alexa Palm Fruit Juice Mitigates AZT Mitochondrial Genotoxici
ISSN 2155-6113

Journal of AIDS & Clinical Research
Open Access

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Research Article

Palm Fruit Juice Mitigates AZT Mitochondrial Genotoxicity and Dose- Dependent Cytotoxicity

Osborne AE1, Sanchez JA1*, Solomon M2, Stopa A1, Wangh LJ1, Sambanthamurthi R3 and Hayes KC1

1Department of Biology, Brandeis University, Waltham, MA, 02454, USA

2Molecular Pharmacology and Chemistry, Sloan-Kettering Institute, New York, NY 10065, USA

3Malaysian Palm Oil Board, Kajang, Selangor, Malaysia

*Corresponding Author:
Sanchez JA
Department of Biology
Brandeis University
Waltham, MA, 02454, USA
Tel: 1-781-736-3111
Fax: 1-781-736-3107
E-mail: [email protected]

Received date: September 18, 2014; Accepted date: December 16, 2014; Published date: December 20, 2014

Citation: Osborne AE, Sanchez JA, Solomon M, Stopa A, Wangh LJ, et al. (2014) Palm Fruit Juice Mitigates AZT Mitochondrial Genotoxicity and Dose-Dependent Cytotoxicity. J AIDS Clin Res 5:400. doi:10.4172/2155-6113.1000400

Copyright: © 2014 Osborne AE, et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.

 

Abstract

Chronic use of 3′-Azido-3′-deoxythymidine (AZT) to treat HIV/AIDS causes mitochondrial dysfunction and the accumulation of mitochondrial mutations. These toxicities have been attributed to increased oxidative damage, among other mechanisms. Palm fruit juice (PFJ), also known as oil palm phenolics (OPP), is a water soluble byproduct of oil extraction from the fruit of the oil palm (Elaeis guineensis) that is rich in antioxidants and other phytochemicals. The capacity of PFJ to mitigate AZT mitochondrial genotoxicity (mutagenesis) as well as dosedependent cytotoxicity were measured in cultured HepG2 cells. In the presence of PFJ, AZT-induced mutations were 35% the number of mutations observed in samples treated with AZT alone in the three regions of the mitochondrial genome examined (HV2, CO2, and ND1). Co-treatment with PFJ increased cell survival in the presence of increasing doses of AZT by up to 350%. These effects were not due to degradation or inactivation of AZT by PFJ. The discovery of the mitigating effects of PFJ provides a potential means of ameliorating AZT-induced mutations and possibly other long-term negative side effects of long-term AZT use.

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