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... ler and Lundberg (1954). Since then many studies have been published on the effects of physical, intellectual, and emotional stress on catecholamine excretion. The results have been somewhat conflicting in regard to the relative increases of adrenaline and of noradrenaline in these situations, and variability between subjects is often considerable. Levi (1967) has shown that there is a quantitative relation between the strain experienced by an individual and his urinary excretion of adrenaline. Euler (1964) believed that adrenaline excretion was increased by stress, whereas noradrenaline increased with physical work ; even the change from recumbency to the upright posture induced a threefold ...
... Everyday work stress also produced increased noradrenaline excretion (Levi, 1967). Friedman et al. (1960) showed increased daytime noradrenaline excretion in a particular personality type, but even the control group showed a greater Discussion ...
... Stress has been shown to affect several brain activities and promote long-term changes in multiple neural systems [27]. Levi and Basuaj [28] found that stress has been shown to cause a decrease in the level of glutathione which protect the tissues from oxidative damage. Gilgun-Sherki et al., [29] suggested that ROS attack glial cellsand neurons which are post-mitotic cells, and therefore they are particularly sensitive to free radicals, leading to neuronal damage. ...
Xanax is an agent with hypnogenic, anxiolytic, anticonvulsant, and muscle relaxant properties and has generally been used as a hypnotic/tranquilizer. The aim of this paper was to investigate the effect of Xanax on acetylcholinesterase and glutathionestransferase enzyme activities on the cerebellar tissues of male mice. Sixty male mice were randomly assigned into four groups (15 mice/each) according to their approximately equal mean body weight. Mice that received orally by gavage 0.5 ml saline solution of 0.9% NaCl were considered as a control mice. Other experimental mice were daily administered orally by gavage with 0.5 ml of different three doses of Xanax (0.5, 1 and 1.5 mg/kg bw), for two months. Biochemical analyses revealed significant decreases in the activities of acetylcholinesterase and glutathionestransferase enzyme in the brain tissues of mice administered with the three doses of Xanax. The major mechanism involved appears to be the result of oxidative stress scavenging action on the neuronal cells of cerebellar cortex of male mice.
... However, blind dependence on synthetics seems to be over and people are returning to the naturals with the hope of safety and security. The aqueous extract of S. nigrum leaves has been reported to play an important role in protection of tissues from oxidative damage [16]. ...
The prophylactic or curative antioxidant efficacy of crude extract and the active constituent of S. nigrum leaves were evaluated in modulating inherent antioxidant system altered due to immobilization stress in rat brain tissues, in terms of measurement of glutathione (GSH), lipid peroxidation (thiobarbituric acid reactive substances, TBARS), and free radical scavenging enzymes activities. Rats were treated with single dose of crude extract of S. nigrum prior to and after 6 h of immobilization stress exposure. Exposure to immobilization stress resulted in a decrease in the brain levels of glutathione, SOD, GST, and catalase, with an increase in thiobarbituric acid reactive substances (TBARS) levels. Treatment of S. nigrum extract and its active constituents to both pre- and poststressed rats resulted in significant modulation in the above mentioned parameters towards their control values with a relative dominance by the latter. Brain is vulnerable to stress induced prooxidant insult due to high levels of fat content. Thus, as a safe herbal medication the S. nigrum leaves extract or its isolated constituents can be used as nutritional supplement for scavenging free radicals generated in the brain due to physical or psychological stress or any neuronal diseases per se.
... The first event and one of the most important consequences of free radical production is the membrane lipoperoxidation. Moreover, stress has been suggested to decrease the levels of glutathione (GSH) and vitamin C and, both substances that play an important role in tissue protection from oxidative damage (Liu et al., 1994; Levi and Basuaj, 2000). In the present study we evaluated thiobarbituric acid reactive substances (TBARS) levels as a consequence of different stressors which could be indicative of oxidative stress. ...
