UMLS:C0011570 - FACTA Search

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Query: UMLS:C0011570 (depression)
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It has been shown that helium has the ability to affect variously the rates of certain metabolic reactions in vitro as compared to nitrogen. An attempt has been made to approximate the sites of action in mouse liver preparations. The following results have been obtained by the substitution of a mixture of 80 per cent helium and 20 per cent oxygen for air: (a) An increase in the rate of oxygen consumption and carbon dioxide production to the same degree, the respiratory quotient remaining unchanged. (b) A decrease in the magnitude of cyanide inhibition. The effectiveness of helium increases with the degree of the cyanide inhibition. (c) No effect on the activity of slices which have been poisoned with fluoride when either lactate or pyruvate has been added as a substrate. (d) A change in the rate, and the slope of the curve of oxygen consumption in liver homogenates which are utilizing pyruvate as a substrate. The use of helium relative to nitrogen under anaerobic conditions causes: (a) A depression of the glycolytic rates in both mouse liver slices and diaphragm. (b) An increase in the carbon dioxide evolution and lactic acid production of mouse liver homogenates oxidizing either glucose and hexose diphosphate, or hexose diphosphate alone. In neither slices nor homogenates does the addition of fluoride and the use of pyruvate as the hydrogen acceptor alter the fundamental response of the preparations. The following hypotheses have been advanced and discussed in order to explain the observed phenomena: 1. Helium does not alter the substrate utilized by the tissue. 2. The gas interferes in some way with the cyanide-cytochrome oxidase bond, but may not affect cytochrome oxidase in the absence of cyanide. 3. The citric acid cycle is not subject to the influence of helium in tissue slices, but is altered in an unexplained fashion in homogenates. It is postulated that a rearrangement of particulate surfaces may be the significant factor here. 4. The glycolytic cycle is the site of both an inhibitory and an acceleratory effect of helium. The locus of the inhibition lies above the aldolase reaction and that of the acceleration between the aldolase and enolase reactions.
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PMID:Effect of helium on the respiration and glycolysis of mouse liver slices. 1303 67

Tethered cord syndrome (TCS) is a stretch-induced functional disorder of the spinal cord. The mechanical cause of TCS is an inelastic structure anchoring the caudal end of the spinal cord that prevents cephalad movement of the lumbosacral cord. Stretching of the spinal cord occurs in patients either when the spinal column grows faster than the spinal cord or when the spinal cord undergoes forcible flexion and extension. Research in patients and experimental animals suggests that there is a link between the clinical dysfunctions that characterize TCS and putative pathophysiological changes that accompany this syndrome. Among these changes are depression of electrophysiological activity and shifts in the reduction/oxidation ratio of cytochrome oxidase. The latter suggests that there is impairment of oxidative metabolism. These putative pathophysiological changes in TCS occur mainly within the lumbosacral cord under excessive tension. The authors discuss the pathophysiology of TCS and examine related symptoms.
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PMID:Pathophysiology of tethered cord syndrome: correlation with symptomatology. 1520 89

The phloroglucinol derivative hyperforin has been recently shown to be a major antidepressant component in the extract of Hypericum perforatum. Experimental studies clearly demonstrated its activity in different behavioral models of depression. Moreover clinical studies linked the therapeutic efficacy of Hypericum extracts to their hyperforin content, in a dose-dependent manner. The molecular mechanism of action of hyperforin is still under investigation. Hyperforin has been shown to inhibit, like conventional antidepressants, the neuronal uptake of serotonin, norepinephrine and dopamine. However, hyperforin inhibits also the uptake of gamma-aminobutyric acid (GABA) and L-glutamate. The uptake inhibition by hyperforin does not involve specific binding sites at the transporter molecules; its mechanism of action seems to be related to sodium conductive pathways, leading to an elevation in intracellular Na(+) concentration. Other additional mechanisms of action of hyperforin, involving ionic conductances as well synaptosomal and vesicular function, have been suggested. In addition to its antidepressant activity, hyperforin has many other pharmacological effects in vivo (anxiolytic-like, cognition-enhancing effects) and in vitro (antioxidant, anticyclooxygenase-1, and anticarcinogenic effects). These effects could be of clinical importance. On the other hand, the role of hyperforin in the pharmacological interactions occurring during Hypericum extract therapy must be fully investigated. Hyperforin seems to be responsible for the induction of liver cytochrome oxidase enzymes and intestinal P-glycoprotein. Several pharmacokinetic studies performed in rats and humans demonstrated oral bioavailability of hyperforin from Hypericum extract. Only recently a new chromatographic method for detection of hyperforin in the brain tissue has been developed and validated. Taking into account the chemical instability of hyperforin, current efforts are directed to the synthesis of new neuroactive derivatives.
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PMID:Role of hyperforin in the pharmacological activities of St. John's Wort. 1549 71

