Oxidative stress in acute human poisoning with organophosphorus insecticides; a case control study

Ranjbar, Akram; Solhi, Hassan; Mashayekhi, Farideh Jalali; Susanabdi, Alireza; Rezaie, Ali; Abdollahi, Mohammad

doi:10.1016/j.etap.2004.10.007

Cited by 143 publications

(83 citation statements)

References 14 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…This protection may be attributed to phosphorylation and activation of endothelial nitric oxide syntheses in endothelial cells through modulation of protein kinase C. A signaling pathways by green tea resulting in endothelial dependant vasorelaxtion (Lorenz et al, 2004). So in our present study demonstrate that, the activity of the MDA in malathion exposed group increased 2 fold compared with that of the control one, these finding is in accordance with Gultekin et al (2001) who reported that MDA values increased with increasing organophosphorous compounds concentration and incubation period (Ranjbar et al, 2005), may be due to Lipid peroxidation was seen in erythrocytes and liver of rats when exposed to malathion orally for 4 weeks at dose of 5,25 and 75 mg/Kg, respectively (Abdollahi et al, 2004) While in groups treated by malathion plus vitamine c or malathion plus green tea there were a significant decrease in MDA values in comparison with malathion group may be due to The protective effect of vitamin c over malathion toxicity is likely to be mediated via the inhibition of free radical generation and enhancement of free radical scavenging activity (Suna et al, 2010) and Green tea prevents the loss of lipophilic antioxidant α-tocopherol by repairing tocopheryl radicals and protection of the hydrophilic antioxidant ascorbate (Skryzdlewska et al, 2002). Therefore, it may decrease the concentration of lipid free radicals and terminate initiation and propagation of lipid peroxidation (Guo et al, 1999).…”

Section: Discussionsupporting

confidence: 82%

Protective Role of Vitamin C and Green Tea Extract on Malathion-Induced Hepatotoxicity and Nephrotoxicity in Rats

Elzoghby¹,

Hamoda²,

Aboubakr³

et al. 2014

American Journal of Pharmacology and Toxicology

View full text Add to dashboard Cite

The present study was designed to determine the modulating effect of green tea and vitamin C against adverse effects of malathion. Animals were divided into four groups 5 rats /group). Group one was used as a control. Group two given malathion (50 mg/kg/day; 1/50 of the LD50 for four weeks). Group three and Group four were given malathion (50 mg/kg/day; 1/50 of the LD50 for four weeks) plus vitamin C (200 mg/kg/day) and plus green tea (36 mg/kg/day) respectively. At the end of the fourth week, the malathion-treated group had significantly lower Red Blood Cell count (RBCs), Hemoglobin concentration (Hb), Packed Cell Volume (PCV%) and leucocytes (WBCs) than the control group. Compared to the control group, the malathion-treated group had significantly higher serum Alkaline Phosphatase (ALP), Alanine aminotransferase (ALT), Aspartate aminotransferase (AST), Lactate Dehydrogenase (LDH), urea, creatinine and uric acid levels than the control group. The malathion treated rats also had significantly lower serum total protein, albumin and globulin levels than the control group, but the malathion plus vitamin C and malathion plus green tea groups did not differ from the control group in terms of these parameters. Moreover, concomitant vitamin C and green tea treatment significantly normalized, at least partially, all of the other hematological and biochemical parameters that were altered by malathion. Liver tissue homogenate in malathion treated group had lower Glutathione (GSH), Glutathione Peroxidase (GSH-PX) and Superoxide Dismutase (SOD) levels accompanied with higher level of Malondialdehyde (MDA) than the control group. Histopathological studies revealed that the malathion-treated, malathion plus vitamin C and malathion plus green tea treated groups exhibited histopathological changes in liver and kidney tissues, although some pathological features were only observed in the malathion-treated group. Thus, vitamin C and green tea can reduce malathion hepatotoxicity and nephrptoxicity.

show abstract

Section: Discussionsupporting

confidence: 82%

Protective Role of Vitamin C and Green Tea Extract on Malathion-Induced Hepatotoxicity and Nephrotoxicity in Rats

Elzoghby¹,

Hamoda²,

Aboubakr³

et al. 2014

American Journal of Pharmacology and Toxicology

View full text Add to dashboard Cite

show abstract

“…It has been reported that oxidative stress is the common pathophysiological pathway of most types of intoxications. The role of increased oxidative stress has been demonstrated in experimental organophosphate, paracetamol, and methotrexate models (12)(13)(14). Recent in vitro and in vivo studies have suggested that oxidative stress is probably responsible for α-amanitininduced hepatotoxicity in studies (7,(15)(16)(17)(18).…”

