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Implementing a new variant load model to investigate the role of mtDNA in oxidative stress and inflammation in a bi-ethnic cohort: the SABPA study

Lookup NU author(s): Dr Joanna Elson

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Abstract

© 2019, © 2019 Informa UK Limited, trading as Taylor & Francis Group. Mitochondrial DNA (mtDNA) variation has been implicated in several common complex and degenerative diseases, including cardiovascular disease. Inflammation is seen as part of many of these conditions. Mitochondria feature in inflammatory pathways and it has been suggested that mtDNA variation or released mtDNA might be important in this phenomenon. To determine if mtDNA is involved in the mechanisms leading up to cardiovascular disease, we investigated the role of these variants in seven indicators of oxidative stress and inflammation. This study was done in participants of the Sympathetic Activity and Ambulatory Blood Pressure in Africans (SABPA) cohort, a South African bi-ethnic cohort (N = 363). We applied a variant load hypothesis, which is an alternative approach to, and moves away from the classic haplogroup association approaches, to evaluate the cumulative effect of non-synonymous mtDNA variants on measurements of serum peroxides, nitric oxide metabolites, 8-hydroxy-deoxyguanosine, thiobarbituric acid reactive substances, whole blood reduced glutathione, C-reactive protein, and tumor necrosis factor alpha. We found no significant relationships between non-synonymous mtDNA variants and the seven biochemical parameters investigated here. Non-synonymous mtDNA variants are unlikely to impact on disease in this cohort, to an appreciable or measurable extent.


Publication metadata

Author(s): Venter M, Malan L, Elson JL, van der Westhuizen FH

Publication type: Article

Publication status: Published

Journal: Mitochondrial DNA Part A: DNA Mapping, Sequencing, and Analysis

Year: 2019

Volume: 30

Issue: 3

Pages: 440-447

Online publication date: 18/01/2019

Acceptance date: 31/10/2018

ISSN (print): 2470-1394

ISSN (electronic): 2470-1408

Publisher: Taylor and Francis Ltd

URL: https://doi.org/10.1080/24701394.2018.1544248

DOI: 10.1080/24701394.2018.1544248


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