Children and adolescents aged 4-16 years with the diagnosis of acute respiratory viral infection with long-lasting fever, manifestations of intoxication syndrome, and catarrhal symptoms were examined. In children and adolescents suffering from frequent diseases and presented with acute respiratory viral infection we found disorders in the immune status (depression of the cellular component, helper/suppressor imbalance, suppressed production of IgA and hyperproduction of IgM, decreased concentration of secretory IgA in the saliva) in comparison with children rarely falling ill. The redox potential and lymphocyte cytochrome C content were decreased in adolescents often falling ill, while the content of cytochrome oxidase did not change. A negative multiple correlation (R=6.8, p<0.005) was detected between the decrease in cytochrome C content and NADP/NADPH redox potential and increase in the immunoregulatory index. ATP content in lymphocyte from adolescents frequently falling ill remained 21% decreased during the first 2 weeks after acute respiratory viral infection, while the ATP/ADP ratio was shifted towards dinucleotide, which also indicated disorders in ATP synthesis in lymphocytes.
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PMID:Relationship between immune status and activity of the lymphocyte energy supply system in adolescents suffering from frequent diseases. 1622 84

The potential toxicity of the herbicide Roundup and its fundamental substance (glyphosate) was tested in bioenergetic functions of isolated rat liver mitochondria. Roundup stimulates succinate-supported respiration twice, with simultaneous collapse of transmembrane electrical potential, while glyphosate used in the same concentrations does not induce any significant effect. Additionally, Roundup depresses state 3 respiration by about 40%, at 15 mM, whereas uncoupled respiration in the presence of FCCP is depressed by about 50%. Depression of uncoupled respiratory activity is mediated through partial inhibition of mitochondrial complexes II and III, but not of complex IV. The phosphorylative system was affected by both a direct and an indirect effect on the F0F1 ATPase activity. The addition of uncoupled concentrations of Roundup to Ca2+-loaded mitochondria treated with Ruthenium Red resulted in non-specific membrane permeabilization, as evidenced by mitochondrial swelling in isosmotic sucrose medium. Therefore, the uncoupling of oxidative phosphorylation is also related to the non-specific membrane permeabilization induced by Roundup. Glyphosate alone does not show any relevant effect on the mitochondrial bioenergetics, in opposition to Roundup formulation products. The differences in the toxicity observed could be either attributed to some products of Roundup or to a synergic effect of glyphosate and formulation products. Bearing in mind that mitochondria is provided with a variety of bioenergetic functions mandatory for the regulation of intracellular aerobic energy production and electrolyte homeostasis, these results question the safety of Roundup on animal health.
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PMID:Comparative effects of the Roundup and glyphosate on mitochondrial oxidative phosphorylation. 1626 81

Ladostigil is a novel drug that inhibits acetyl and butyrylcholinesterase, and monoamine oxidase (MAO) A and B selectively in the brain. It reverses memory deficits induced by chronic inhibition of cortical cytochrome oxidase in rats and has anxiolytic and antidepressant-like activity in prenatally-stressed rats. Ladostigil also prevents oxidative-nitrative stress induced in astrocytes in the hippocampal CA1 region following icv injection of STZ in rats which also impairs their episodic memory. The unique combination of ChE and MAO enzyme inhibition combined with neuroprotection makes ladostigil a potentially useful drug for the treatment of dementia in subjects that also have extrapyramidal dysfunction and depression.
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PMID:Ladostigil, a novel multifunctional drug for the treatment of dementia co-morbid with depression. 1701 66