Homocysteine levels are affected by diet factors such as vitamin deficiencies, non-diet factors such as genetic disorders, and stress exposure. Hyperhomocysteinemia has been implicated in several disorders, including cardiovascular disease, depression, schizophrenia, Alzheimer's and Parkinson's disease. Since sex differences play a role both in stress responses and in susceptibility to various diseases, the objective of this study was to evaluate possible alterations in homocysteine metabolism including cysteine, folate, and vitamin B6, and oxidative stress markers in female rats exposed to different types of acute stress. Female rats were randomly distributed into eight groups according to stress manipulation (restraint, swimming, cold and control) and estrous cycle (diestrus and estrus). In general no significant differences were seen between rats in estrus and diestrus. Restraint stress was the only type of stress that altered homocysteine concentrations (+ 33% relative to controls). An increase in levels of thiobarbituric acid reactive substances (TBARS) and a decrease in total glutathione (GSHt) concentration were also observed in animals subjected to restraint and swimming stress, suggesting the possibility of oxidative damage. Thus, both the homocysteine results and the oxidative stress data indicated that restraint stress was the most powerful stress manipulation in female rats, as previously observed in male rats.These findings indicate that hormonal and gonadal differences do not interfere with stress responses related to homocysteine metabolism and suggest that putative gender-related differences in homocysteine responses are probably not involved in the differential prevalence of some diseases in human males and females.
... Recently various stresses have been associated with enhanced free radical generation causing oxidative stress [3]. One of the most important consequences of the generation of free radical is the peroxidation of membrane lipids.Moreover, stress has been suggested to decrease the level of glutathione (GSH) and vitamin C which play an important role in protection of tissues from oxidative damage [5,6]. Next to the huge group of polyphenols,especially tocopherols, ascorbic acid and carotenoids have been associated with antioxidative properties [7]. ...
In the present study we examined immobilization stress-induced antioxidant defense changes in rat plasma and also observed the antioxidant effects of pre and post vitamins A, E and C administration (15 mg/Kg of body weight) individually and in combination (vit E + C) on these alterations.Following immobilization stress the circulating activities of superoxide dismutase, catalase and glutathione-S-transferase were decreased, while the level of thiobarbituric acid reactive substances (TBARS) was increased as compared to non-stressed control rats. Post treatment with individual vitamins A, E and C (after exposure to stress) resulted in a less marked alteration of plasma TBARS levels and activities of SOD, GST and catalase as compared to pre vitamin stress or stress alone treatments. Both pre and post vitamin treatments were effective in preventing stress induced derangement of free radical metabolism with a relative dominance by latter. The combined treatment with vitamin E and C did not show any additive antioxidant effect on restraint stress induced altered free radical metabolism, rather a predominant effect similar to vitamin E alone was observed. The prevention of oxidative stress generated in response to restraint stress by the vitamins can be summarized as: vitamin (E + C) i.e. vit E > vit C > vit A, thus combined vitamin (E + C) treatment though showed maximum preventive effect, but was similar to vitamin E treatment alone, in terms of the circulating activities of SOD, GST, catalase and TBARS levels.
Environmental noise is a well‐recognized health risk and part of the external exposome—the World Health Organization estimates that 1 million healthy life years are lost annually in Western Europe alone due to noise‐related complications, including increased incidence of hypertension, heart failure, myocardial infarction, and stroke. Previous data suggest that noise works through two paired pathways in a proposed reaction model for noise exposure. As a nonspecific stressor, chronic low‐level noise exposure can cause a disruption of sleep and communication leading to annoyance and subsequent sympathetic and endocrine stress responses leading to increased blood pressure, heart rate, stress hormone levels, and in particular more oxidative stress, being responsible for vascular dysfunction and representing changes of the internal exposome. Chronic stress generates cardiovascular risk factors on its own such as increased blood pressure, blood viscosity, blood glucose, and activation of blood coagulation. To this end, persistent chronic noise exposure increases cardiometabolic diseases, including arterial hypertension, coronary artery disease, arrhythmia, heart failure, diabetes mellitus type 2, and stroke. The present review discusses the mechanisms of the nonauditory noise‐induced cardiovascular and metabolic consequences, focusing on mental stress signaling pathways, activation of the hypothalamic–pituitary–adrenocortical axis and sympathetic nervous system, the association of these activations with inflammation, and the subsequent onset of oxidative stress and vascular dysfunction.
Die letzten Jahrzehnte brachten eine erhebliche Ausweitung unserer Kenntnisse über Physiologie und Pathologie des hypothalamo-neurohypophysären Systems, als dessen Aufgaben vorzugsweise die Regulation des Wasserhaushaltes, die Anregung der Wehentätigkeit und gewisse Vorgänge bei der Lactation erkannt wurden.
