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)

The primary defence mechanism of myocytes against peroxides and peroxide-derived peroxyl and alkoxyl radicals is the glutathione redox cycle. The purpose of the present study was to increase the turnover rate of this cycle by stimulating the glutathione peroxidase catalysed reaction (2GSH-->GSSG), the glutathione reductase catalysed reaction (GSSG-->2GSH), or both. Neonatal rat heart cell cultures were subjected to a standardized protocol of oxidative stress using 80 mumol.l-1 cumene hydroperoxide (CHPO) for 0-90 min. The consequences of this protocol were described in terms of cellular concentrations of GSH, GSSG, NADPH and ATP, formation of malondialdehyde (MDA), release of GSSG and of ATP catabolites, depression of contraction frequency, cellular calcium overload, and enzyme release. Trolox-C, an analogue of vitamin E, accelerated the glutathione peroxidase reaction leading to lowering of GSH concentration and the GSH/GSSG ratio, less MDA formation, diminished negative chronotropy, delayed calcium overload, and less enzyme release. Glucose was used to accelerate the glutathione reductase reaction by supplying NADPH, leading to higher GSH concentration and a higher GSH/GSSG ratio, less MDA formation, diminished negative chronotropy, unchanged development of calcium overload, and less enzyme release. As a full turn of the glutathione redox cycle involves both the peroxidase and the reductase reactions, the combination of Trolox-C and glucose was superior to either of the two alone: 90 min following addition of CHPO together with Trolox-C and glucose, the GSH concentration and the GSH/GSSG ratio were almost normal, MDA formation was extremely low, calcium overload was markedly delayed, and enzyme release hardly occurred at all. Cells remained beating in the observation period of 30 min. We conclude that the capacity of the glutathione redox cycle to withstand oxidative stress can be increased by stimulation of either the peroxidase reaction or the reductase reaction, and that optimal redox cycling is achieved by stimulation of both reactions.
 ...
PMID:Protection of myocytes against free radical-induced damage by accelerated turnover of the glutathione redox cycle. 767 3

Classical glutathione peroxidase (GPX) is a useful Se-dependent parameter for determining Se status, but loss of GPX activity alone cannot explain the full effects of Se deficiency. The recent identification of type I thyroxine 5'-deiodinase as a Se-dependent enzyme provides a new potentially critical role for Se. To develop a model of impaired growth due to Se deficiency, second generation deficient weanling rats were fed a Se-deficient amino acid diet with adequate vitamin E and methionine. Initial growth rates of deficient males and females were 53 and 63%, respectively, of rats fed 0.1 micrograms Se/g diet. In short-term experiments with deficient males, liver Se and GPX activity were reduced 99%, liver glutathione-s-transferase activity was increased 114%, plasma thyroxine concentrations were increased 67%, plasma triiodothyronine was decreased 23% and the plasma triiodothyronine:thyroxine ratio was decreased 55%, compared with rats fed 0.2 micrograms Se/g diet. When deficient rats were injected on d 14 with 0, 1, 5 or 10 micrograms Se/100 g, rats grew 4.45, 7.62, 7.17 and 9.05 g/d, respectively, over the next 7 d. Injection with 10 micrograms Se/100 g restored plasma thyroxine and triiodothyronine concentrations 7 d later. Rats injected with 1 microgram Se/100 g rat had significantly altered plasma thyroxine and triiodothyronine concentrations 1 but not 7 d after injection. Infusion of Se-deficient rats with 438 ng triiodothyronine/d for 7 d restored plasma triiodothyronine concentrations but did not increase growth rate compared with rats infused with saline. This model produced a significant growth depression that was significantly reversed by as little as 1 microgram Se/100 g rat, but not by triiodothyronine infusion, suggesting that other Se-dependent roles in addition to 5'-deiodinase and GPX are necessary for adequate growth.
 ...
PMID:Growth and plasma triiodothyronine concentrations are modified by selenium deficiency and repletion in second-generation selenium-deficient rats. 772 88

Cardiac myocytes were exposed to concentrations of potassium antimonyl tartrate (PAT) ranging from 1 to 1000 microM for 1 to 24 hr. Toxicity was assessed by measuring lactate dehydrogenase (LDH) release and by monitoring chronotropic depression. Lipid peroxidation was assessed by measuring the release of thiobarbituric acid reactive substances (TBARS). PAT produced a concentration- and time-dependent depression in chronotropy and an increase in the release of LDH and TBARS. A 4-hr exposure to 100 microM PAT stopped beating and induced significant increases in TBARS and LDH release in the myocyte cultures. The lipid peroxidation and LDH release induced by 100-200 microM PAT at 4 hr could be prevented by pretreatment of the cardiac myocytes with vitamin E or by the simultaneous addition of other antioxidants. Vitamin E continued to protect against lipid peroxidation up to 18 hr after the addition of 100 microM PAT, but failed to provide significant protection against LDH release at this time-point. Both 50 and 100 microM PAT decreased cardiac myocyte glutathione (GSH) levels after a 4-hr exposure. A series of thiol-containing compounds was evaluated for their effects on PAT toxicity. The addition of dithiothreitol, GSH, and 2-mercaptoethanol afforded some degree of protection against lipid peroxidation and LDH release up to 18 hr after the addition of 100 microM PAT. These results suggest that PAT induces lipid peroxidation in cultured cardiac myocytes but that other mechanisms may contribute to cell death with long-term exposures to PAT. Our results also suggest that PAT interacts with thiol-containing compounds.
 ...
PMID:Antimony-induced oxidative stress and toxicity in cultured cardiac myocytes. 783 69

