Literature DB >> 26721193

Doxorubicin toxicity changes myocardial energy metabolism in rats.

Rong Wu1, Hui-Lin Wang1, Hai-Lun Yu2, Xiao-Hua Cui1, Meng-Ting Xu1, Xu Xu2, Jian-Ping Gao3.   

Abstract

BACKGROUND: Doxorubicin (DOX) is an antitumor antibiotics used against malignancies. But its toxicity limits the therapy of DOX.
OBJECTIVE: The purpose of this study was to evaluate DOX toxicity and the alteration of energy metabolism after short term and long term treatment.
METHODS: Male Sprague-Dawley rats were randomly assigned to four groups: Short term control group, short term DOX treatment group, long term control group and long term DOX treatment group. In short term treated group, rats were injected with DOX i.p. at a dose of 2.5 mg/kg every 48 h for six equal injections. In long term, treated group, rats were tail-intravenously injected with DOX at a dose of 3 mg/kg once a week for four weeks. At the end of the experiment, histopathological changes, general blood biomarkers, endogenous antioxidant enzymes, cardiac energy metabolism and related mRNA expression of AMPK signal pathway were determined.
RESULTS: DOX induced prominent oxidative stress, a higher mortality rate, histological and ECG changes, obvious cardiac hypertrophy, acute cardiac damage and cardiac energy impairment in short term treatment rats. In long term treatment rats, DOX caused serious nephropathy and systolic dysfunction, terrible cardiac energy impairment, clear alteration of substrate utilization and AMPK signal pathway.
CONCLUSION: DOX treatment can induce different damages after short term and long term treatment. In short term treatment group, rats experienced a terrible mortality rate about 40%, the acute cardiac damage, cardiac energy impairment and an early heart failure which are potential connected with reduction of glucose utilization. In the long term treatment group, serious nephropathy and obvious changes of mRNA expressions of AMPK signal pathway were observed. Meanwhile, the serious cardiac energy impairment and substrate utilization alteration denote an obviously heart failure. This study could be helpful to develop therapy strategies of DOX complications for clinical application.
Copyright © 2015 Elsevier Ireland Ltd. All rights reserved.

Entities:  

Keywords:  AMPKα2; Doxorubicin; Myocardial energy metabolism; Toxicity

Mesh:

Substances:

Year:  2015        PMID: 26721193     DOI: 10.1016/j.cbi.2015.12.010

Source DB:  PubMed          Journal:  Chem Biol Interact        ISSN: 0009-2797            Impact factor:   5.192


  8 in total

1.  The Prophylactic Effect of Pinocembrin Against Doxorubicin-Induced Cardiotoxicity in an In Vitro H9c2 Cell Model.

Authors:  Nonhlakanipho F Sangweni; Malebogo Moremane; Sylvia Riedel; Derick van Vuuren; Barbara Huisamen; Lawrence Mabasa; Reenen Barry; Rabia Johnson
Journal:  Front Pharmacol       Date:  2020-08-05       Impact factor: 5.810

2.  Cardioprotective effects of sodium thiosulfate against doxorubicin-induced cardiotoxicity in male rats.

Authors:  Maryam Shekari; Narges Khalilian Gortany; Mina Khalilzadeh; Alireza Abdollahi; Homanaz Ghafari; Ahmad Reza Dehpour; Mahmoud Ghazi-Khansari
Journal:  BMC Pharmacol Toxicol       Date:  2022-05-25       Impact factor: 2.605

Review 3.  Autophagy and mitophagy in the context of doxorubicin-induced cardiotoxicity.

Authors:  Navid Koleini; Elissavet Kardami
Journal:  Oncotarget       Date:  2017-07-11

4.  Advantages of prophylactic versus conventionally scheduled heart failure therapy in an experimental model of doxorubicin-induced cardiomyopathy.

Authors:  Mária Lódi; Dániel Priksz; Gábor Áron Fülöp; Beáta Bódi; Alexandra Gyöngyösi; Lilla Nagy; Árpád Kovács; Attila Béla Kertész; Judit Kocsis; István Édes; Zoltán Csanádi; István Czuriga; Zoltán Kisvárday; Béla Juhász; István Lekli; Péter Bai; Attila Tóth; Zoltán Papp; Dániel Czuriga
Journal:  J Transl Med       Date:  2019-07-19       Impact factor: 5.531

Review 5.  The Role of AMPK Activation for Cardioprotection in Doxorubicin-Induced Cardiotoxicity.

Authors:  Kerstin N Timm; Damian J Tyler
Journal:  Cardiovasc Drugs Ther       Date:  2020-04       Impact factor: 3.727

Review 6.  Regulated cell death pathways in doxorubicin-induced cardiotoxicity.

Authors:  Effimia Christidi; Liam R Brunham
Journal:  Cell Death Dis       Date:  2021-04-01       Impact factor: 8.469

7.  Lapatinib induces mitochondrial dysfunction to enhance oxidative stress and ferroptosis in doxorubicin-induced cardiomyocytes via inhibition of PI3K/AKT signaling pathway.

Authors:  Lei Sun; Hua Wang; Dan Xu; Shanshan Yu; Lin Zhang; Xiaopeng Li
Journal:  Bioengineered       Date:  2022-01       Impact factor: 3.269

8.  Toxicity and Safety Evaluation of Doxorubicin-Loaded Cockleshell-Derived Calcium Carbonate Nanoparticle in Dogs.

Authors:  Abubakar Danmaigoro; Gayathri Thevi Selvarajah; Mohd Hezmee Mohd Noor; Rozi Mahmud; Md Zuki Abu Bakar
Journal:  Adv Pharmacol Sci       Date:  2018-06-24
  8 in total

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