TY - JOUR
T1 - The effects of prolonged stress exposure on the brain of rats and insights to understand the impact of work-related stress on caregivers
AU - Pujo, Jean Marc
AU - Fitriani, Dewi Yunia
AU - Ben Saad, Hajer
AU - Ghariani, Marwa
AU - Dghim, Amel
AU - Mellouli, Manel
AU - Burin, Antoine
AU - Mutricy, Remi
AU - Houcke, Stephanie
AU - Roujansky, Ariane
AU - Mansyur, Muchtaruddin
AU - Nkontcho, Flaubert
AU - de Toffol, Bertrand
AU - Ben Amara, Ibtissem
AU - Kallel, Hatem
N1 - Publisher Copyright:
Copyright © 2023 Pujo, Fitriani, Ben Saad, Ghariani, Dghim, Mellouli, Burin, Mutricy, Houcke, Roujansky, Mansyur, Nkontcho, de Toffol, Ben Amara and Kallel.
PY - 2023
Y1 - 2023
N2 - Introduction: Stress exposure is a significant concern in the healthcare sector. This animal model study aims to reproduce caregivers’ working conditions and determine their impact on the brain. Method: Twenty-four healthy male rats of the Wistar strain were divided into four groups. Three groups were submitted each to one stressor for 21 days, while the fourth group was used as a control. Stressors were food and water deprivation (FW), permanent illumination (PI), and forced swimming (FS). At the end of the experiment, rats were euthanized, and stress biomarkers, biological parameters, and DNA damage were measured. Results: Prooxidant biomarker rates increased in the different groups (+50 to +75%) compared to the control (p < 0.0001). Urinary corticosterone rates increased in all stressed animals, mainly in the PI group, with changes of up to +50% compared to the control group. Acetylcholinesterase levels decreased to −50% (p < 0.0001 for the three exposed groups). Total ATPase, (Na+/K+)-ATPase, and Mg2+-ATPase activities decreased in all stressed groups. The percentage of brain cell congestion and apoptosis was 3% for the FW group (p < 0.0001), 2% for the PI group (p < 0.0001), and 4% for the FS group (p < 0.0001) compared to the control (0.8%). DNA damage was observed in all exposed groups. Finally, we noticed behavioral changes and a depression-like syndrome in all stressed rats. Conclusion: Stressful conditions such as the working environment of caregivers can trigger several pathophysiological processes leading to oxidative, neurochemical, and hypothalamic–pituitary–adrenal disorders. These changes can progress to cell damage and apoptosis in the brain and trigger psychological and physical disorders.
AB - Introduction: Stress exposure is a significant concern in the healthcare sector. This animal model study aims to reproduce caregivers’ working conditions and determine their impact on the brain. Method: Twenty-four healthy male rats of the Wistar strain were divided into four groups. Three groups were submitted each to one stressor for 21 days, while the fourth group was used as a control. Stressors were food and water deprivation (FW), permanent illumination (PI), and forced swimming (FS). At the end of the experiment, rats were euthanized, and stress biomarkers, biological parameters, and DNA damage were measured. Results: Prooxidant biomarker rates increased in the different groups (+50 to +75%) compared to the control (p < 0.0001). Urinary corticosterone rates increased in all stressed animals, mainly in the PI group, with changes of up to +50% compared to the control group. Acetylcholinesterase levels decreased to −50% (p < 0.0001 for the three exposed groups). Total ATPase, (Na+/K+)-ATPase, and Mg2+-ATPase activities decreased in all stressed groups. The percentage of brain cell congestion and apoptosis was 3% for the FW group (p < 0.0001), 2% for the PI group (p < 0.0001), and 4% for the FS group (p < 0.0001) compared to the control (0.8%). DNA damage was observed in all exposed groups. Finally, we noticed behavioral changes and a depression-like syndrome in all stressed rats. Conclusion: Stressful conditions such as the working environment of caregivers can trigger several pathophysiological processes leading to oxidative, neurochemical, and hypothalamic–pituitary–adrenal disorders. These changes can progress to cell damage and apoptosis in the brain and trigger psychological and physical disorders.
KW - acetylcholine
KW - apoptosis
KW - brain damage
KW - corticosterone
KW - healthcare
KW - oxidative stress
KW - stress
UR - http://www.scopus.com/inward/record.url?scp=85179966311&partnerID=8YFLogxK
U2 - 10.3389/fnbeh.2023.1288814
DO - 10.3389/fnbeh.2023.1288814
M3 - Article
AN - SCOPUS:85179966311
SN - 1662-5153
VL - 17
JO - Frontiers in Behavioral Neuroscience
JF - Frontiers in Behavioral Neuroscience
M1 - 1288814
ER -