The Protective Effect of Vitamin E in Pyrethroid-induced Oxidative Stress in Rat Tissues

Kale, Manisha; Rathore, Nisha; John, Susan; Bhatnagar, Deepak; Nayyar, Shashi; Kothari, Vineeta

doi:10.1080/13590849961500

Cited by 11 publications

(9 citation statements)

References 2 publications

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“…Cypermethrin was also report to induce the level of MDA with a concomitant increase in ROS [19] . The increased level of MDA observed in ECM inhalation was also reported as a result of pyrethroid insecticides exposure by several authors [20][21][22][23][24] . The current value of SOD activity represent a significant decrease in ECM-intoxicated groups (p≤0.001).…”

Section: Discussionsupporting

confidence: 64%

Chronic toxicity of ectomethrin: A biochemical and histological study

Othman

Mahmoud

2019

Egyptian Journal of Histology

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Introduction: Ectomethrin (ECM) a synthetic pyrethroid, has broad spectrum use in agriculture, domestic and veterinary medical applications. Its prolonged and indiscriminate use has both acute and chronic toxicity in non-target species including humans. Aim of the work: To evaluate the toxic effects of ECM inhalation in rats, and its recovery after stopping the treatment. Materials and Methods: A total of forty Wistar male albino rats were divided into four groups. First group served as control group and received no treatment. Second group; ECM45 was administered 0.3 ml/kg/day of ECM daily by inhalation for 45 days. Third group; ECM90 group was administered the same ECM dose for 90 days. The forth group is the recovery group; Rec30 was administered the same dose of ECM by inhalation for 90 days, then the inhalation was stopped and the animals were left to recover without any treatment for another 30 days. At the end of the experiment, blood and tissue samples were obtained. Results: ECM-intoxication revealed significant alterations in the oxidative stress parameters, malondialdehyde and superoxide dismutase in all treated groups. However, these alterations were attenuated in the recovery group and tended to approach normal levels. Histopathologically, ECM-intoxication revealed dramatic changes in liver and lung tissues and induced minor changes in the heart. The liver showed ballooning degeneration, focal lymphocytic aggregation, pyknotic nuclei, dilated central vein, collapsed sinusoidal spaces, focal necrosis and vascular degeneration. The lung revealed marked respiratory inflammation and focal necrosis and the heart showed myocardial hypertrophy. The recovery group had less severe complications in investigated tissues. Conclusion: ECM inhalation resulted in severe biochemical and histological alterations that were attenuated after stopping inhalation.

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Section: Discussionsupporting

confidence: 64%

Chronic toxicity of ectomethrin: A biochemical and histological study

Othman

Mahmoud

2019

Egyptian Journal of Histology

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“…significant protection against the elevation of TBARS levels in cerebral and hepatic tissues, induced by cypermethrin (Giray et al, 2001). Pretreatment with Vitamin E reduced the LPO in cypermethrin and fenvalerate treated rats (Kale et al, 1999b). Studies show that fenugreek seeds have antioxidant properties.…”

Section: Discussionmentioning

confidence: 97%

“…The levels of TBARS decreased significantly and the activities of SOD, catalase, GPx and GST were close to the normal control. Earlier studies have shown that antioxidants play a protective role in CM induced toxicity by reducing the LPO and oxidative stress (Atehassin et al, 2005;Kale et al, 1999b). Pretreatment of rats with Vitamin E or allopurinol provided Comparing the retention time with those for standard flavonoids, the extract is found to contain -1-.Quercetin , 2-Vitexin , 3-Orientin , 4-Naringenin, 5-Diadzein, 6-Tricin.…”

Section: Discussionmentioning

confidence: 97%

Effect of some socio-economic activities on fish diversity of lagoon systems in Ogun waterside Local Government of Ogun State, Nigeria

Sushma¹,

Devasena²

2010

International Journal of Biological and Chemical Sciences

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Cypermethrin, a Type II pyrethroid pesticide is commonly used in agriculture and many other domestic applications for pest control. Studies have shown that cypermethrin induces lipid peroxidation and alters the antioxidant status in non-target organisms. Fenugreek, a source of several polyphenols and flavonoids is a potent antioxidant. Hence in the present study we have investigated the possible effect of germinated fenugreek extract supplementation in counteracting the cypermethrin induced oxidative stress in erythrocytes of rats. Male Wistar rats were treated with 25 mg/kg weight (1/10 LD 50 ) of cypermethrin and aqueous extract of germinated fenugreek (GFaq) (10%) for 60 days. Our results show that lipid peroxidation, an index of oxidative stress, significantly increased in circulation in cypermethrin-treated rats. The activities of SOD, CAT, GPx, GST in RBCs also decreased concomitantly in the cypermethrin treated rats. Treatment with aqueous extract of germinated fenugreek brought the values to near normal showing that fenugreek ameliorates cypermethrin-induced oxidative stress. HPLC analysis of the aqueous extract of germinated fenugreek showed the presence of flavonoids.

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“…Previous studies report the involvement of ROS in pyrethroid toxicity, in particular it increases lipid peroxidation and alters the antioxidant system in plasma membrane of heart cells [52,53].…”

Section: Discussionmentioning

confidence: 99%

Purine Bases Oxidation and Repair Following Permethrin Insecticide Treatment in Rat Heart Cells

2010

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Pollutants including insecticides have been recently reported to be a risk factor involved in various diseases. Permethrin, a member of the family of synthetic pyrethroids, is widely used as insecticide in agriculture and other domestic applications. To investigate possible cardiotoxicity, we had examined different concentrations of permethrin on the freshly isolated rat heart cells using the alkaline comet assay. A significant difference in % tail DNA between all concentrations of permethrin (5, 10, 20 microM) and vehicle (control) without enzymes and with Fpg-treated cells were measured. The results indicated that permethrin induced oxidative damage to purine bases in the heart cells. Pyrimidines oxidation was evaluated using Endonuclease III (Endo III), but the results did not reveal any significant changes. After permethrin exposure, cells were studied to evaluate their DNA repair capacity. A complete DNA repair at 10 and 20 microM was measured after 30 and 60 min of repair intervals. Significant change in plasma membrane fluidity at different depths of bilayer was measured following permethrin treatment. Membrane fluidity in the hydrophilic-hydrophobic region was reduced, while the hydrophobic inner resulted more fluid following permethrin treatment of heart cells. This work points to standardize conditions applicable to ex vivo cells following in vivo treatment in order to study the cardiotoxicity of insecticide.

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The Protective Effect of Vitamin E in Pyrethroid-induced Oxidative Stress in Rat Tissues

Cited by 11 publications

References 2 publications

Chronic toxicity of ectomethrin: A biochemical and histological study

Chronic toxicity of ectomethrin: A biochemical and histological study

Effect of some socio-economic activities on fish diversity of lagoon systems in Ogun waterside Local Government of Ogun State, Nigeria

Purine Bases Oxidation and Repair Following Permethrin Insecticide Treatment in Rat Heart Cells

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