In the recent decade, there has been increasing concern on the hazard effect of drugs on different species. Stressful life events contribute to the development of many neurodegenerative and neuropsychiatric disorders including depression and anxiety. Alprazolam (ALP) is commonly used and approved for the medical treatment of panic and anxiety disorders, such as generalized anxiety or social anxiety disorders. Thus, it was of a particular interest to investigate the effect of ALP on the neurons of cerebellar cortex of mice, where mice have genomic similarities to human. So, biochemical, histological and ultrastructural investigations are reported on the cerebellum of adult male mice subjected to three different doses of ALP, for two months. These doses were equivalent to the human therapeutic doses as 0.5, 1 and 1.5 mg. In a dose dependant manner, significant decreases in the levels of both acetylcholine enzyme activities and total glutathione are recorded, indicating that the activity of acetylcholine esterase was inhibited by free radical formation. Little histopathological changes were observed in the cerebellar cortex of mice administered with 0.5 mg ALP. Marked alterations were observed in the Purkinje neurons of cerebellar cortex of mice administered with 1 and 1.5 mg ALP, where unstained haloes are seen around most of these cells. Their nuclei were eccentrically placed, and pyknotic. The intracellular structure of Purkinje cells showed dilatation of both rER and Golgi apparatus. Many small vesicles near the Golgi bodies were accumulated to form clusters, probably indicate disturbance in the vesicular transport between rER and Golgi apparatus. These results reflect the injured effect of high dose ALP on brain activity, performing in the possible ultrastructural abnormalities as well as its oxidative stress.
Bei klinisch gesunden und NNR-insuffizienten Hunden wurden mit der kompetitiven Proteinbindungsanalyse die Cortisolkonzentrationen in Plasma und Harn bestimmt. Bei den gesunden Tieren variierte die basale Plasma-cortisolkonzentration bei täglich mehrfacher Bestimmung zwischen 0,16 und 4,24 (z = 1,48) μg/100 ml und bei nur einmaliger morgendlicher Blutentnahme zwischen 0,50 und 1,70 (z = 0,98) μg/100 ml. Nach exogener ACTH-Stimulation kam es stets zu einem raschen Anstieg des Plasmacortisols, die im Mittel höchste Konzentration wurde mit z = 13,2 (v = 7,9–21,0) μg/100 ml zur 120. Minute bestimmt.
A critical investigation of the separation of free noradrenaline and adrenaline from urine samples revealed serious errors
during sample pretreatment using Al2O3 as adsorbant. An exact and rapid pH adjustment of the sample, using thymol-blue as indicator, proved to be the chief prerequisite
for precise and accurate results. Increasing temperature and pH favour the oxidative decomposition of the catecholamines during
routine analysis. This was examined, using the radiotracer method and liquid scintillation counting.
The aim of this study was to investigate the possible protective role of vitamin A, C, and E on aflatoxin B(1)-induced in human lymphocytes using biochemical approaches. The control group received dimethyl sulfoxide, the second group of cultures were administered aflatoxin B(1) (AFB(1)) at a dose of 5 muM. The other group of cultures were treated with AFB(1)+vitamin A (0.5 and 1.0 and 1.5 microM) and AFB(1)+vitamin C (25, 50, and 100 microM) and AFB(1)+vitamin E (40, 100, and 200 microM). The results of this experiment show that AFB(1) significantly decreased the level of GSH and the activities of superoxide dismutase and GPx and increased level of malondialdehyde. Simultaneous supplementation with vitamin A, C, and E restored these parameters to that of normal range. In conclusion, vitamin A, C, and E exhibited protective effects in human lymphocytes by inhibiting AFB(1)-induced ROS generation.
Résumé L'administration du pimozide, un bloqueur spécifiquement dopaminergique, à des rats intacts et hypophysectomisés, a pour résultats une augmentation du CRF hypothalamique, une diminution concomitante du poids pituitaire ainsi qu'une réaction réduite à l'≪ether stress≫. Ces données indiquent l'existence d'une mécanisme dopaminergique dans le contrôle de libération du MECRF.
Normally, neural, hormonal, haemodynamic, and renal mechanisms all function in a highly integrated way to preserve sodium and water homeostasis. There are two major objectives. The first is to keep the concentration of sodium in the extracellular fluid (ECF) within very tight limits Together with its associated anions, sodium constitutes more than ninety per cent of the total solute in the ECF, and it controls the distribution of water between the cells and the extracellular space. Large deviations in ECF sodium concentration from normal cause the cells to shrink or swell. This can have disastrous effects, particularly on brain function. The body protects the sodium concentration constantly by finely adjusting the water content of the ECF. This is achieved through the secretion and action of antidiuretic hormone (ADH) to control water loss from the kidney. The thirst mechanism helps by controlling the fluid intake to some extent. The second objective is to keep the total sodium content of the ECF within narrow confines, and thereby to maintain a normal ECF volume. Given that sodium is the major cation of the ECF and that the body adjusts the water around it to maintain a normal sodium concentration, then the total number of sodium ions in the ECF will determine the ECF volume. Large deviations in the ECF sodium content from normal cause fluctuations in the circulating blood volume. Both volume contraction and expansion can have disastrous consequences on brain function, particularly in the presence of brain damage. Normally ECF sodium is regulated by many closely coordinated mechanisms which adjust the amount of sodium lost through the kidneys (Schrier and Anderson 1980). Minor alterations in renal tubular reabsorption can have a profound effect on sodium balance, since the filtered load of sodium is enormous in relation to the amount excreted (Leader, Lancet 1984).
