Toxicological evaluation of subchronic use of pioglitazone in mice

نویسندگان

  • Ayman El-Meghawry El-Kenawy Department of Pathology, College of Medicine, Taif University, Taif, KSA|Department of Molecular Biology, GEBRI, University of Sadat City, Egypt
  • Hosam-Eldin Hussein Osman Department of Anatomy, College of Medicine, Taif University, Al-Azhar University, Taif, KSA
  • Said Said Elshama Department of Forensic Medicine and Clinical Toxicology, College of Medicine, Taif University, Suez Canal University, Taif, KSA
چکیده مقاله:

Objective(s): Pioglitazone (Actos) is one of the most controversial recent oral antidiabetic drugs. It was originally authorized in the European Union in 2000, and approved as an oral monotherapy for overweight second type of diabetic patients in 2002. It belongs to the thiazolidinedione group which some of its members have been withdrawn from the market due to the hepatotoxicity or cardiotoxicity effects.This studyinvestigates sub-chronic use of pioglitazone induced toxicity in mice by the assessment of renal and liver function tests, cardiac enzymes, and some hematological indices with histological changes of liver, kidney, heart, and bladder. Materials and Methods: 120 albino mice were divided into four groups; 30 in each. The first group (control) received water, second (diabetic) group received alloxan only, while the third and the fourth groups received alloxan with 200 and 400 mg/kg/day of pioglitazone, respectively for 90 days. Results: Prolonged use of pioglitazone induced significant abnormalities of hepatic, renal, and cardiac biomarkers and some hematological indices associated with histopathological changes in the liver, kidney, heart, and bladder that increased based on administered dose. Conclusion: Subchronic use of pioglitazone leads to hepatic, renal, cardiac, hematological, and bladder affection depending on the applied dose.

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toxicological evaluation of subchronic use of pioglitazone in mice

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عنوان ژورنال

دوره 19  شماره 7

صفحات  712- 719

تاریخ انتشار 2016-07-01

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