مرکز اطلاعات علمی Scientific Information Database (SID) - Trusted Source for Research and Academic Resources

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Information Journal Paper

Title

EFFECTS OF ENZYME INDUCTION AND/OR GLUTATHIONE DEPLETION ON METHIMAZOLE-INDUCED HEPATOTOXICITY IN MICE AND THE PROTECTIVE ROLE OF N-ACETYLCYSTEINE

Pages

  21-28

Abstract

 Purpose: METHIMAZOLE is the most convenient drug used in the management of hyperthyroid patients. However, associated with its clinical use is HEPATOTOXICITY as a life threatening adverse effect. The exact mechanism of METHIMAZOLE-induced HEPATOTOXICITY is still far from clear and no protective agent has been developed for this toxicity.Methods: This study attempts to evaluate the HEPATOTOXICITY induced by METHIMAZOLE at different experimental conditions in a MICE model. METHIMAZOLE-induced HEPATOTOXICITY was investigated in different situations such as enzyme-induced and/or GLUTATHIONE-depleted animals.Results: METHIMAZOLE (100 mg/kg, i.p) administration caused HEPATOTOXICITY as revealed by increase in serum alanine aminotransferase (ALT) activity as well as pathological changes of the liver. Furthermore, a significant reduction in hepatic GLUTATHIONE content and an elevation in lipid peroxidation were observed in METHIMAZOLE-treated MICE. Combined administration of L-buthionine sulfoximine (BSO), as a GLUTATHIONE depletory agent, caused a dramatic change in METHIMAZOLE-induced HEPATOTOXICITY characterized by hepatic necrosis and a severe elevation of serum ALT activity. ENZYME INDUCTION using phenobarbital and/or b-naphtoflavone beforehand, deteriorated METHIMAZOLE-induced HEPATOTOXICITY in MICE. N-acetyl cysteine (300 mg/kg, i.p) administration effectively alleviated hepatotoxic effects of METHIMAZOLE in both GLUTATHIONE-depleted and/or enzyme-induced animals.Conclusion: The severe hepatotoxic effects of METHIMAZOLE in GLUTATHIONE-depleted animals, reveals the crucial role of GLUTATHIONE as a cellular defense mechanism against METHIMAZOLE-induced HEPATOTOXICITY. Furthermore, the more hepatotoxic properties of METHIMAZOLE in enzyme-induced MICE, indicates the role of reactive intermediates in the HEPATOTOXICITY induced by this drug. The protective effects of N-ACETYLCYSTEINE could be attributed to its radical/reactive metabolite scavenging, and/or antioxidant properties as well as GLUTATHIONE replenishment activities.

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    • Cite

    APA: Copy

    HEIDARI, REZA, BABAEI, HOSSEIN, ROSHANGAR, LEILA, & EGHBAL, MOHAMMAD ALI. (2014). EFFECTS OF ENZYME INDUCTION AND/OR GLUTATHIONE DEPLETION ON METHIMAZOLE-INDUCED HEPATOTOXICITY IN MICE AND THE PROTECTIVE ROLE OF N-ACETYLCYSTEINE. ADVANCED PHARMACEUTICAL BULLETIN, 4(1), 21-28. SID. https://sid.ir/paper/331733/en

    Vancouver: Copy

    HEIDARI REZA, BABAEI HOSSEIN, ROSHANGAR LEILA, EGHBAL MOHAMMAD ALI. EFFECTS OF ENZYME INDUCTION AND/OR GLUTATHIONE DEPLETION ON METHIMAZOLE-INDUCED HEPATOTOXICITY IN MICE AND THE PROTECTIVE ROLE OF N-ACETYLCYSTEINE. ADVANCED PHARMACEUTICAL BULLETIN[Internet]. 2014;4(1):21-28. Available from: https://sid.ir/paper/331733/en

    IEEE: Copy

    REZA HEIDARI, HOSSEIN BABAEI, LEILA ROSHANGAR, and MOHAMMAD ALI EGHBAL, “EFFECTS OF ENZYME INDUCTION AND/OR GLUTATHIONE DEPLETION ON METHIMAZOLE-INDUCED HEPATOTOXICITY IN MICE AND THE PROTECTIVE ROLE OF N-ACETYLCYSTEINE,” ADVANCED PHARMACEUTICAL BULLETIN, vol. 4, no. 1, pp. 21–28, 2014, [Online]. Available: https://sid.ir/paper/331733/en

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