TY - JOUR
T1 - Underlying inflammation has no impact on the oxidative stress response to acute mental stress
AU - Wadley, Alex J
AU - Veldhuijzen van Zanten, Jet J C S
AU - Paine, Nicola J
AU - Drayson, Mark T
AU - Aldred, Sarah
N1 - Copyright © 2014 Elsevier Inc. All rights reserved.
PY - 2014/8
Y1 - 2014/8
N2 - INTRODUCTION: Mental stress is considered to be a trigger for acute myocardial infarction (MI), with inflammation thought to provide a mechanism. Inflammation is reciprocally linked to oxidative stress, which has also been implicated in MI. The purpose of this study was to assess the effects of experimentally-induced inflammation on the oxidative stress response to mental stress in healthy participants.METHODS: Healthy males undertook one of two inflammatory stimuli: typhoid vaccination (Vaccination paradigm, N=17) or eccentric exercise (Eccentric exercise paradigm, N=17). All participants completed a mental arithmetic stress task twice (within-subject design): 6h after the inflammatory stimulus, and during a control non-inflammation condition. Blood samples were taken before, immediately and 30min after the stress task. Plasma was assessed for interleukin-6 (IL-6), protein carbonyls (PC), lipid hydroperoxides (LOOH), total antioxidant capacity (TAC) and nitric oxide metabolites (NOx).RESULTS: Vaccination paradigm: IL-6, PC and NOx were significantly higher in the vaccination condition, relative to the control condition (p<.05). PC, TAC, LOOH and NOx were unchanged in response to mental stress in both the vaccination and control conditions. Eccentric Exercise paradigm: IL-6 and TAC were significantly higher in the eccentric exercise condition (p<.05), relative to the control condition. PC, TAC and NOx were unchanged in response to mental stress in both the eccentric exercise and control conditions.CONCLUSIONS: Two different inflammatory paradigms were successful in increasing selective plasma markers of inflammation and oxidative stress prior to a mental stress task. However, experimentally induced transient inflammation had no impact on mental stress-induced changes in plasma LOOH, PC, TAC or NOx in young healthy participants.
AB - INTRODUCTION: Mental stress is considered to be a trigger for acute myocardial infarction (MI), with inflammation thought to provide a mechanism. Inflammation is reciprocally linked to oxidative stress, which has also been implicated in MI. The purpose of this study was to assess the effects of experimentally-induced inflammation on the oxidative stress response to mental stress in healthy participants.METHODS: Healthy males undertook one of two inflammatory stimuli: typhoid vaccination (Vaccination paradigm, N=17) or eccentric exercise (Eccentric exercise paradigm, N=17). All participants completed a mental arithmetic stress task twice (within-subject design): 6h after the inflammatory stimulus, and during a control non-inflammation condition. Blood samples were taken before, immediately and 30min after the stress task. Plasma was assessed for interleukin-6 (IL-6), protein carbonyls (PC), lipid hydroperoxides (LOOH), total antioxidant capacity (TAC) and nitric oxide metabolites (NOx).RESULTS: Vaccination paradigm: IL-6, PC and NOx were significantly higher in the vaccination condition, relative to the control condition (p<.05). PC, TAC, LOOH and NOx were unchanged in response to mental stress in both the vaccination and control conditions. Eccentric Exercise paradigm: IL-6 and TAC were significantly higher in the eccentric exercise condition (p<.05), relative to the control condition. PC, TAC and NOx were unchanged in response to mental stress in both the eccentric exercise and control conditions.CONCLUSIONS: Two different inflammatory paradigms were successful in increasing selective plasma markers of inflammation and oxidative stress prior to a mental stress task. However, experimentally induced transient inflammation had no impact on mental stress-induced changes in plasma LOOH, PC, TAC or NOx in young healthy participants.
U2 - 10.1016/j.bbi.2014.03.009
DO - 10.1016/j.bbi.2014.03.009
M3 - Article
C2 - 24675034
SN - 0889-1591
VL - 40
SP - 182
EP - 190
JO - Brain, Behaviour, and Immunity
JF - Brain, Behaviour, and Immunity
ER -