Activation of the hypothalamic-pituitary-adrenal stress axis induces cellular oxidative stress

Spiers, Jereme G.; Chen, Hsiao-Jou Cortina; Sernia, Conrad; Lavidis, Nickolas A.

doi:10.3389/fnins.2014.00456

Cited by 174 publications

(168 citation statements)

References 68 publications

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“…Clearly GC, by blocking production of inflammatory cytokines, could remove a major stimulus of OS. On the other hand, activation of the HPAA, by increasing metabolic rate and glucose availability, can result in increased OS (146) and, in agreement with this hypothesis, administration of corticosterone to rats causes an increase in biomarkers of OS, lipid peroxides and protein carbonyls (132).…”

Section: Brain-body Interactions Of Stress Os and Inflammationsupporting

confidence: 64%

Oxidative Stress and Inflammation Induced by Environmental and Psychological Stressors: A Biomarker Perspective

Ghezzi

Floridi

Boraschi

et al. 2018

Antioxidants & Redox Signaling

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Section: Brain-body Interactions Of Stress Os and Inflammationsupporting

confidence: 64%

Oxidative Stress and Inflammation Induced by Environmental and Psychological Stressors: A Biomarker Perspective

Ghezzi

Floridi

Boraschi

et al. 2018

Antioxidants & Redox Signaling

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“…40,41 As reviewed by Picard et al, 13 chronic neuroendocrine and metabolic stress may lead to mitochondrial dysfunction and accumulation of mtDNA damage. Activation of the HPA axis increases the demand for energy production, 42 the primary function of the mitochondria. Owing to the mitochondria's relatively poor ability to repair its own DNA and the production of reactive oxygen species, the increased metabolic rate leads to cell damage and fragmentation of mtDNA.…”

Section: Discussionmentioning

confidence: 99%

Stress: A deadly weapon

Peñagarikano

2016

Sci. Transl. Med.

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Preclinical data suggest that chronic stress may cause cellular damage and mitochondrial dysfunction, potentially leading to the release of mitochondrial DNA (mtDNA) into the bloodstream. Major depressive disorder has been associated with an increased amount of mtDNA in leukocytes from saliva samples and blood; however, no previous studies have measured plasma levels of free-circulating mtDNA in a clinical psychiatric sample. In this study, free circulating mtDNA was quantified in plasma samples from 37 suicide attempters, who had undergone a dexamethasone suppression test (DST), and 37 healthy controls. We hypothesized that free circulating mtDNA would be elevated in the suicide attempters and would be associated with hypothalamic-pituitaryadrenal (HPA)-axis hyperactivity. Suicide attempters had significantly higher plasma levels of free-circulating mtDNA compared with healthy controls at different time points (pre-and post-DST; all P-values o2.98E − 12, Cohen's d ranging from 2.55 to 4.01). Pre-DST plasma levels of mtDNA were positively correlated with post-DST cortisol levels (rho = 0.49, P o 0.003). Suicide attempters may have elevated plasma levels of free-circulating mtDNA, which are related to impaired HPA-axis negative feedback. This peripheral index is consistent with an increased cellular or mitochondrial damage. The specific cells and tissues contributing to plasma levels of free-circulating mtDNA are not known, as is the specificity of this finding for suicide attempters. Future studies are needed in order to better understand the relevance of increased free-circulating mtDNA in relation to the pathophysiology underlying suicidal behavior and depression.

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“…This may have important implications for neurodegenerative conditions involving redox-sensitive regions. These observations highlight that maintenance of a balanced redox state is critical for normal cellular homeostatic function and relies heavily on hormonal cues from the neuroendocrine stress system [5].…”

Section: Introductionmentioning

confidence: 97%

Effect of Ubiquinol on Serum Reproductive Hormones of Amenorrhic Patients

Thakur¹,

Littaru

Funahashi

et al. 2015

Ind J Clin Biochem

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In neuroendocrine system the increase in oxidative status is produced by a glucocorticoid-dependent and transcriptional increase in pro-oxidative drive, with concurrent inhibition of the antioxidant defense system, ultimately leading to increased neuronal cell death. Functional hypothalamic disturbances and neuroendocirne aberrations have both short and long term consequences for reproductive health. Understandably, an impaired or diminished hypothalamic-pituitary-ovarian axis leads to anovulation and hypoestrogenism. Anovulation is directly linked to the neurohormonal and hormonal background of Functional Hypothalamic Amenorrhea. Impairment of pulsatile Gonadotropin Releasing Hormone secretion causes the impairment of pulsatile Lutenizing Hormone (LH) and Follicle Stimulating Hormone (FSH) secretion. The importance of oxidative stress in various pituitary disorders suggesting a possible clinical usefulness of antioxidant molecules like the lipophilic antioxidant Ubiquinol. Coenzyme Q10 or Ubiquinol is an essential part of the cell energy-producing system of mitochondria. However, it is also a powerful lipophilic antioxidant, protecting lipoproteins and cell membranes from autooxidation. Due to these unique actions Ubiquinol is used in clinical practice as an antioxidants for neurodegenerative diseases. So to identify the role of Ubiquinol on reproductive hormones FSH and LH, we have included 50 infertile patients of age group of 20-40, which are mostly amenorrhic. Out of 50 only 30 patients were in continuous follow up after supplementing them with 150 mg of Ubiquinol every day for 4 months. The hormonal levels were estimated by Enzyme Linked Immuno Sorbent Assay technique at follicular phase. The result suggests that FSH concentration is increased up to three times (from 3.10 ± 2.70 to 10.09 ± 6.93) but remains within the normal limit (P \ 0.05). LH values were found doubled (P \ 0.05) than its normal range (from 14.83 ± 10.48 to 27.85 ± 22.30). The Prolactin values were decreased while Progesterone values were high but not in the significant range (P [ 0.05). The supplementation of 150 mg of Ubiquinol may reduce the oxidative stress in neuroendocrine system which further improves the function of diminished HPA axis. Hence increased level of FSH and LH may be due to reduced oxidative stress by Ubiquinol.

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Activation of the hypothalamic-pituitary-adrenal stress axis induces cellular oxidative stress

Cited by 174 publications

References 68 publications

Oxidative Stress and Inflammation Induced by Environmental and Psychological Stressors: A Biomarker Perspective

Oxidative Stress and Inflammation Induced by Environmental and Psychological Stressors: A Biomarker Perspective

Stress: A deadly weapon

Effect of Ubiquinol on Serum Reproductive Hormones of Amenorrhic Patients

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