Systemic Oxidative Stress markers in animal model for Depression

TY - CONF

T1 - Systemic Oxidative Stress markers in animal model for Depression

AU - Bouzinova, Elena

N1 - Conference code: 38

PY - 2013/7/11

Y1 - 2013/7/11

N2 - Involvement of oxidative stress (OxS) in development of major depressive disorder has recently become evident, though mechanisms behind this remain elusive. We analyzed therefore OxS pathways in rat Chronic Mild Stress (CMS) model of depression. Rats are exposed to chronic unpredictable mild stressors and Sucrose Consumption Tests (measure of hedonic state) were performed. Some rats developed the anhedonia-like symptoms, which were evident after 4 weeks of CMS protocol. During 5th to 8th weeks of CMS anhedonic rats were treated with a selective serotonin reuptake inhibitor Escitalopram (i.p., 5 mg/kg/day). Saline injections were done to control the vehicle effect. Escitalopram treated rats were sub-divided into 2 groups: responders and non-responders, according to their hedonic state and compared to non-stressed rats, treated with either saline or Escitalopram. Measurement of total glutathione and malondialdehyde (MDA) in lungs, heart, skeletal muscles, liver, saphenous, mesenteric, and tail arteries were used as estimates for OxS. In heart, glutathione was increased in CMS rats in comparison with non-stressed vehicle group. Accordingly, an estimate for free radical activity, MDA, was significantly lower in vehicle-treated anhedonic rats in comparison with both non-stressed groups and CMS non-responders group. Similarly, glutathione concentration in liver was significantly higher in vehicle-treated anhedonic group compared to all other groups. In lungs, glutathione was significantly elevated in Escitalopram-treated non-stressed rats and in CMS non-responders group (over 500 µmol/ml), while it was negligible in all other experimental groups. Glutathione was lower in tail arteries from non-stressed vehicle group than in all others groups. In contrast, glutathione was significantly higher in mesenteric small arteries from the non-stressed Escitalopram-treated group than in other CMS groups. No significant changes in the OxS markers were seen in skeletal muscles and saphenous arteries. No differences between the groups in MDA were seen in any tissue with the exception of heart.Thus, we have demonstrated tissue specific changes in the OxS markers in rats exposed to CMS and developed anhedonia-like symptoms. SSRI antidepressant treatment affected OxS pathways and related recovery was observed only in liver and lungs.

AB - Involvement of oxidative stress (OxS) in development of major depressive disorder has recently become evident, though mechanisms behind this remain elusive. We analyzed therefore OxS pathways in rat Chronic Mild Stress (CMS) model of depression. Rats are exposed to chronic unpredictable mild stressors and Sucrose Consumption Tests (measure of hedonic state) were performed. Some rats developed the anhedonia-like symptoms, which were evident after 4 weeks of CMS protocol. During 5th to 8th weeks of CMS anhedonic rats were treated with a selective serotonin reuptake inhibitor Escitalopram (i.p., 5 mg/kg/day). Saline injections were done to control the vehicle effect. Escitalopram treated rats were sub-divided into 2 groups: responders and non-responders, according to their hedonic state and compared to non-stressed rats, treated with either saline or Escitalopram. Measurement of total glutathione and malondialdehyde (MDA) in lungs, heart, skeletal muscles, liver, saphenous, mesenteric, and tail arteries were used as estimates for OxS. In heart, glutathione was increased in CMS rats in comparison with non-stressed vehicle group. Accordingly, an estimate for free radical activity, MDA, was significantly lower in vehicle-treated anhedonic rats in comparison with both non-stressed groups and CMS non-responders group. Similarly, glutathione concentration in liver was significantly higher in vehicle-treated anhedonic group compared to all other groups. In lungs, glutathione was significantly elevated in Escitalopram-treated non-stressed rats and in CMS non-responders group (over 500 µmol/ml), while it was negligible in all other experimental groups. Glutathione was lower in tail arteries from non-stressed vehicle group than in all others groups. In contrast, glutathione was significantly higher in mesenteric small arteries from the non-stressed Escitalopram-treated group than in other CMS groups. No significant changes in the OxS markers were seen in skeletal muscles and saphenous arteries. No differences between the groups in MDA were seen in any tissue with the exception of heart.Thus, we have demonstrated tissue specific changes in the OxS markers in rats exposed to CMS and developed anhedonia-like symptoms. SSRI antidepressant treatment affected OxS pathways and related recovery was observed only in liver and lungs.

KW - depression

KW - oxidative stress

M3 - Poster

T2 - Federation of European Biochemical Societies CONGRESS 2013 “Mechanisms in Biology”

Y2 - 6 July 2013 through 11 July 2013

ER -