Broiler chicks were kept on feeds amended by the addition of 240 mg monensin and 15 mg selenium with or without 200 mg vitamin E/kg. After 12 days, birds in different groups were orally administered three doses of 250 mg monensin and 5 mg selenium/kg body weight. In the second experiment, after four weeks of adaptation on amended feeds, similar groups were orally administered 40 mg monensin and 1 mg selenium/kg body weight on alternate days for four weeks. Monensin increased the liver iron level. Selenium increased the hepatic levels of selenium and iron while variable degrees of depression occurred in copper, zinc, manganese and magnesium levels. Concurrent administration of monensin and selenium significantly increased the liver selenium levels. A marked decrease in body weight and increased mortality were recorded due to concurrent administration of monensin and selenium.
 ...
PMID:Concurrent oral administration of monensin and selenium to broiler chickens: effects on concentration of different elements in the liver. 801 40

Vitamin E, an antioxidant present in all cellular membranes, is associated with protein complexes in the inner mitochondrial membranes and may affect oxidative changes which occur in these organelles when heart tissue is subjected to hypoxia. The effect of 60 min hypoxia, after a 30 min normoxic equilibration period, on the function and the production of reactive oxygen species (ROS) by cardiac mitochondria from rats fed vitamin E sufficient or deficient diets for 9 weeks was examined. Mitochondria from the hearts of rats fed vitamin E deficient diets had 40-fold less vitamin E and were more susceptible to lipid peroxidation, as compared to heart mitochondria from rats fed vitamin E sufficient diet. Perfusion with normoxic, but not hypoxic, media significantly decreased cardiac vitamin E in deficient, but not sufficient rats. Hypoxia decreased the production of ROS by mitochondria from vitamin E sufficient hearts, compared to normoxia. A similar level of ROS production was seen after hypoxia in mitochondria from vitamin E deficient hearts. However, vitamin E deficiency alone decreased the production of ROS by mitochondria from normoxic hearts, relative to vitamin E sufficient animals. Under all conditions where the production of ROS was decreased, 1 microM calcium increased production to the maximum levels seen in vitamin E sufficient, normoxic heart mitochondria. Mitochondrial function was depressed in mitochondria from hypoxic hearts as compared to mitochondria from normoxic hearts of vitamin E sufficient rats. A similar depression of mitochondrial function was not seen in mitochondria from hypoxic hearts of vitamin E deficient rats. Compensatory changes in response to long-term vitamin E deficiency may be responsible for the differences in response to hypoxia of mitochondria from vitamin E sufficient and deficient rats.
 ...
PMID:Modulation of rat heart mitochondrial function and the production of reactive oxygen by vitamin E deficiency. 802 35

Broiler chicks fed lead or selenium for varying periods were later intoxicated with two levels of either of these elements. In this way different groups of chicks were exposed to lead or selenium alone or a combination of these two. Lead caused increased liver concentrations of lead and iron. Selenium administration increased liver selenium and iron levels while liver copper decreased. Concurrent administration of lead and selenium greatly enhanced the accumulation of both elements in the liver and increased the liver iron. Lead partially counteracted the depression of liver copper caused by selenium. Mortality due to concurrent exposure to lead and selenium was lower when vitamin E was added to the feed. Body weights were markedly suppressed by selenium. The concurrent administration of lead partially alleviated the growth depression caused by selenium. Selenium fed birds had increased relative weights of liver and heart but this increase was of lesser degree in birds given both elements.
 ...
PMID:Effects of oral administration of toxic levels of lead and selenium upon concentration of different elements in the liver of broiler chicks. 813 71

Exposure of rats to high dietary levels of sodium saccharin (NaSac) started in utero produce physiological effects at 30 days post-birth that are similar to those found in pups of iron-deficient dams. These similarities suggest that some of the changes due to NaSac are secondary to iron deficiency. The present experiment investigated whether the effects of 7.5% dietary NaSac in the newborn rat could be prevented by dietary iron and/or folate supplementation. The NaSac-related effects prevented by iron supplementation included anaemia, decreased serum iron and folate, increased serum cholesterol and triglyceride and increased serum vitamin E. Folate supplementation prevented NaSac-induced depression of serum folate and increase in serum vitamin E. Although bladder hyperplasia was increased by dietary iron and/or folate supplementation, the majority of the urinary chemistry changes associated with NaSac treatment were not affected. The results show that some physiological changes associated with NaSac treatment in the newborn rat may occur as a consequence of iron deficiency rather than a direct effect of NaSac treatment. These changes may be independent of the urinary and bladder effects, which are not reversed by iron supplementation.
 ...
PMID:Effects of dietary iron and folate supplementation on the physiological changes produced in weanling rats by sodium saccharin exposure. 822 26

