Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0018799 (heart disease)
34,133 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We have shown that E-type prostaglandins are potent relaxant of the lamb ductus arteriosus at low, but not high, oxygen tensions, and that their effect is possibly controlled by the rate of endogenous PG synthesis. These findings, together with the demonstration of the contractile effect of PG synthesis blockers on the hypoxic ductus in vitro and in vivo and of the relaxant effect of GSH in vitro, strongly suggest that E-type prostaglandins are responsible for maintaining ductus patency during fetal life. The endoperoxide intermediates may act in concert with PGEs. While our findings argue against the idea that PGF2alpha mediates the oxygen-induced constriction, they suggest that suppression of PGE activity in a high oxygen environment might be important to the initiation of ductus closure at birth. An extension of this concept is that continued patency of the ductus after birth results from either the excessive formation of PGEs or from the persistence of a "fetal-like" response of ductal muscle to endogenous or bloodborne PGEs, or both. The present scheme of PGE action is amenable to practical applications. Our work and that of Elliott et al. (15) prove that PGEs can be used to reopen a constricted ductus in children with cyanotic congenital heart disease, thus improving their change of survival during subsequent corrective surgery. Conversely, treatment with blockers of PG synthesis is envisaged as an alternative to surgery for closing a persistent ductus.
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PMID:Prostaglandins: a possible regulator of muscle tone in the ductus arteriosus. 99 35

Lipoperoxide changes and the effect of reduced glutathione (GSH) on that were investigated in cardiopulmonary bypass and endotoxin shock states. In human cardiopulmonary bypass, 26 patients with congenital heart disease were studied and the following results were obtained. Serum lipoperoxide concentration in control group increased in 30 and 60 min after bypass. On the other hand, in the reduced glutathione pretreatment group (100 mg/kg), this change was not observed. In both groups, beta-glucuronidase activity had a tendency to increase after bypass, and it had a close correlation between serum lipoperoxide concentration and beta-glucuronidase activity. In endotoxin shock rats, the results were as follows. 3 hours after injection of endotoxin (10 mg/kg), hepatic lipoperoxide concentration increased and superoxide dismutase (SOD) activity decreased, and hepatic Chemiluminescence counts had a tendency to increase. There was no significant change in serum lipoperoxide concentration after 3 hr, but a significant elevation was observed only after 6 hr. In the reduced glutathione pretreatment group (1,000 mg/kg), serum and hepatic lipoperoxide concentration, hepatic SOD activity, and hepatic Chemiluminescence counts were unchanged. These results suggest that lipoperoxide may increase in shock states and GSH administration may be useful to inhibit lipoperoxide formation.
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PMID:[The effect of reduced glutathione on the changes of lipid-peroxide concentration in shock states--clinical and experimental studies]. 399 53

There is a strong possibility that lipid peroxide (LPO) exerts a great influence on the persistence of pulmonary vascular obstruction (PVO) after radical operation of congenital heart disease with pulmonary hypertension (PH). We investigated the relationship between LOP and PVO, and discussed the effects of scavengers. Fourteen cases of infantile open heart surgery were investigated. LPO, superoxide dismutase SOD and reduced glutathione (GSH) were measured in blood and lung tissue. In the cases of PH group, the levels of lung tissue and plasma LPO showed significantly higher than those of PS group (p < 0.05) before and after radical operation. The levels of Pp/Ps and pulmonary vascular resistance (PVR) of PH cases showed still higher than those of PS group (p < 0.05) even after radical operation. In addition, the levels of plasma and lung tissue SOD, lung tissue GSH of PH cases were lower than those of PG group. These suggest that LPO plays an important role as the cause of PVO before operation and which remains unchanged even after operation. It is to be expected that increase of the free radical scavengers will be effective to suppress the generation of LPO and at last to reduce the level of PVR after operation.
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PMID:[Lipid peroxide and free radical scavengers in congenital heart disease with pulmonary hypertension]. 827 69

