Protective effect of thymoquinone and aminoguanidine against paraquat induced cardiotoxicity: possible role of nitric oxide synthase
MJFCT-Mansoura Journal of Forensic Medicine and Clinical Toxicology. 2001; 9 (1): 53-66
Dans Anglais
| IMEMR
| ID: emr-57771
ABSTRACT
Paraquat induced cardiotoxicity is due to oxidative damage produced by free radicals generations. The present study was undertaken to investigate whether inhibition of nitric oxide synthase by aminoguanidine, an inhibitor of nitric oxide [NO] synthase, can protect against paraquat-induced cardiomyopathy and to investigate whether thymoquinone, a potent superoxide radical scavenger, can protect against paraquat-induced cardiotoxicity in rats. Administration of paraquat, 50 mg/kg I P induce cardiotoxicity as indicated by a significant increase in the level of lipid peroxide, significant depletion of the reduced glutathione in heart tissue and significant decrease in the activity of antioxidant enzymes glutathione peroxidase [EC 1.11.1.9] and catalase [EC 1.11.1.6]. Oral administration of aminoguanidine [50 mg/100 mL in drinking water] or thymoquinone [5 mg/100 mL in drinking water] for 5 days before 2 days after single injection of paraquat [50 mg/kg, IP] leads to return of lactate dehydrogenase [EC 1.1.1.27] and creatine phosphokinase [EC 2.7.3.2] to normal values
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Indice:
Méditerranée orientale
Sujet Principal:
Rats
/
Système cardiovasculaire
/
Catalase
/
Stress oxydatif
/
Nitric oxide synthase
/
Agents protecteurs
/
Creatine kinase
/
Lactate dehydrogenases
/
Glutathione peroxidase
Limites du sujet:
Animaux
langue:
Anglais
Texte intégral:
Mansoura J. Forensic Med. Clin. Toxicol.
Année:
2001
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