Chronic variable stress induces oxidative stress and decreases butyrylcholinesterase activity in blood of rats

Abstract

Depressive disorders, including major depression, are serious and disabling, whose mechanisms are not clearly understood. Since life stressors contribute in some fashion to depression, chronic variable stress (CVS) has been used as an animal model of depression. In the present study we evaluated some parameters of oxidative stress [thiobarbituric acid reactive substances (TBARS), catalase (CAT), superoxide dismutase (SOD) and glutathione peroxidase (GPx)], and inflammatory markers (interleukin 6, C reactive protein, tumor necrosis factor-alpha and nitrites), as well as the activity of butyrylcholinesterase in blood of rats subjected to chronic stress. Homocysteine and folate levels also were measured. Stressed animals were submitted to different mild stressors for 40 days. After CVS, a reduction in weight gain was observed in the stressed group, as well as an increase in immobility time in the forced swimming test as compared with controls. Stressed animals presented a significant increase on TBARS and SOD/CAT ratio, but stress did not alter GPx activity and any inflammatory parameters studied. CVS caused a significant inhibition on serum butyrylcholinesterase activity. Stressed rats had higher plasmatic levels of homocysteine without differences in folate levels. Although it is difficult to extrapolate our findings to the human condition, the alterations observed in this work may be useful to help to understand, at least in part, the pathophysiology of depressive disorders.

Chronic Variable Stress Alters Inflammatory and Cholinergic Parameters in Hippocampus of Rats

“…CVS chronic variable stress The CVS procedure was developed as an animal model of depression that presents three important characteristics: the inducing conditions are relatively realistic, the focus of the model is a core symptom of depression, anhedonia, and the protracted time course of the model is suitable for investigating the effects of chronic drug treatments [31]. A series of publications have reported that the CVS procedure causes decreased intake of sucrose solutions (or pellets) [32][33][34][35], impairments in other measures of hedonic reactivity such as place preference conditioning [36,37] and brain stimulation reward [38,39], decreased sexual and aggressive behaviors [40,41] and self-care [42][43][44], in addition to changes in sleep architecture [39,45]. Moreover, these behavioral changes are reversed by chronic treatment with all classes of clinically-effective antidepressant drugs, but not by drugs known to be ineffective as antidepressants.…”

Oxidative Stress and Major Depression

“…Its activity altered in numbers of diseases [29,30,37]. SOD activity found to be decreased in different depressive animal model [38,39]. Rybka et al, reported low levels of SOD in the cases of major depression as compared to healthy controls but this was not significant [22].…”

Antidepressive effect of paroxetine in a rat model

“…Malondialdehyde (MDA) is a product of lipid peroxidation caused by reactive oxygen species and is therefore an indicator of lipid oxidation injury [9]. Tagliari and Lucca observed an obvious decrease in SOD and CAT activities with increasing MDA levels in chronic unpredicted mild stress-induced or variable stress-induced depressive rats [7,10]. Therefore, another aim of antidepression treatment would be to increase the activity of SOD and CAT and decrease the levels of MDA.…”

“…Oxidative stress in the brain may also be involved in the development of depression [7]. Free radicals, which play a role in mitosis, are mainly scavenged by elements of the antioxidative stress system, including superoxide dismutase (SOD) and catalase (CAT).…”