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AMELIORATIVE EFFECT OF GALLIC ACID ON DOXORUBICIN INDUCED CARDIOTOXICITY IN ADULT WISTAR RATS
Author(s) -
Adejumobi Olumuyiwa A,
Orotusin Oyetola,
Oyagbemi Ademola,
Adedapo Adeolu,
Olaogun Charles,
Omóbòwálé Temidayo Olutayo
Publication year - 2016
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.30.1_supplement.960.2
Subject(s) - gallic acid , cardiotoxicity , glutathione , lactate dehydrogenase , pharmacology , doxorubicin , superoxide dismutase , chemistry , oxidative stress , toxicity , catalase , histopathology , antioxidant , biochemistry , medicine , chemotherapy , enzyme , pathology
Doxorubicin is a potent antineoplastic anthracycline drug however, its use is greatly limited by its toxic side effects which occurs by formation of reactive oxygen species that disruption of cell function. This present study was conducted to assess the possible cardioprotective effect of gallic acid against doxorubicin‐ induced cardiotoxicity in rats. In this study, sixty (60) male Wistar rats were divided into six groups. Group A was the control. Group B rats was intoxicated with Doxorubicin (Dox) at 15 mg/kg body weight i.p. Group C pre‐treated with 60 mg/kg Gallic Acid (GA) orally for 7 days prior to administration of Dox 15 mg/kg, Group D pre‐treated with 120 mg/kg Gallic Acid (GA) orally for 7 days prior to administration of Dox 15 mg/kg, Group E received 60 mg/kg Gallic Acid (GA) orally alone for 7 days and Group F received 120 mg/kg Gallic Acid (GA) orally alone for 7 days. The parameters of study were cardiac antioxidant status, serum biomarker of cardiac damage and electrocardiography measurements. Exposure of rats to doxorubicin led to a significant (p < 0.05) decrease in cardiac glutathione peroxadise (GPx), glutathione‐S‐transferase (GST), reduced glutathione (GSH) content, superoxide dismutase (SOD) and catalase (CAT) activity. Similarly, a significant (p < 0.05) increase in protein thiol was recorded in doxorubicin treated rats while it was reduced in those pre‐treated with GA. Dox also caused elevation of Creatinine kinase‐muscle brain (CK‐MB) and Lactate Dehydrogenase (LDH). Histopathology of rats exposed to Dox showed focal areas of infiltration by inflammatory cells and degeneration of myofibres. Electrocardiography results showed a significant decrease in heart rate; increase in P wave duration, R‐amplitude, PR interval, QRS and QT‐segment prolongation. Pre‐treatment with GA significantly alleviated Dox associated ECG abnormalities, restored the antioxidant enzyme and decreased serum Creatinine kinase‐muscle brain CK‐MB and LDH. However, administration of GA alone in a set of groups led to a significant prolongation of QT interval which could predispose to the potentially fatal ventricular tachycardia, torsades de pointes . All these findings confirm the efficacy of GA against Dox induced cardiotoxicity but caution must be taken in its use. Support or Funding Information None