Social Stress-Induced Oxidative DNA Damage Is Related to Prospective Cardiovascular Risk
Psychosocial stress increases cardiovascular risk, which coincides with enhanced oxidative DNA damage. Increased sympathetic tone-related catecholamine release causes oxidative stress, which contributes to catecholamine-related cardiotoxicity. Therefore, we tested the hypothesis whether acute psycho...
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| Format: | Article |
| Language: | English |
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MDPI AG
2020-11-01
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| Series: | Journal of Clinical Medicine |
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| Online Access: | https://www.mdpi.com/2077-0383/9/11/3783 |
| _version_ | 1797547046860750848 |
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| author | Christiane Waller Dae-Sup Rhee Michael Gröger Manuela Rappel Tanja Maier Markus Müller Edit Rottler Katharina Nerz Christopher Nerz Sebastian Brill Horst-Peter Becker Peter Radermacher |
| author_facet | Christiane Waller Dae-Sup Rhee Michael Gröger Manuela Rappel Tanja Maier Markus Müller Edit Rottler Katharina Nerz Christopher Nerz Sebastian Brill Horst-Peter Becker Peter Radermacher |
| author_sort | Christiane Waller |
| collection | DOAJ |
| description | Psychosocial stress increases cardiovascular risk, which coincides with enhanced oxidative DNA damage. Increased sympathetic tone-related catecholamine release causes oxidative stress, which contributes to catecholamine-related cardiotoxicity. Therefore, we tested the hypothesis whether acute psychosocial stress induces oxidative DNA damage, its degree being related to the cardiovascular risk profile and depending on the sympathetic stress response. After assessment of the prospective cardiovascular Münster score (PROCAM) to determine the risk of acute myocardial infarction, 83 male and 12 female healthy volunteers underwent the Trier social stress test for groups (TSST-G). Heart rate variability was quantified by measuring the standard deviation (SDNN) and root mean square of successive differences (RMSSD) between normal-to-normal inter-beat intervals. Salivary α-amylase (sAA) activity was assessed as a surrogate for noradrenaline plasma concentrations. Oxidative DNA damage was determined using whole-blood single-cell gel electrophoresis (“tail moment” in the “comet assay”). A total of 33 subjects presented with a prospective risk of myocardial infarction (risk+) vs. 59 subjects without risk (risk-). The TSST-G stress significantly increased blood pressure, heart rate, and sAA in both groups, while oxidative DNA damage was only increased in the risk+ group. Immediately after the TSST-G, the “tail moment” showed significant inverse linear relations with both SDNN and RMSSD. Acute psychosocial stress may cause oxidative DNA damage, the degree of which is directly related to the individual cardiovascular risk profile and depends on the stress-induced increase in the sympathetic tone. |
| first_indexed | 2024-03-10T14:37:49Z |
| format | Article |
| id | doaj.art-5778729a5b1f4b7e8450bbc09ac0f9fc |
| institution | Directory Open Access Journal |
| issn | 2077-0383 |
| language | English |
| last_indexed | 2024-03-10T14:37:49Z |
| publishDate | 2020-11-01 |
| publisher | MDPI AG |
| record_format | Article |
| series | Journal of Clinical Medicine |
| spelling | doaj.art-5778729a5b1f4b7e8450bbc09ac0f9fc2023-11-20T22:00:59ZengMDPI AGJournal of Clinical Medicine2077-03832020-11-01911378310.3390/jcm9113783Social Stress-Induced Oxidative DNA Damage Is Related to Prospective Cardiovascular RiskChristiane Waller0Dae-Sup Rhee1Michael Gröger2Manuela Rappel3Tanja Maier4Markus Müller5Edit Rottler6Katharina Nerz7Christopher Nerz8Sebastian Brill9Horst-Peter Becker10Peter Radermacher11Klinik für Psychosomatische Medizin und Psychotherapie, Universitätsklinik der Paracelsus Medizinischen Privatuniversität, 90419 Nürnberg, GermanyKlinik für Psychosomatische Medizin und Psychotherapie, Universitätsklinikum, 89081 Ulm, GermanyInstitut für Anästhesiologische Pathophysiologie und