Section: Introductionmentioning

confidence: 99%

The role of oxidative stress in α-amanitin-induced hepatotoxicityin an experimental mouse model

et al. 2017

View full text Add to dashboard Cite

Background/aim: This study aimed to evaluate oxidative stress markers of liver tissue in a mouse α-amanitin poisoning model with three different toxin levels. Materials and methods:The mice were randomly divided into Group 1 (control), Group 2 (0.2 mg/kg), Group 3 (0.6 mg/kg), and Group 4 (1.0 mg/kg). The toxin was injected intraperitoneally and 48 h of follow-up was performed before sacrifice.Results: Median superoxide dismutase activities of liver tissue in Groups 3 and 4 were significantly higher than in Group 1 (for both, P = 0.001). The catalase activity in Group 2 was significantly higher, but in Groups 3 and 4 it was significantly lower than in Group 1

show abstract

“…OPs are known to produce oxidative stress by generating free radicals and modifying the antioxidant defence system. Many studies have already indicated that enzymes associated with antioxidant defence mechanisms are altered under the infl uence of OPs, and that lipid peroxidation is one of the molecular mechanisms involved in OP-induced cytotoxicity (8,11,13,(29)(30)(31)(35)(36)(37)(38). Further supportive evidence comes from studies indicating diazinon-induced free radical damage to pancreatic B-cells as the cause of hyperglycaemia in animals (17,30).…”

Section: Figure 6 Insulin Release From Islets Of Langerhans Incubatedmentioning

confidence: 60%

Comparative Effects of Calcium Channel Blockers, Autonomic Nervous System Blockers, and Free Radical Scavengers On Diazinon-Induced Hyposecretion Of Insulin From Isolated Islets of Langerhans in Rats

Pourkhalili

Pournourmohammadi

Rahimi

et al. 2009

Archives of Industrial Hygiene and Toxicology

Self Cite

View full text Add to dashboard Cite

Hyperglycaemia has been observed with exposure to organophosphate insecticides. This study was designed to compare the effects of calcium channel blockers, alpha-adrenergic, beta-adrenergic, and muscarinic receptor blockers, and of free radical scavengers on insulin secretion from diazinon-treated islets of Langerhans isolated from the pancreas of rats using standard collagenase digestion, separation by centrifugation, and hand-picking technique. The islets were then cultured in an incubator at 37 °C and 5 % CO 2 . In each experimental set 1 mL of 8 mmol L -1 glucose plus 125 µg mL -1 or 625 µg mL -1 of diazinon were added, except for the control group, which received 8 mmol L -1 glucose alone. The cultures were then treated with one of the following: 30 µmol L -1 atropine, 100 µmol L -1 ACh + 10 µmol L -1 neostigmine, 0.1 µmol L -1 propranolol, 2 µmol L -1 nifedipine, 50 µmol L -1 phenoxybenzamine, or 10 µmol L -1 alphatocopherol. In all experiments, diazinon signifi cantly reduced glucose-stimulated insulin secretion at both doses, showing no dose dependency, as the average inhibition for the lower dose was 62.20 % and for the higher dose 64.38 %. Acetylcholine and alpha-tocopherol restored, whereas atropine potentiated diazinoninduced hyposecretion of insulin. Alpha-, beta-and calcium channel blockers did not change diazinoninduced effects. These fi ndings suggest that diazinon affects insulin secretion mainly by disturbing the balance between free radicals and antioxidants in the islets of Langerhans and by inducing toxic stress.

show abstract

Oxidative stress in acute human poisoning with organophosphorus insecticides; a case control study

Cited by 143 publications

References 14 publications

Protective Role of Vitamin C and Green Tea Extract on Malathion-Induced Hepatotoxicity and Nephrotoxicity in Rats

Protective Role of Vitamin C and Green Tea Extract on Malathion-Induced Hepatotoxicity and Nephrotoxicity in Rats

The role of oxidative stress in α-amanitin-induced hepatotoxicityin an experimental mouse model

Comparative Effects of Calcium Channel Blockers, Autonomic Nervous System Blockers, and Free Radical Scavengers On Diazinon-Induced Hyposecretion Of Insulin From Isolated Islets of Langerhans in Rats

Contact Info

Product

Resources

About