The effects of vitamin E on the erythrocyte and heart tissue cholinesterase, NO and MDA levels in the acute organophosphate toxicity

We have examined the effect of subchronic methidathion (MD) administration on heart damage, and have evaluated possible ameliorating effects of a combination of vitamins E and C against MD toxicity. The experimental groups were: control group, rats treated with 5 mg/kg MD and rats treated with 5 mg/kg body weight MD plus vitamin E and vitamin C (MD+Vit). The groups were given MD by gavage 5 days a week for four weeks at a dose level of 5 mg/kg/day (MD and MD+Vit) by using corn oil as the vehicle. Vitamin E and vitamin C were injected at doses of 50 mg/kg i.m. and 20 mg/kg i.p., respectively, after the treatment with MD in the MD+Vit group. The levels of malondialdehyde (MDA) were determined in the heart tissue, and the levels of cardiac troponin I (TnI) in serum. An autoanalyser was used to determine the serum activities of cholinesterase (ChE). Histopathological examination was carried out in the heart tissue. MDA significantly increased in the MD group as compared to controls (P <0.01). When MD was given concurrently with vitamins E and C, the increase in MDA was significantly less (P <0.01). ChE activity significantly decreased in the MD group as compared to controls (P <-0.01). When MD was given concurrently with vitamins E and C, the decrease in ChE activity was significantly higher (P <-0.05). The serum TnI levels significantly increased in the MD group as compared to controls (P <-0.01). When MD was given concurrently with vitamins E and C, the increase in the serum TnI was significantly less (P <-0.01). MD caused the diffuse loss of striation and myocytolysis of the cardiomyocytes, whereas the combination of vitamins E and C caused a significant decrease in these effects of MD. In conclusion, subchronic MD administration caused heart damage and, in addition, treatment with a combination of vitamins E and C after the administration of MD reduced heart damage caused by MD.

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α-Tocopherol mediated amelioration of camptothecin-induced free radical damage to avert cardiotoxicities

Human & Experimental Toxicology ◽

10.1177/0960327114533577 ◽

2014 ◽

Vol 34 (4) ◽

pp. 380-389 ◽

Cited By ~ 4

Author(s):

K Singh ◽

M Bhori ◽

T Marar

Keyword(s):

Antioxidant Enzymes ◽

Free Radical ◽

Vitamin E ◽

Protective Efficacy ◽

Antineoplastic Agent ◽

Lipid Peroxides ◽

Heart Tissue ◽

Free Radical Scavengers ◽

Cancer Therapies ◽

Free Radical Damage

Reactive oxygen species (ROS) such as [Formula: see text], hydrogen peroxide, and OH− are highly toxic to cells. Cellular antioxidant enzymes and free radical scavengers normally protect a cell from toxic effects of ROS. However, when generation of ROS overtakes the antioxidant defense of the cells, it leads to various pathological conditions. The present study investigated the protective efficacy of α-tocopherol on the peroxidative damage and abnormal antioxidant levels in the myocardial tissue of camptothecin (CPT), administered at the dosage of 6 mg/kg/day in male Wistar rats. CPT-administered rats showed significant increase ( p < 0.001) in lipid peroxidation and abnormal changes in the activities/levels of antioxidant enzymes (catalase, superoxide dismutase, glutathione peroxidase, glutathione reductase, glutathione S-transferase) and nonenzymic antioxidants (reduced glutathione and vitamin E). Alterations in the levels of tissue alkaline phosphatase, lactate dehydrogenase ( p < 0.01), alanine transaminase ( p < 0.001), and aspartate transaminase ( p < 0.001) were also observed in CPT-treated rats. In contrast, rats pretreated with α-tocopherol showed significant revision of elevated levels of lipid peroxides and abnormal antioxidant enzyme activity suggesting the ameliorative property of vitamin E. Histopathological alterations in the heart tissue observed after CPT administration were also protected in animals that were pretreated with vitamin E. Based on our results, we conclude that supplementation of vitamin E may improve the efficacy of standard and experimental cancer therapies by subsiding the toxic effect of the antineoplastic agent.

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Cardioprotective effect of lemon grass as evidenced by biochemical and histopathological changes in experimentally induced cardiotoxicity

Human & Experimental Toxicology ◽

10.1177/0960327110386391 ◽

2010 ◽

Vol 30 (8) ◽

pp. 1073-1082 ◽

Cited By ~ 9

Author(s):

K. Gayathri ◽

KS Jayachandran ◽

Hannah R Vasanthi ◽

G. Victor Rajamanickam

Keyword(s):

Vitamin E ◽

Myocardial Necrosis ◽

Heart Tissue ◽

Cardioprotective Effect ◽

Albino Rats ◽

Enzymatic Antioxidants ◽

Group V ◽

Lemon Grass ◽

Heart Homogenate ◽

Wistar Albino Rats

Isoproterenol is a synthetic catecholamine found to cause toxicity leading to severe stress in the myocardium of experimental animals. The aim of the present study is to evaluate the cardioprotective effect of Cymbopogon citratus, which is used as a culinary item and commonly known as lemon grass (LG), in isoproterenol-induced cardiotoxicity. Male Wistar albino rats were segregated into five different groups as follows. Groups I and II rats were treated with vehicle. Groups III and IV rats were treated with 100 and 200 mg/kg b.wt. of LG. Group V with 100 mg/kg b.wt. of vitamin E. Myocardial necrosis was induced in Groups II, III, IV and V on 58th and 59th day using isoproterenol at a dose of 85 mg/kg twice at 24-hour interval. Animals were sacrificed on the 60 th day. LG pretreatment exhibited cardioprotective activity as evidenced by decreased activity of cardiac markers in serum and increased the same in heart homogenate (p < 0.05). LG administration decreased the toxic events of lipid peroxidation (TBARS) in both serum and heart tissue, by increasing the level of enzymatic antioxidants and non-enzymatic antioxidants significantly in both heart homogenate and serum sample (p < 0.05). The histopathological observations also revealed that the cardioprotective effect of LG extract was observed at a dose of 200 mg/kg b.wt. The results of the present study reveal that LG is cardioprotective and antilipid peroxidative by increasing various antioxidants at a dose of 200 mg/kg b.wt., which is comparable with that of vitamin E.

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