Research Article

Val16Ala-SOD2 polymorphism modulates hypothalamic-pituitary-adrenal axis molecules and BDNF levels in healthy adults under no psychological stress

Published: May 27, 2020
Genet. Mol. Res. 19(2): GMR18586 DOI: https://doi.org/10.4238/gmr18586
Cite this Article:
I.Eda Cruz Jung, T. Duarte, I.B.M. da Cruz, B. .O.Turra, B. Chitolina, J.R. Motta, M.A.E. Montano, V. .F.Azzolin, E.E. Ribeiro, M.M.M.F. Duarte, F. Barbisan (2020). Val16Ala-SOD2 polymorphism modulates hypothalamic-pituitary-adrenal axis molecules and BDNF levels in healthy adults under no psychological stress. Genet. Mol. Res. 19(2): GMR18586. https://doi.org/10.4238/gmr18586
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Abstract

Chronic psychological stress alters the hypothalamic–pituitary–adrenal axis (HPA-axis), triggering chronic oxidative-inflammatory states that are associated with physical and psychiatric conditions. However, it is not clear if basal oxidative-inflammatory states triggered by genetic variation affect the HPA-axis by altering cortisol, adrenocorticotropic hormone (ACTH) and dehydroepiandrosterone sulfate (DHEA-S) levels. Humans have a single nucleotide polymorphism (SNP) found in manganese-dependent superoxide dismutase (Val16Ala-SOD2, rs4880), which has two alleles (V and A) which affect the basal efficacy of SOD2 antioxidant enzyme in the mitochondria. The VV-genotype, which presents low SOD2-efficacy, has been associated with chronic inflammatory states, as well as higher risk of depression and self-reported psychological stress. Therefore, basal oxidative imbalance could have some influence on modulation of HPA-axis physiology. We tested this hypothesis comparing morning blood levels of cortisol, ACTH and DHEA-S and other biochemical markers in 90 healthy adult university students previously genotyped for the SOD2-SNP (30 volunteers for each genotype, 26.5 ± 8.7 years old). Only volunteers who self-reported no perception of psychological stress were included in the study. The VV group had higher morning cortisol and ACTH, and lower DHEA-S and brain-derived neurotrophic factor (BDNF) than A-allele subjects. These results indicate some influence of S-imbalance on modulation of this molecule. Therefore, we suggest that genetically controlled pro-oxidative and inflammatory states could modulate physiological markers for stress and neurogenesis.

 

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