Verfahrensentwicklung, Universitätsklinikum, 89081 Ulm, GermanyKlinik für Psychosomatische Medizin und Psychotherapie, Universitätsklinikum, 89081 Ulm, GermanyKlinik für Psychosomatische Medizin und Psychotherapie, Universitätsklinikum, 89081 Ulm, GermanyKlinik für Psychosomatische Medizin und Psychotherapie, Universitätsklinik der Paracelsus Medizinischen Privatuniversität, 90419 Nürnberg, GermanyKlinik für Psychosomatische Medizin und Psychotherapie, Universitätsklinikum, 89081 Ulm, GermanyInstitut für Anästhesiologische Pathophysiologie und Verfahrensentwicklung, Universitätsklinikum, 89081 Ulm, GermanyInstitut für Anästhesiologische Pathophysiologie und Verfahrensentwicklung, Universitätsklinikum, 89081 Ulm, GermanyKlinik für Allgemein-, Viszeral- und Thoraxchirurgie, Bundeswehrkrankenhaus, 89081 Ulm, GermanyBundeswehrkrankenhaus, 10115 Berlin, GermanyInstitut für Anästhesiologische Pathophysiologie und Verfahrensentwicklung, Universitätsklinikum, 89081 Ulm, GermanyPsychosocial stress increases cardiovascular risk, which coincides with enhanced oxidative DNA damage. Increased sympathetic tone-related catecholamine release causes oxidative stress, which contributes to catecholamine-related cardiotoxicity. Therefore, we tested the hypothesis whether acute psychosocial stress induces oxidative DNA damage, its degree being related to the cardiovascular risk profile and depending on the sympathetic stress response. After assessment of the prospective cardiovascular Münster score (PROCAM) to determine the risk of acute myocardial infarction, 83 male and 12 female healthy volunteers underwent the Trier social stress test for groups (TSST-G). Heart rate variability was quantified by measuring the standard deviation (SDNN) and root mean square of successive differences (RMSSD) between normal-to-normal inter-beat intervals. Salivary α-amylase (sAA) activity was assessed as a surrogate for noradrenaline plasma concentrations. Oxidative DNA damage was determined using whole-blood single-cell gel electrophoresis (“tail moment” in the “comet assay”). A total of 33 subjects presented with a prospective risk of myocardial infarction (risk+) vs. 59 subjects without risk (risk-). The TSST-G stress significantly increased blood pressure, heart rate, and sAA in both groups, while oxidative DNA damage was only increased in the risk+ group. Immediately after the TSST-G, the “tail moment” showed significant inverse linear relations with both SDNN and RMSSD. Acute psychosocial stress may cause oxidative DNA damage, the degree of which is directly related to the individual cardiovascular risk profile and depends on the stress-induced increase in the sympathetic tone.https://www.mdpi.com/2077-0383/9/11/3783Trier stress test for groupsPROCAM scoresingle-cell gel electrophoresisheart rate variabilitynoradrenaline |
| spellingShingle | Christiane Waller Dae-Sup Rhee Michael Gröger Manuela Rappel Tanja Maier Markus Müller Edit Rottler Katharina Nerz Christopher Nerz Sebastian Brill Horst-Peter Becker Peter Radermacher Social Stress-Induced Oxidative DNA Damage Is Related to Prospective Cardiovascular Risk Journal of Clinical Medicine Trier stress test for groups PROCAM score single-cell gel electrophoresis heart rate variability noradrenaline |
| title | Social Stress-Induced Oxidative DNA Damage Is Related to Prospective Cardiovascular Risk |
| title_full | Social Stress-Induced Oxidative DNA Damage Is Related to Prospective Cardiovascular Risk |
| title_fullStr | Social Stress-Induced Oxidative DNA Damage Is Related to Prospective Cardiovascular Risk |
| title_full_unstemmed | Social Stress-Induced Oxidative DNA Damage Is Related to Prospective Cardiovascular Risk |
| title_short | Social Stress-Induced Oxidative DNA Damage Is Related to Prospective Cardiovascular Risk |
| title_sort | social stress induced oxidative dna damage is related to prospective cardiovascular risk |
| topic | Trier stress test for groups PROCAM score single-cell gel electrophoresis heart rate variability noradrenaline |
| url | https://www.mdpi.com/2077-0383/9/11/3783 |
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