Abstract
Childhood maltreatment (CM) is associated with an increased risk for the development of psychiatric and somatic disorders in later life. A potential link could be oxidative stress, which is defined as the imbalance between the amount of reactive oxygen species (ROS) and the neutralizing capacity of anti-oxidative defense systems. However, the findings linking CM with oxidative stress have been inconsistent so far. In this study, we aimed to further explore this association by investigating biological markers of DNA and lipid damage due to oxidation in a comprehensive approach over two study cohorts of postpartum women (study cohort I and study cohort II). The severity of CM experiences (maltreatment load) was assessed in both studies using the Childhood Trauma Questionnaire. In study cohort I (N = 30), we investigated whether CM was associated with higher levels of structural DNA damage in peripheral blood mononuclear cells (PBMC) by two methods that are highly sensitive for detecting nuclear DNA strand breaks (comet assay and γH2AX staining). In study cohort II (N = 117), we then assessed in a larger cohort, that was specifically controlled for potential confounders for oxidative stress measurements, two established serum and plasma biomarkers of oxidative stress, one representing oxidative DNA and RNA damage (8-hydroxy-2′-deoxyguanosine and 8-hydroxyguanosine; 8-OH(d)G) and the other representing lipid peroxidation (8-isoprostane). In study cohort I, the analyses revealed no significant main effects of maltreatment load on cellular measures of nuclear DNA damage. The analyses of peripheral oxidative stress biomarkers in study cohort II revealed a significant main effect of maltreatment load on free 8-isoprostane plasma levels, but not on total 8-isprostane plasma levels and 8-OH(d)G serum levels. Taken together, by combining different methods and two study cohorts, we found no indications for higher oxidative DNA damages with higher maltreatment load in postpartum women. Further research is needed to investigate whether this increase in free 8-isoprostane is a marker for oxidative stress or whether it is instead functionally involved in ROS-related signaling pathways that potentially regulate inflammatory processes following a history of CM.
Highlights
The experience of emotional, physical and/or sexual abuse, as well as emotional and/or physical neglect during childhood may cast a long shadow on adult health: A growing body of literature has shown that individuals with a history of Childhood maltreatment (CM) are at greater risk to develop both mental and physical disorders later in life [1]
In study cohort I (N = 30), we investigated whether CM was associated with higher levels of oxidative DNA damage in peripheral blood mononuclear cells (PBMC) by two methods that are highly sensitive for detecting nuclear DNA strand breaks
With regard to lipid peroxidation, we found that an increasing maltreatment load was significantly associated with a higher probability for increased plasma levels of free 8-isoprostane, but not with plasma levels of total 8-isoprostane in study cohort II
Summary
The experience of emotional, physical and/or sexual abuse, as well as emotional and/or physical neglect during childhood (i.e., childhood maltreatment [CM]) may cast a long shadow on adult health: A growing body of literature has shown that individuals with a history of CM are at greater risk to develop both mental and physical disorders later in life [1]. Accumulating research supports the hypothesis that CM is biologically embedded and exerts a long-lasting influence on stress-responsive systems [2, 3], research elucidating the causal pathways underlying the association of CM with adult health outcomes is sparse The research investigating this potential link focuses more and more on oxidative stress, which is defined as the imbalance between the amount of reactive oxygen species (ROS) and the neutralizing capacity of anti-oxidative defense systems [4]. While the comet assay is a direct measure for DNA single and double strand breaks [9], γH2AX plays a role in signaling DNA double strand breaks and initiating their repair by supporting the recruitment and localization of DNA repair proteins [10] If such oxidative damages accumulate over time, they may have detrimental effects both at the cellular and at the systemic level [6, 11]
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