Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0011570 (depression)
 172,036 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In vitro E-rosette formation, lymphocyte mitogenesis, and natural killer (NK) cell activity of human blood lymphocytes were strongly inhibited by high concentrations (10(-4) M) of sodium selenite, sodium selenate, and selenium dioxide. Lower concentrations (10(-5) or 10(-7) M) also inhibited E-rosette formation and natural killer cell activity against K-562 tumor cells. Lymphocyte transformation induced by concanavalin A (con A) or pokeweed mitogen (PWM) was also inhibited by all selenium compounds tested, but only at the highest concentrations (10(-5) and 10(-4) M). There was depression of the total number of viable lymphocytes following incubation with selenium dioxide only at a high concentration (10(-4) M). Interferon production was enhanced at lower levels (10(-9) to 10(-6)M) of selenium dioxide while a higher concentration (10(-5) and 10(-4)M) appeared to inhibit its production. The mechanism of inhibition by selenium compounds (10(-4) M) is due, in part, to the decrease of viable lymphocytes. It is unclear how other and lower concentrations (10(-7) or 10(-9) M) of selenium compounds inhibit E-rosette formation, NK activity, or K-562 tumor cell growth.
 ...
PMID:Effects of selenium in vitro on human T-lymphocyte functions and K-562 tumor cell growth. 241 67

Four different canine mammary tumor (CMT) cell lines and a nonneoplastic primary culture of mammary cells were examined for their in vitro responsiveness to selenium supplementation. These cell lines were found to vary in their metabolic response to increasing concentrations of selenium. Sensitivity to selenium, as sodium selenite, increased with increasing concentrations of this trace element in all of the neoplastic lines. These data also suggest that increasing the plating density of tumor cells further increases the sensitivity to selenium. A relatively selenium-sensitive cell line (CMT-13) and relatively insensitive cell line (CMT-11) were characterized on the basis of reduced growth resulting from selenium supplementation. Increasing the concentration of selenium to 0.75 microgram/ml depressed the growth of CMT-13 and CMT-11 cells by 75% and 11%, respectively, while no inhibition was observed in nonneoplastic cells. These cell lines also varied in their sensitivity to different forms of selenium. Selenodiglutathione was the most effective form of selenium examined that inhibited tumor cell growth. The sensitivity of the neoplastic lines was selenodiglutathione much greater than sodium selenite much greater than selenocystine greater than selenomethionine. None of the forms of selenium examined inhibited the growth of the nonneoplastic mammary cells in culture. Supplementation with sodium selenite (1 microgram Se per ml) for 60 min resulted in a dramatic depression in RNA biosynthesis in CMT-13, but not CMT-11 or nonneoplastic cells.
 ...
PMID:Differential effects of selenium on normal and neoplastic canine mammary cells. 242 32

In 20 hospitalized male chronic alcoholic patients, plasma adrenocorticotrophic hormone (ACTH) levels were estimated by radioimmunoassay and cortisol levels by the competitive protein binding (CPB) method with radioactive selenium-75 on admission and during abstinence along with rating of the degree of depression immediately after the acute phase of the ethanol withdrawal syndrome was over. Duration of drinking ranged from 5 to 25 years and average daily ethanol intake was between 100 and 150 g. Plasma ACTH levels were found to be raised in drinking chronic alcoholics. There was a positive and statistically significant correlation between depression ratings and plasma ACTH concentrations (r = + 0.379; P less than 0.05). In chronic alcoholism the negative feedback mechanism seems to be disturbed between plasma ACTH and cortisol levels which are not normalised after 1 week of total abstinence. Chronic ethanol ingestion might have a direct stimulatory effect on the adrenal cortex leading to dysregulation of the hypothalamo-pituitary-adrenocortical axis.
 ...
PMID:Relationship between plasma adrenocorticotrophic hormone and cortisol concentrations in chronic alcoholic patients with depression. 253 88