Neurohumors: In “chemical synaptic transmission” the messenger substance elicits strictly localized postsynaptic responses of very short duration in effector cells that are contiguous with the respective presynaptic terminals. The active principles (e. g., acetylcholine, noradrenaline) lack several essential attributes of endocrine substances and are, therefore, more appropriately classified as “chemical transmitters”, “neurotransmitters”, or “neurohumors” in contradistinction to “neurohormones”. Electron micrographs of cholinergic neurons show small electron-lucent vesicles that are especially abundant in presynaptic areas. There is circumstantial evidence that these “synaptic vesicles” are intracellular storage sites of acetylcholine. Adrenergic axons and terminals (with deposits of noradrenaline as demonstrated by fluorescence microscopy) contain varying amounts of dense-core vesicles which seem to harbor some of this catecholamine.
Résumé L'occlusion de la carotide, l'épuisement du sodium du plasma et l'effet de la pression de perfusion rénale ont été utilisés pour étudier les niveaux d'acide gras non-estérifié dans la veine rénale. Dans la présente recherche, le système nerveux sympathique controlait la libération vers les reins de l'acide gras non-estérifié. Apparemment, l'épuisement du sodium n'affecte pas les niveaux normaux de repos de cet acide dans la veine rénale.
A preliminary study was carried out to determine the interrelation between ‘ moderato ’ acoustical stimulation and certain physiological changes. It has been shown that ‘ subjective importance ’ of the noise was a material factor effecting changes in skin resistance. Further studies were made of the effect of whole-day exposure to aircraft noise, typewriter noise and white noise. The noises of high subjective importance, the aircraft and the typewriter, both showed measurable physiological changes, whereas that of low subjective importance (white noise) showed no significant change compared with control levels. Estimations from four subjects showed a marked decrease in 24-hour urinary 17-ketosteroid and eosinophils, and an increase in total white cell count, lymphocytes and neutrophils. It is suggested that ‘ moderato ’ noise does not appear to act as a ‘ conventional ’ stressor and it is further postulated that it may result in a characteristic syndrome which is comparable with a mild form of anxiety-depression.
Stress is known to affect synaptic plasticity, dendritic morphology and induces neurotoxic damage in humans, probably through generation of free radicals. Both ex vivo antioxidant vitamins and in vivo free radical scavenging enzymes exist. In the present study, restraint stress induced pro-oxidant status of rat brain was evaluated in terms of measurement of glutathione (GSH), lipid peroxidation (thiobarbituric acid reactive substances, TBARS) and free radical scavenging enzymes activities. The efficacy of antioxidant vitamins A, E and C alone and in combination was also evaluated in modulating inherent antioxidant system in stressed rats.
Rats were treated with vit A, E and C alone (15 mg/kg of body weight) and in combination vitamins (E and C) prior to and after 6 h of restraint stress exposure. Both nonstressed and stressed rats were handled simultaneously. Pro-oxidant status of brain tissue was evaluated by determining the levels of GSH, TBARS and activities of superoxide dismutase (SOD), glutathione-S-transferase (GST) and catalase (CAT).
Restraint stress induced a decrease in the level of GSH and the activities of SOD, GST and catalase, while the levels of TBARS were found elevated. Both pre-stress and post-stress vitamin treatments (either alone or combined) resulted in alteration of these parameters towards their controls values with a relative dominance by latter. Vitamin E was found most effective in restoring inherent antioxidant system, no additive effect was observed in combined vitamin treatment as expected.
Immobilization of rats generated oxidative stress in rat brain, by decreasing the activities of SOD, GST, catalase and glutathione levels, while increasing the lipid peroxidation. Post stress vitamin E treatment was found most effective than vitamins A and C in enhancing the levels of glutathione and activities of SOD, GST and catalase and decreasing lipid peroxidation. Thus vitamin E can be given as a nutritional supplement for scavenging free radical generated in the brain tissues in order to reduce oxidative stress.
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