The objective of this update is to give an overview of the effects of dietary nutrients on the structure and certain functions of the brain. As any other organ, the brain is elaborated from substances present in the diet (sometimes exclusively, for vitamins, minerals, essential amino-acids and essential fatty acids, including omega- 3 polyunsaturated fatty acids). However, for long it was not fully accepted that food can have an influence on brain structure, and thus on its function, including cognitive and intellectuals. In fact, most micronutrients (vitamins and trace-elements) have been directly evaluated in the setting of cerebral functioning. For instance, to produce energy, the use of glucose by nervous tissue implies the presence of vitamin B1; this vitamin modulates cognitive performance, especially in the elderly. Vitamin B9 preserves brain during its development and memory during ageing. Vitamin B6 is likely to benefit in treating premenstrual depression. Vitamins B6 and B12, among others, are directly involved in the synthesis of some neurotransmitters. Vitamin B12 delays the onset of signs of dementia (and blood abnormalities), provided it is administered in a precise clinical timing window, before the onset of the first symptoms. Supplementation with cobalamin improves cerebral and cognitive functions in the elderly; it frequently improves the functioning of factors related to the frontal lobe, as well as the language function of those with cognitive disorders. Adolescents who have a borderline level of vitamin B12 develop signs of cognitive changes. In the brain, the nerve endings contain the highest concentrations of vitamin C in the human body (after the suprarenal glands). Vitamin D (or certain of its analogues) could be of interest in the prevention of various aspects of neurodegenerative or neuroimmune diseases. Among the various vitamin E components (tocopherols and tocotrienols), only alpha-tocopherol is actively uptaken by the brain and is directly involved in nervous membranes protection. Even vitamin K has been involved in nervous tissue biochemistry. Iron is necessary to ensure oxygenation and to produce energy in the cerebral parenchyma (via cytochrome oxidase), and for the synthesis of neurotransmitters and myelin; iron deficiency is found in children with attention-deficit/hyperactivity disorder. Iron concentrations in the umbilical artery are critical during the development of the foetus, and in relation with the IQ in the child; infantile anaemia with its associated iron deficiency is linked to perturbation of the development of cognitive functions. Iron deficiency anaemia is common, particularly in women, and is associated, for instance, with apathy, depression and rapid fatigue when exercising. Lithium importance, at least in psychiatry, is known for a long time. Magnesium plays important roles in all the major metabolisms: in oxidation-reduction and in ionic regulation, among others. Zinc participates among others in the perception of taste. An unbalanced copper metabolism homeostasis (due to dietary deficiency) could be linked to Alzheimer disease. The iodine provided by the thyroid hormone ensures the energy metabolism of the cerebral cells; the dietary reduction of iodine during pregnancy induces severe cerebral dysfunction, actually leading to cretinism. Among many mechanisms, manganese, copper, and zinc participate in enzymatic mechanisms that protect against free radicals, toxic derivatives of oxygen. More specifically, the full genetic potential of the child for physical growth ad mental development may be compromised due to deficiency (even subclinical) of micronutrients. Children and adolescents with poor nutritional status are exposed to alterations of mental and behavioural functions that can be corrected by dietary measures, but only to certain extend. Indeed, nutrient composition and meal pattern can exert either immediate or long-term effects, beneficial or adverse. Brain diseases during aging can also be due to failure for protective mechanism, due to dietary deficiencies, for instance in anti-oxidants and nutrients (trace elements, vitamins, non essential micronutrients such as polyphenols) related with protection against free radicals. Macronutrients are presented in the accompanying paper.
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PMID:Effects of nutrients (in food) on the structure and function of the nervous system: update on dietary requirements for brain. Part 1: micronutrients. 1706 9

Mitochondrial dysfunction has been implicated as a contributing factor in epileptic seizures. Present studies were carried out to decipher seizure-dependent changes in mitochondrial function and ultrastructure in the chronic condition of temporal lobe epilepsy (TLE) induced by pilocarpine in rat hippocampus. Enzyme assay revealed significant depression of the activity of mitochondrial- and nuclear-encoded cytochrome oxidase (COX). Conversely, the activity of nuclear-encoded succinate dehydrogenase (SDH) remained unchanged. Discernible mitochondrial ultrastructural damage, varying from swelling to disruption of membrane, was observed in the hippocampus. Quantitative real-time PCR and Western blotting showed the expression of mitochondrial-encoded COX subunit III (COXIII) dropped significantly during the chronic seizure activity; the corresponding expression of COX subunit IV (COXIV) displayed no significant change. Most likely, our results suggest that dysfunction of mitochondrial COX respiratory enzyme and mitochondrial ultrastructural damage in the hippocampus are associated with prolonged seizure during experimental TLE and mitochondria are more vulnerable to epilepsy.
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PMID:Mitochondrial dysfunction and ultrastructural damage in the hippocampus of pilocarpine-induced epileptic rat. 1709 49