Supplementation with increasing quantities of selenium (Se), as sodium selenite, to cultures of rat mammary epithelial cells resulted in a proportional depression in 7,12-dimethylbenz[a]anthracene (DMBA) binding to DNA. A depression in the two major anti bay-region dihydrodiol epoxide-deoxyribonucleoside adducts largely accounted for the reduced binding. DMBA-DNA binding in freshly isolated mammary cells from rats fed a diet containing 2.0 p.p.m. Se and incubated in culture with DMBA for 24 h was decreased 32% compared to binding in cells obtained from rats fed 0.1 p.p.m. Se. DMBA-DNA binding in mammary cells obtained from rats fed supplemental Se for 2 weeks or more was depressed compared to that occurring in cells from unsupplemented rats. The reduced ability of cells obtained from rats previously fed a 2.0 p.p.m. Se diet to activate DMBA to intermediates capable of binding to DNA became increasingly apparent with the duration of exposure to the carcinogen. Consistent with the in vitro supplementation study, cells isolated from rats previously fed a diet containing 2.0 p.p.m. Se had a reduced occurrence of the two major anti dihydrodiol epoxide adducts. The depression in DMBA binding following selenite supplementation, both in vitro and in vivo, supports the ability of Se to inhibit the initiation phase of carcinogenesis.
 ...
PMID:In vitro and in vivo effects of sodium selenite on 7,12-dimethylbenz[a]anthracene--DNA adduct formation in isolated rat mammary epithelial cells. 253 14

Selenium poisoning occurs worldwide in nearly all domestic animals. Acute selenium poisoning is associated with feeding high levels or injecting excessive amounts of selenium and is usually fatal. The acute poisoning may cause gastrointestinal disturbance, muscle weakness, depression of the central nervous system, prostration and death (1-2). Chronic selenium poisoning in cattle, sheep and horses may result from the consumption of seleniferous plants over an extended period of time. Chronic selenium results in ataxia, incoordination, partial blindness, paralysis, loss of hair or wool, abnormal hoof growth and possibly abnormal changes in behavior (1). There is little information regarding the clinical signs and pathology of selenium toxicosis in marine mammals. Likewise, there is little information regarding normal tissue levels or toxicologically significant levels of selenium in these species. The results of these investigations in sea lions, based on clinical signs, pathologic findings and tissue levels of selenium, suggest subacute or chronic selenium poisoning was most likely from dietary fish high in selenium.
 ...
PMID:Selenium toxicosis in three California sea lions (Zalophus californianus). 261 40

Young chicks exhibited a 61% reduction in weight gain when a corn-soybean meal diet was supplemented with 15 mg/kg Se provided as Na selenite. The same level of Se provided as selenomethionine depressed weight gain by 32%. Supplementing the high selenite diet with isoarsenous (14 mg/kg As) additions of As2O5, As2O3, phenylarsonic acid, phenylarsine oxide and roxarsone ameliorated the Se-induced growth depression: As2O5 almost totally restored growth rate; As2O3, phenylarsonic acid and phenylarsine oxide gave intermediate responses; and roxarsone gave only a small ameliorative growth response. Arsanilic acid was without effect in stimulating growth rate of selenite-intoxicated chicks. Dietary addition of .4% L-cysteine produced a growth response in selenite intoxicated chicks that was somewhat greater than that obtained with roxarsone; administering both roxarsone and cysteine corrected growth better than either compound given singly. Both roxarsone and As2O5 also effectively ameliorated the Se-toxicity growth depression caused by selenomethionine (15 mg Se/kg) supplementation, but cysteine showed no efficacy against morbidity caused by this form of Se. Liver Se concentration was elevated 10-fold by selenite and 25-fold by selenomethionine supplementation. The arsenic compounds had varying effects on liver Se, whereas cysteine tended to increase Se concentration. These findings suggest that both inorganic and organic arsenicals as well as cysteine ameliorate selenium toxicity by different mechanisms.
 ...
PMID:Amelioration of selenium toxicity by arsenicals and cysteine. 271 21

To shed light on the causes of Kaschin-Beck disease, which can be prevented by supplementation of the diet with sodium selenite, the interactions between inorganic selenium compounds (selenite and selenate) and humic/fulvic acid were investigated. Selenate was found to be slowly reduced to selenite by humic acid in acidic solution. Selenite was adsorbed on manganese dioxide and iron(III) oxide from solution to a much greater degree than on kaolin, humic acid, Yongshu soil, or silicon dioxide. Feeding mice a diet supplemented with sodium selenite increased the selenium concentration in the kidney, liver, spleen, lung, heart and blood. A diet containing sodium selenite and fulvic acid caused the selenium concentrations in the organs, with the exception of the spleen, to be lower than observed with the selenite-only diet. Selenium and fulvic acid increase the activity of glutathione peroxidase. Sodium selenite and fulvic acid injected in combination into the abdominal cavity of mice and rats were less toxic than either substance alone. Selenite and fulvic acid applied separately enhanced the luminosity of photobacterium phosphoreum T-3 at low concentrations but depressed the luminosity at higher concentrations. Selenite and fulvic acid in combination caused a larger enhancement and a smaller depression of the luminosity than observed with either substance alone. The hypothesis is formulated that Kaschin-Beck disease is caused by selenium levels insufficient to prevent the toxic effects of the organic compounds present in the drinking water of the regions in which the disease is endemic.
 ...
PMID:The effects of humic acid on the chemical and biological properties of selenium in the environment. 295 9

