Impairment of several immune functions in anxious women

Arranz, Lorena; Guayerbas, Noelia; Fuente, Mónica De la

doi:10.1016/j.jpsychores.2006.07.030

Cited by 85 publications

(67 citation statements)

References 40 publications

(57 reference statements)

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“…This behavioral trait may be analogous to certain human personality traits associated with naturally-elevated glucococorticoid production in certain individuals (Arranz et al, 2007;Zobel et al, 2004). The results of the current study suggest that females with such personalities may physiologically mimic the effects of chronic environmental stress.…”

Section: Discussionsupporting

confidence: 53%

Female temperament, tumor development and life span: Relation to glucocorticoid and tumor necrosis factor α levels in rats

Cavigelli

Bennett

Michael

et al. 2008

Brain, Behavior, and Immunity

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Behavioral characteristics closely associated with specific physiological profiles present an important area of research in understanding health disparities. In particular, glucocorticoid overproduction may be an important factor moderating disease progression; natural variance in production of this steroid has been proposed as one mechanism underlying individual differences in health and disease. In the current paper, we examined immune parameters in female rats of two different behavioral types previously shown to have differential glucocorticoid production and life spans. We categorized young female rats according to their behavioral response to novelty (high-or low-locomotion), and compared their glucocorticoid production, adrenal size, thymus size, tumor necrosis factor-α (TNF-α) production, tumor development and life span. As expected, high-locomotion females produced more glucocorticoids and had larger adrenal glands during young adulthood than did low-locomotion females. High-locomotion females had significantly smaller thymuses and reduced TNF-α levels compared to low-locomotion, suggesting altered immune function in young adulthood. Finally, highlocomotion females had shorter life spans than did low-locomotion females, and this was particularly true in females that developed pituitary tumors, but not in those that developed mammary tumors. These results, along with other published findings, suggest that high-locomotion rodent females experience life-long elevations in glucocorticoid responses to novelty, and that these elevated levels may be comparable to chronic stress. This naturally-occurring endocrine profile may influence immune responses which in turn could affect disease susceptibility. Variance in immune function across personality types may be partially moderated by natural variance in glucocorticoid production.

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Section: Discussionsupporting

confidence: 53%

Female temperament, tumor development and life span: Relation to glucocorticoid and tumor necrosis factor α levels in rats

Cavigelli

Bennett

Michael

et al. 2008

Brain, Behavior, and Immunity

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“…The study on social phobia also found a reversal of these disturbances following 8 wk of citalopram treatment (Atmaca et al, 2004). A study of anxious women found reduced total antioxidant capacity among this group compared with non-anxious controls, in conjunction with several parameters of impaired immune functioning (Arranz et al, 2007). A case series has reported improvement in trichotillomania, pathological nail-biting and skin-picking, conditions that have similarities with obsessivecompulsive disorder, using NAC (Odlaug and Grant, 2007).…”

Section: Human Studiesmentioning

confidence: 96%

Oxidative stress in psychiatric disorders: evidence base and therapeutic implications

Berk

Dean

et al. 2008

Int. J. Neuropsychopharm.

861

569

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Oxidative stress has been implicated in the pathogenesis of diverse disease states, and may be a common pathogenic mechanism underlying many major psychiatric disorders, as the brain has comparatively greater vulnerability to oxidative damage. This review aims to examine the current evidence for the role of oxidative stress in psychiatric disorders, and its academic and clinical implications. A literature search was conducted using the Medline, Pubmed, PsycINFO, CINAHL PLUS, BIOSIS Previews, and Cochrane databases, with a time-frame extending to September 2007. The broadest data for oxidative stress mechanisms have been derived from studies conducted in schizophrenia, where evidence is available from different areas of oxidative research, including oxidative marker assays, psychopharmacology studies, and clinical trials of antioxidants. For bipolar disorder and depression, a solid foundation for oxidative stress hypotheses has been provided by biochemical, genetic, pharmacological, preclinical therapeutic studies and one clinical trial. Oxidative pathophysiology in anxiety disorders is strongly supported by animal models, and also by human biochemical data. Pilot studies have suggested efficacy of N-acetylcysteine in cocaine dependence, while early evidence is accumulating for oxidative mechanisms in autism and attention deficit hyperactivity disorder. In conclusion, multi-dimensional data support the role of oxidative stress in diverse psychiatric disorders. These data not only suggest that oxidative mechanisms may form unifying common pathogenic pathways in psychiatric disorders, but also introduce new targets for the development of therapeutic interventions.