In this study, superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px) activities and malondialdehyde (MDA) levels were measured in heart tissues from guinea pigs treated with gentamicin and gentamicin plus vitamin E combination. Mean values were compared with those of the controls treated with only physiological saline solution. The activities of SOD and GSH-Px were found to be lower and the MDA level higher in the hearts from gentamicin-treated animals compared with those of the controls. In the gentamicin plus vitamin E group, however, tissue SOD activity was found to be increased and MDA level decreased significantly relative to the gentamicin group. GSH-Px activity was lowest in this group. Results suggest that gentamicin suppresses SOD and GSH-Px activities in heart tissue, thereby making the tissue more vulnerable to oxidative stress and peroxidative attacks, an important indicator of which is increased MDA level in the heart tissues from gentamicin-treated guinea pigs. This effect might be deleterious when gentamicin is used after cardiac surgery since a potential risk of free radical injury exists in the heart tissue during and/or after cardiac surgery owing to ischaemia and reperfusion processes, and, possibly, in the management of the patients with certain types of heart disease. Our results showed that vitamin E given concomitantly with gentamicin could protect the heart tissue against free radical injury.
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PMID:The effects of gentamicin on the activities of glutathione peroxidase and superoxide dismutase enzymes and malondialdehyde levels in heart tissues of guinea pigs. 952 93

N-acetylcysteine (NAC), the acetylated variant of the amino acid L-cysteine, is an excellent source of sulfhydryl (SH) groups, and is converted in the body into metabolites capable of stimulating glutathione (GSH) synthesis, promoting detoxification, and acting directly as free radical scavengers. Administration of NAC has historically been as a mucolytic agent in a variety of respiratory illnesses; however, it appears to also have beneficial effects in conditions characterized by decreased GSH or oxidative stress, such as HIV infection, cancer, heart disease, and cigarette smoking. An 18-dose oral course of NAC is currently the mainstay of treatment for acetaminophen-induced hepatotoxicity. N-acetylcysteine also appears to have some clinical usefulness as a chelating agent in the treatment of acute heavy metal poisoning, both as an agent capable of protecting the liver and kidney from damage and as an intervention to enhance elimination of the metals.
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PMID:Clinical applications of N-acetylcysteine. 957 47

The purpose of this study was to examine the relationship between arterial hypertension (HTN), chronic heart disease (CHD), and selenium (Se) status. Blood and plasma Se concentrations and Se-dependent GSH-Px activities were determined in 40 patients (HTN = 20; CHD = 20) and 17 healthy volunteers aged 41 to 66 years. Whole blood and plasma Se concentrations were significantly lower in the patients with HTN (19.1% and 26.3%, respectively) and CHD (33.1% and 29.4%, respectively) compared with the values obtained in the controls. The hypertensive patients had lower plasma Se-GSH-Px (26.7%), and those with CHD had both lower whole blood (19.5%) and plasma Se-GSH-Px activities (30.2%). A significant positive correlation between plasma Se-GSH-Px activity and ejection fraction (EF) was found in patients with CHD. There were significant correlations between plasma and whole blood Se concentration, plasma Se concentration and Se-GSH-Px activity, and whole blood Se and Se-GSH-Px activity. Our results showed that hypertensive patients and those with CHD had lower Se levels compared with controls. We conclude that low Se content might be a risk factor for development of HTN and CHD.
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PMID:Blood and plasma selenium levels and GSH-Px activities in patients with arterial hypertension and chronic heart disease. 972 4

N-acetylcysteine (NAC) is the acetylated precursor of both the amino acid L-cysteine and reduced glutathione (GSH). Historically it has been used as a mucolytic agent in chronic respiratory illnesses as well as an antidote for hepatotoxicity due to acetaminophen overdose. More recently, animal and human studies of NAC have shown it to be a powerful antioxidant and a potential therapeutic agent in the treatment of cancer, heart disease, HIV infection, heavy metal toxicity, and other diseases characterized by free radical oxidant damage. NAC has also been shown to be of some value in treating Sjogren's syndrome, smoking cessation, influenza, hepatitis C, and myoclonus epilepsy.
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PMID:N-acetylcysteine. 1105 17