The nonlactating period should be regarded as a preparatory phase for the next lactation, rather than a rest phase from the preceding one. During the early dry period, a diet should be provided that meets nutrient requirements for energy, protein, calcium, phosphorus, selenium, vitamins, and other minerals. This can usually be accomplished by feeding a blend of roughages with little or no grain and providing a vitamin and mineral supplement. The diet during the late dry period, or transitional stage, should provide increased energy (an additional 3 to 4 Mcal), and a PP preventive regimen can be instituted at this time. Five to six pounds of concentrate containing 200 gm of an ammonium sulfate and chloride mixture and 6 gm of niacin can be added to the diet to aid in the transition to lactation. Feeding of high-calcium, lactating-cow grain mix should be avoided until after parturition. Stress should be minimized at and after parturition, and a quiet maternity area should be available. The normal depression in dry matter intake at parturition should be minimized; feeding high-quality roughages at this time is beneficial. Concentrate consumption should be increased gradually following parturition, and careful attention to the soluble and undegradable protein fractions of the diet is warranted. In group feeding situations, introduction to the energy-dense, high-lactation ration should probably be avoided for the first 10 to 14 days postpartum, until the cow is acclimated to the forage mix. Body overconditioning should be avoided. However, attempts to manipulate body condition during the dry period tend to be unrewarding and counterproductive. Following these guidelines should reduce the incidence of metabolic diseases in high-producing dairy cattle.
 ...
PMID:Feeding the dry cow to avoid metabolic disease. 306 14

Studies were conducted to determine the relationship between dietary vitamin E (VE) and the development of nutritional pancreatic atrophy (NPA) in selenium (Se)-deficient chicks. Selenium- and VE-depleted chicks reared on a low Se, amino acid-based diet containing 100 IU VE (as all-rac-alpha-tocopheryl acetate) per kilogram were found to have exceedingly low pancreatic activities of Se-dependent glutathione peroxidase (SeGSHpx) at 8 d of age. Supplementation of the purified diet with 500 or 1,000 IU VE/kg prevented both NPA and the associated growth depression. Use of graded dietary VE levels showed that addition of at least 300 IU/kg was required to overcome the growth depression associated with severe Se deficiency. Although tissue alpha-tocopherol concentrations increased linearly with increasing dietary levels of VE, the response in pancreas was less than (about one-half of) those in liver and heart and, unlike the response in heart, was not affected by dietary Se level. That protection against NPA involved the antioxidant action of VE was suggested by results showing that NPA is promoted by high dietary levels of linoleic acid, that high VE levels correct membrane unsaturated fatty acid losses due to Se deficiency and that NPA is prevented by high levels of other antioxidants. It is suggested that the normally low activities of SeGSHpx and concentrations of alpha-tocopherol in the pancreas may predispose that organ to lesions due to oxidative stress under conditions of severe nutritional Se deficiency that results in further depletion of SeGSHpx. This situation may be overcome by feeding VE at 15-20-fold excesses over the levels normally regarded as nutritionally required.
 ...
PMID:Influence of dietary vitamin E on nutritional pancreatic atrophy in selenium-deficient chicks. 357 59

Acute selenium (Se) toxicosis was evaluated in 20 female crossbred sheep, 8 to 14 mo of age. Five groups of 4 sheep each were given 0.4, 0.6, 0.7, 0.8, or 1.0 mg Se/kg body weight IM. The LD50 for sodium selenite was 0.7 mg Se/kg body weight with a standard error of 0.035 over a 192 hr observation period. The most evident clinical signs were dyspnea and depression. At necropsy, the most consistent lesions in animals which received 0.7, 0.8, and 1.0 mg Se/kg body weight were edematous lungs and pale mottled hearts. Highest tissue Se concentrations in declining order were found in the liver, kidney and heart.
 ...
PMID:Acute selenium toxicosis in sheep. 360 43


<< Previous 1 2 3 4 5 6 7 8 9 10 Next >>