Mitochondrial function as related to psychological distress in health care professionals

OBJECTIVE: The present study evaluated the association of psychological distress and radiation exposure as a work-related stressor with mitochondrial function in healthcare professionals. METHODS: Health care professionals at a regional hospital in Italy were evaluated for physical health and psychological measures using self-report questionnaires (n = 41; mean age 47.6 ± 13.1 years; 66% women). In a second sample, individuals exposed to elevated levels of ionizing radiation (IR: likely effective dose exceeding 6 mSv/year; (n = 63, mean age 45.8 ± 8.8 years; 62% women) were compared to health care workers with low IR (n = 57; mean age 47.2 ± 9.5 years; 65% women) because exposure to a toxic agent might act as a (work-related) stressor. Associations were examined between psychological factors (GHQ-12, PSS), work ability (WAI) and IR-exposure at the workplace with markers of mitochondrial function, including mitochondrial redox activity (MRA), mitochondrial membrane potential (ΔΨm), mitochondrial DNA copy number (mtDNAcn), biogenesis and mtDNA damage response (mtDDR) measured from peripheral blood mononuclear cells (PBMCs). RESULTS: All participants were in good physical health. Individuals reporting high levels of psychological distress showed lower mitochondrial biogenesis as indicated by PGC-1α and lower NRF2 expression (2.5 ± 1.0 vs 1.0 ± 0.9 rel exp, p = .035 and 31.5 ± 5.0 vs 19.4 ± 6.9 rel exp, p = .013, respectively). However, exposure to toxic agents (IR) was primarily associated with mitochondrial metabolism and reduced mtDNA integrity. Participants with IR exposure displayed higher mitochondrial redox activity (4480 ± 1202 MFI/min vs 3376 ± 983 MFI/min, p < .001) and lower ΔΨm (0.89 ± 0.09 MFI vs 0.95 ± 0.11 MFI, p = .001), and reduced mtDNA integrity (1.18 ± 0.21 rel exp vs 3.48 ± 1.57 rel exp, p < .001) compared to non-exposed individuals. CONCLUSIONS: This study supports the notion that psychological distress and potential stressors related to toxic agents might influence various aspects of mitochondrial biology, and that chronic stress exposure can lead to molecular and functional recalibrations among mitochondria.