The Potential Role of Thioctic Acid in the Attenuation of Doxorubicin Induced-Cardiotoxicity

Hayder M Al kuraishy¹*, Reem G Hussein² and Ali I Al Gareeb¹

Received: May 21, 2018;   Published: May 24, 2018

DOI: 10.32474/OAJOM.2018.01.000120

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Abstract

During 1950s in Italy a soil sample was isolated and found new strains of Streptomyces peucetius bacteria from which a new antibiotic was extracted with potent effect against murine tumors, this antibiotic named daunorubicin [1]. In 1960s, a clinical trial was done on the drug and result a successful in treating acute leukemia and lymphoma, and finally a new antibiotic was discovered which named adriamycin which change to doxorubicin. Doxorubicin has a potent antitumor activity more than daunorubicin with a higher therapeutic index [2]. In 1967 the cardiotoxicity due to danurubicin was approved, the greatest risk of doxorubicin-induced toxicity is cardiotoxicity, so administration of doxorubicin should be doselimited [3]. Doxorubicin changes the structure and function of cardiomyocytes, the genes that cause this are the brain natriuretic peptide (BNP) and atrial natriuretic peptide (ANP) which are highly expressed in doxorubicin-induce cardiotoxicity, so; these two genes are responsible for cardiac hypertrophy [4]. The molecular mechanism behind this event involves formation of oxygen free radicals and iron oxidation. Since doxorubicin known to affect multiple biomarkers, the assessment of troponins and specific natriuretic peptides (pro BNP and DNP) is believed to predict doxorubicin-induced cardiotoxicity in early stages [5].

Introduction| Mechanism of Doxorubicin-Induced Cardiotoxicity| Conclusion| References|