Protein kinase A (PKA) activation has been implicated in early-phase ischemic preconditioning. We recently found that during ischemia PKA activation causes inactivation of cytochrome-c oxidase (CcO) and contributes to myocardial damage due to ischemia-reperfusion. It may be that beta-adrenergic stimulation during ischemia via endogenous catecholamine release activates PKA. Thus beta-adrenergic stimulation may mediate both myocardial protection and damage during ischemia. The present studies were designed to determine the role of the beta(1)-adrenergic receptor (beta(1)-AR) in myocardial ischemic damage and ischemic preconditioning. Langendorff-perfused rabbit hearts underwent 30-min ischemia by anterior coronary artery ligation followed by 2-h reperfusion. Occlusion-reperfusion damage was evaluated by delineating the nonperfused volume of myocardium at risk and volume of myocardial necrosis after 2-h reperfusion. In some hearts ischemic preconditioning was accomplished by two 5-min episodes of global low-flow ischemia separated by 10 min before coronary occlusion-reperfusion. Orthogonal electrocardiograms were recorded, and coronary flow was monitored by a drip count. Three hearts from each experimental group were used to determine mitochondrial CcO and aconitase activities. Two-hour reperfusion after occlusion caused an additional decrease in CcO activity vs. that after 30-min occlusion alone. Blocking the beta(1)-AR during occlusion-reperfusion reversed CcO activity depression and preserved myocardium at risk for necrosis. Similarly, mitochondrial aconitase activity exhibited a parallel response after occlusion-reperfusion as well as for the other interventions. Furthermore, classic ischemic preconditioning had no effect on CcO depression. However, blocking the beta(1)-AR during preconditioning eliminated the cardioprotection. If the beta(1)-AR was blocked after preconditioning, the myocardium was preserved. Interestingly, in both of the latter cases the depression in CcO activity was reversed. Thus the beta(1)-AR plays a dual role in myocardial ischemic damage. Our findings may lead to therapeutic strategies for preserving myocardium at risk for infarction, especially in coronary reperfusion intervention.
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PMID:beta1-Adrenoreceptor activation contributes to ischemia-reperfusion damage as well as playing a role in ischemic preconditioning. 1723 52

Stressful experiences and genetic predisposition have both independent and interactive contributions to the development of depression. The serotonergic system is involved in the development of depression, and administration of neurotoxins that specifically compromise its function leads to symptoms of affective disorders. In order to find out which brain regions are most affected by stress, partial serotonergic denervation and their combination, chronic variable stress (CVS) was applied for 3 week. Serotonergic denervation was elicited by parachloroampetamine (PCA, 2mg/kg), and cytochrome oxidase histochemistry was used to characterize the long-term levels of neuronal oxidative energy metabolism. PCA pretreatment blocked the increase in oxidative activity in chronically stressed rats in medial preoptic area, cortical and medial amygdala. PCA raised oxidative activity compared to control animals in substantia nigra and ventrolateral division of laterodorsal thalamus. CVS reduced the oxidative activity induced by PCA in suprachiasmatic hypothalamus, anteroventral thalamus, hippocampal CA3 region and cortical amygdala. In the dorsal part of the anterior olfactory nucleus chronic stress blocked the decrease in oxidative activity evoked by PCA. Conclusively, partial serotonergic denervation with PCA and chronic variable stress both had independent effects on long-term energy metabolism in several rat brain structures, tending to increase it. However, partial serotonergic denervation by parachloroampetamine and chronic variable stress had in many brain regions an interactive effect on energy metabolism, each factor reducing the effect of the other, which could reflect the weakening of adaptive mechanisms.
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PMID:Changes in regional long-term oxidative metabolism induced by partial serotonergic denervation and chronic variable stress in rat brain. 1788 57

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