared to the controls. Toxicity due to AlP appears to result as a consequence of both-energy insufficiency and oxidative stress, with a possible and preferential interaction with the tissue cytochromes.
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severe hypoglycemia following acute Aluminum Phosphide rice tablet poisoning a case report and review of the literature
Acta medica Iranica, 2012Co-Authors: Omid Mehrpour, Mohammad Abdollahi, Abbas Aghabiklooei, Surjit SinghAbstract:Aluminum Phosphide (AlP) as 3 g tablet is widely used in Iran to protect stored food grains from pests. Hyperglycemia following its ingestion has been already reported in the recent years but severe hypoglycemia is uncommon. Here, we report a 19 year old male who attempted suicide with one tablet of AlP and demonstrated severe hypoglycemia. Despite restoration of blood glucose concentration to normal, he failed to respond to supportive treatment and died. The possible mechanisms leading to severe hypoglycemia are discussed. Though severe hypoglycemia is rare following AlP poisoning, physicians managing such patients should be aware of it.
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cytochrome c oxidase inhibition in 26 Aluminum Phosphide poisoned patients
Clinical Toxicology, 2006Co-Authors: Surjit Singh, Ashish Bhalla, Suresh K Verma, Amarpreet Kaur, Kiran Dip GillAbstract:Introduction. Aluminum Phosphide (ALP) is used worldwide to fumigate grain. ALP poisoning, though reported from different parts of world, is most common in north, northwest and central India. In the presence of moisture, ALP liberates phosphine, which is highly toxic. The mechanism of action of phosphine is not known though experimental studies show that it inhibits cytochrome-c oxidase leading to inhibition of mitochondrial oxidative phosphorylation. Patients and Methods. We estimated cytochrome-c oxidase activity in platelets of patients who had ingested ALP and compared them with those in healthy controls and in patients with shock due to other causes (cardiogenic shock, septic shock and hemorrhagic shock). Results. After analysis of variance using Kruskal-Wallis test followed by Mann Whitney U test, significant inhibition of cytochrome-c oxidase activity could be found in ALP-poisoned patients compared to healthy controls (z = −5.513, p < 0.001) and in patients with shock due to other causes (z = −2.3...