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“…Recent studies have shown that social phobia, depression, anxiety, and other neuropsychiatric disorders result in signs of oxidative stress such as increased reactive oxygen generation and decreased antioxidant capacity (Arranz et al, 2007;Bouayed et al, 2007). There is increasing evidence that oxidative stress in neurons is involved in pathological manifestations of many neurological disorders.…”

mentioning

confidence: 99%

Reversal of Oxidative Stress-Induced Anxiety by Inhibition of Phosphodiesterase-2 in Mice

Masood

Nadeem²,

Mustafa³

et al. 2008

J Pharmacol Exp Ther

202

168

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The pathogenesis of several neuropsychiatric disorders, including anxiety and depression, has been linked to oxidative stress, in part via alterations in cyclic nucleotide signaling. Phosphodiesterase-2 (PDE2), which regulates cGMP and cAMP signaling, may affect anxiety-related behavior through reduction of oxidative stress. The present study evaluated the effects of oxidative stress on behavior and assessed the anxiolytic effects of the PDE2 inhibitor Bay 60-7550 [(2-(3,4-Treatment of mice with L-buthionine-(S,R)-sulfoximine (300 mg/kg), an inducer of oxidative stress, caused anxiety-like behavioral effects in elevated plusmaze, open-field, and hole-board tests through the NADPH oxidase pathway; these effects were antagonized by Bay 60-7550 (3 mg/kg) and apocynin (3 mg/kg), an inhibitor of NADPH oxidase. The Bay 60-7550-mediated decrease in oxidative stress (i.e., superoxide anion and reactive oxygen species generation in cultured neurons and total antioxidant capacity and lipid peroxides in amygdala and hypothalamus) and expression of NADPH oxidase subunits (i.e., p47 phox and gp91 phox expression in amygdala, hypothalamus, and cultured neurons) was associated with increased cGMP and phosphorylation of vasodilator-stimulated phosphoprotein at Ser239, suggesting an important role of cGMP-protein kinase G signaling in reduction of anxiety. Overall, the present results indicate that oxidative stress induces anxiety-like behavior in mice and that PDE2 inhibition reverses it through an increase in cGMP signaling. Thus, PDE2 may be a novel pharmacological target for treatment of anxiety in neuropsychiatric and neurodegenerative disorders that involve oxidative stress.Anxiety and fear are normal emotional responses to threatening stimuli. These responses are abnormal in human anxiety disorders, such as panic disorder, post-traumatic stress disorder, social phobias, and generalized anxiety disorder. The development of anxiety/stress-related disorders involves complex interactions among various body mechanisms involving the limbic system and the hypothalamic-pituitaryadrenal axis; their interactions play a significant role in the manifestation of disease pathology (Chrousos and Gold, 1992;Ray et al., 1993). Exposure to stressful stimuli produces widespread physiological and behavioral effects in animals. In recent studies, oxidative stress has been shown to be associated with anxiety in different behavioral models (Gingrich, 2005;Hovatta et al., 2005;Berry et al., 2007).The nervous system, due to enriched concentrations of polyunsaturated fatty acids, is particularly susceptible to the deleterious effects of oxidative stress; this can lead to loss of membrane integrity, protein damage, and neuronal dysfunction. Recent studies have shown that social phobia, depression, anxiety, and other neuropsychiatric disorders result in signs of oxidative stress such as increased reactive oxygen generation and decreased antioxidant capacity (Arranz et al., 2007;Bouayed et al., 2007). There is increasing evidence that oxidati...

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Impairment of several immune functions in anxious women

Cited by 85 publications

References 40 publications

Female temperament, tumor development and life span: Relation to glucocorticoid and tumor necrosis factor α levels in rats

Female temperament, tumor development and life span: Relation to glucocorticoid and tumor necrosis factor α levels in rats

Oxidative stress in psychiatric disorders: evidence base and therapeutic implications

Reversal of Oxidative Stress-Induced Anxiety by Inhibition of Phosphodiesterase-2 in Mice

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