Oxidative stress due to excessive reactive oxygen species (ROS) and depleted antioxidants such as glutathione (GSH) can give rise to apoptotic cell death in acutely diabetic hearts and lead to heart disease. At present, the source of these cardiac ROS or the subcellular site of cardiac GSH loss [i.e., cytosolic (cGSH) or mitochondrial (mGSH) GSH] has not been completely elucidated. With the use of rotenone (an inhibitor of the electron transport chain) to decrease the excessive ROS in acute streptozotocin (STZ)-induced diabetic rat heart, the mitochondrial origin of ROS was established. Furthermore, mitochondrial damage, as evidenced by loss of membrane potential, increases in oxidative stress, and reduction in mGSH was associated with increased apoptosis via increases in caspase-9 and -3 activities in acutely diabetic hearts. To validate the role of mGSH in regulating cardiac apoptosis, L-buthionine-sulfoximine (BSO; 10 mmol/kg ip), which blocks GSH synthesis, or diethyl maleate (DEM; 4 mmol/kg ip), which inactivates preformed GSH, was administered in diabetic rats for 4 days after STZ administration. Although both BSO and DEM lowered cGSH, they were ineffective in reducing mGSH or augmenting cardiomyocyte apoptosis. To circumvent the lack of mGSH depletion, BSO and DEM were coadministered in diabetic rats. In this setting, mGSH was undetectable and cardiac apoptosis was further aggravated compared with the untreated diabetic group. In a separate group, GSH supplementation induced a robust amplification of mGSH in diabetic rat hearts and prevented apoptosis. Our data suggest for the first time that mGSH is crucial for modulating the cell suicide program in short-term diabetic rat hearts.
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PMID:Cardiomyocyte apoptosis induced by short-term diabetes requires mitochondrial GSH depletion. 1580 31

Studies on the lipid peroxidation and antioxidant changes and their significance during myocardial injury have provided a new insight into the pathogenesis of heart disease. The heart failure subsequent to myocardial infarction may be associated with an antioxidant deficit as well as increased myocardial oxidative stress. The present study was designed to evaluate the effect of the combination of ferulic acid and ascorbic acid on antioxidant defense system and lipid peroxidation against isoproterenol (ISO)-induced myocardial infarction in rats. Induction of rats with isoproterenol (150 mg/kg body weight daily, i.p.) for 2 days resulted in a marked elevation in lipid peroxidation, serum marker enzymes (LDH, CPK, GOT, and GPT), and a significant decrease in activities of endogenous antioxidants (SOD, GPx, GST, CAT, and GSH). Pre-co-treatment with the combination of ferulic acid (20 mg/kg body weight/day) and ascorbic acid (80 mg/kg body weight/day) orally for 6 days, significantly attenuated these changes when compared to the individual treatment groups. Histopathological observations were also in correlation with the biochemical parameters. Thus, ferulic acid and ascorbic acid significantly counteracted the pronounced oxidative stress effect of ISO by the inhibition of lipid peroxidation, restoration of antioxidant status, and myocardial marker enzymes levels. In conclusion, these findings indicate the synergistic protective effect of ferulic acid and ascorbic acid on lipid peroxidation and antioxidant defense system during ISO-induced myocardial infarction and associated oxidative stress in rats.
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PMID:Synergistic interactions of ferulic acid with ascorbic acid: its cardioprotective role during isoproterenol induced myocardial infarction in rats. 1644 96

Oxidative stress is common in inflammatory processes of many diseases, including the Chagas' disease, which is characterized by chronic inflammation. The present study is a sequence of a related publication [Oliveira TB, Pedrosa RC, Wilhelm Filho D. Oxidative stress in chronic cardiopathy associated with Chagas' disease. Int J Cardiol in press.] on the same subjects, which showed an increase in oxidative stress associated with the progression of the severity of the disease. Components of the antioxidant system and oxidative biomarkers present in the blood were measured in the same chronic chagasic patients (n=40), before and after vitamin E (800 IU/day) and vitamin C (500 mg/day) supplementation for 6 months. Antioxidant enzymes and contents of reduced glutathione in erythrocytes and plasma TBARS contents were analyzed in four groups of patients in different stages of chronic Chagas heart disease (n=10 each group, groups I, II, III, and IV) according to the Los Andes classification. After the combined vitamin supplementation, TBARS and protein carbonyl levels were decreased in plasma, whilst red cell GSH contents were increased in group I. The vitamin E contents found in the plasma were inversely related to the severity of the disease. No differences in gamma-glutamiltransferase activities were detected but the myeloperoxidase levels were decreased in patients at the initial stages, whilst seric nitric oxide levels were increased in groups II and III. After the antioxidant supplementation, CAT activity was increased in group II, GPx activity was increased in group I, GR activity was increased in groups I and II, whilst the GST activity was decreased in groups II, III and IV. The results clearly indicate that the antioxidant supplementation was able to counteract the progressive oxidative stress associated with the disease. New perspectives for the treatment of Chagas' disease might include an antioxidant therapy in order to attenuate the consequences of oxidative insult related to this disease.
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PMID:Antioxidant therapy attenuates oxidative stress in chronic cardiopathy associated with Chagas' disease. 1732 77


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