Platelet thromboxane (TX) production was examined in response to dietary copper. Groups of eight rats were fed copper-deficient, -marginal, and -adequate diets providing 0.5, 1.7, and 7.5 micrograms Cu/g, respectively, with controlled dietary Se and vitamin E. Platelets were purified and washed by centrifugation. Separate platelet samples from each rat were challenged with 10 micrograms/ml of collagen and 1 unit/ml (27.3 nM) of thrombin in Tyrode's buffer, 2.0 mM Ca2+. Platelet copper-dependent superoxide dismutase (CuSOD) activity showed a significant depression with reduced diet copper, but platelet glutathione peroxidase activity was unaffected. Challenged platelet TX production showed a significant 1.5- to 2.5-fold increase in response to both dietary copper deficiency and marginality, with highly significant negative correlations between challenged platelet TX production and platelet CuSOD activity and between TX production and copper status (liver copper). Endogenous (unchallenged) platelet lipid hydroperoxide concentrations, measured as free fatty acid hydroperoxides by a glutathione-disulfide-specific glutathione reductase recycling assay, showed a nonsignificant 47-67% increase in copper deficiency. Pooled data showed a significant 71% increase in platelet lipid hydroperoxides in copper deficiency. Platelet TX production showed a significant correlation with endogenous lipid hydroperoxides. The results suggest that dietary copper insufficiency increases platelet TX synthesis through changes in CuSOD in a dose-responsive (diet copper and platelet CuSOD activity) manner, and that platelet TX synthesis is influenced by lipid hydroperoxides (peroxide tone).
 ...
PMID:Thromboxane production in copper-deficient and marginal platelets: influence of superoxide dismutase and lipid hydroperoxides. 842 6

Administration of tetracycline was believed to be associated with an adverse drug reaction in a cat. Clinical signs consisted of anorexia, ptyalism, and signs of depression. The most noticeable biochemical abnormality was a markedly high serum alanine transaminase activity. Treatment consisted of vitamin E and selenium injections and feeding via a gastrostomy tube. Abnormalities noticed on histologic examination of hepatic tissue were centrilobular fibrosis, mild diffuse cholangiohepatitis, and mild hepatic lipidosis. The lipidosis was believed to have resulted from tetracycline administration, whereas the more chronic lesions (hepatic fibrosis and mild cholangiohepatitis) were believed to have resulted from preexisting, subclinical hepatic disease. Because serum alanine transaminase activity returned to reference ranges and the anorexia and ptyalism resolved with cessation of tetracycline administration, these abnormalities were believed to have represented an adverse drug reaction. Treatment of the cat with vitamin E and selenium was instituted on the basis of reported preventive and therapeutic effects in albino rats with tetracycline-induced hepatic lesions. Whether these compounds had any role in accelerating clinical recovery in this cat is uncertain.
 ...
PMID:Increased alanine transaminase activity associated with tetracycline administration in a cat. 844 8

We investigated the effects of chronic volume overload in the absence or presence of vitamin E supplements on the cardiac function and contractility, cardiac malondialdehyde (MDA)--a lipid peroxidation product--cardiac antioxidant enzyme activity and antioxidant reserve in canine model. The dogs were divided into three groups of seven dogs each: group I, control; group II, mitral regurgitation (MR) of 4 months duration; and group III, MR of 4 months duration receiving vitamin E (40 U/kg/daily) orally. MR was created by detaching two or more chordae tendinae to raise left atrial pressure to 2.5 to three times normal. MR produced a decrease in the index of myocardial contractility with little change in myocardial function. Decrease in myocardial (left and right ventricles) contractility was associated with an increase in cardiac MDA, and a decrease in cardiac antioxidant reserve and antioxidant enzyme activity. Prevention of volume overload-induced decrease in myocardial contractility by vitamin E was associated with a decrease in cardiac MDA and an increase in cardiac antioxidant reserve and glutathione peroxidase activity towards control levels. Superoxide dismutase and catalase activity remained depressed in vitamin E-treated group. The results indicate that chronic volume overload decreases the contractility of both right and left ventricles and is associated with oxidative stress in both ventricles. These results support the hypothesis that oxygen free radicals are involved in the chronic volume overload-induced cardiac depression.
 ...
PMID:Oxidative stress as a mechanism of cardiac failure in chronic volume overload in canine model. 872 69


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