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Query: UMLS:C1260386 (
GSH
)
38,102
document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)
The effect of high doses of ascorbic acid (AA) (200 mg/kg body weight, s. c.) on the values of some biochemical parameters has been studied in guinea pigs (glucose, lactic acid, SH substances and
GSH
in blood, proteins and urea, and the LDH, MDH, ASAT, ALAT, and gamma-GT activities in the serum, the
acid phosphatase
activity in the liver, the gamma-GT activities in the liver and the kidney, and on the levels of SH substances and
GSH
in various organs). Ascorbic acid was administered to the animals in a single dose or in dialy doses for different periods (4 days, 2 weeks, and 7 weeks). The majority of the studied parameters showed a transient increase or decrease of the values which, however, after long term AA administration mostly returned to normal values. After 7 weeks, the level of urea in the serum remained increased (by approximately 30%) contrary to the decreased level of lactic acid, the gamma-GT activity in the serum, and the
GSH
level in some organs. In the experimental series carried out in the different seasons of the year, the results differed in some cases especially after short term AA administration. However, in a few cases, even the values obtained from the control animals tended to differ. If similar changes are to be expected in man after AA administration, then on the basis of our results it can be assumed that in the indicated cases the therapeutic long-term application of large AA doses does not present any hazard to the patient.
...
PMID:[Biochemical changes in guinea pigs after the application of high doses of ascorbic acid]. 3 29
The effects of thyrotropin-releasing hormone (TRH) on a group of 12 normal euthyroid subjects (8 males, 4 females) were analyzed through the metabolic response of oxidoreduction chains of red cells and leucocytes of venous blood. During the reaction of the pituitary-thyroid glandular system (increase of circulating TSH and T-3) to hypothalamic stimulation, the authors have demonstrated: (1) a significant reduction in erythrocytic
GSH
rate with no anomaly of in vitro stability; (2) an obvious stimulation of the two dehydrogenases of the leucocyte pentose shunt: G6PD and 6PGD. Regarding red cells, the same enzymes do not undergo any quantitative modification, and no behavioral difference of
acid phosphatase
is observed. The authors also refer to the biochemical mechanism which is involved for regulation of the oxidoreductive metabolism in the molecular response to hormonal or hrehormonal solicitations.
...
PMID:Effects of thyrotropin-releasing hormone on the erythrocyte and leucocyte enzyme activities in man. 80 52
An acid cholesteryl ester hydrolase activity associated with a fraction containing mitochondria and lysosomes from rat lactating mammary glands was found to have a pH optimum of 5.0. Its sedimentation pattern was closely related to that of the lysosomal enzyme markers
acid phosphatase
and beta-glucuronidase, suggesting that the activity is associated with the lysosomes. The enzyme was strongly inhibited by Cu2+, but was inhibited little by other divalent metal ions. Acid cholesteryl ester hydrolase activity was almost completely abolished by p-hydroxy-mercuribenzoate, but this effect was reversed in the presence of an equimolar concentration of reduced glutathione (
GSH
), indicating that the enzyme requires free sulfhydryl groups for activity. These properties are similar to those of acid, lysosomal cholesteryl ester hydrolases found in other tissues. Acid cholesteryl ester hydrolase activity was 8-14 fold higher in mammary tissue from lactating as compared to virgin rats. Neutral cholesteryl ester hydrolase activities associated with the microsomal and cytosolic subcellular fractions were also increased in lactating glands, but to a lesser extent. In addition, a 2-fold increase in the activities of both the acid and microsomal neutral enzymes was seen during the first few days of lactation, while the cytosolic neutral activity remained constant. These results suggest that mammary gland cholesteryl ester hydrolases have a role in the regulation of cholesterol metabolism in mammary cells, and in the provision of cholesterol for secretion into milk.
...
PMID:Cholesterol metabolism in the rat lactating mammary gland: the role of cholesteryl ester hydrolase. 180 94
The interstitial transudate was investigated in isolated perfused rat hearts. Capillary permeability and the kinetics of interstitial uptake and release were characterized using four different marker molecules (mol wt 522 to 2 X 10(6)). The half-time (t1/2) values (less than 30 to 170 s) and the interstitial concentration after 30 min (100-44% of arterial concentration) reflected the order and inverse order of their molecular weights, respectively. Creatine kinase (CK) and glutathione (
GSH
) were measured during control state, hypoxia, and anoxia, followed by reoxygenation. Interstitial concentrations of CK and
GSH
were higher by a factor of 100 and 8, respectively, compared with the venous effluent. During hypoxia (PO2 = 110 mmHg, i.e., O2 supply = 30% of demand) and reoxygenation there was a significant increase only in the interstitial (not venous) release of CK and
GSH
, which was further increased during anoxia. Ischemia (75 min) and reperfusion cause no interstitial release of lysosomal (
acid phosphatase
) and mitochondrial (glutamate dehydrogenase) enzymes despite a massive loss of cytosolic enzymes. Examination of the interstitial transudate allows characterization of capillary transfer and provides a very sensitive measure of sarcolemmal release phenomena.
...
PMID:Intra- and extracellular markers in interstitial transudate of perfused rat hearts. 245 35
Male Sprague-Dawley rats were treated with clofibrate (CLOF) in the diet for 2 years or with 4 i.p. injections of either diethylnitrosamine (DEN) or benzidine (BZ) followed by phenobarbital (PB) in the diet for 67 weeks, or just with PB for 41 weeks. Animals were killed at frequent intervals, some while still on treatment and others after 3 or 6 months withdrawal of treatment. The livers were subjected to cytochemical measurements of the parenchyma, foci, nodules and carcinomas. The parenchyma of the CLOF groups showed, in general, increases in glucose-6-phosphate dehydrogenase (G-6PD), alpha-glycerophosphate dehydrogenase (alpha-GPD), 5'-nucleotidase (5'-Nu),
acid phosphatase
(AP) and catalase and decreases in uricase and glutathione (
GSH
). CLOF induced a low incidence of
GSH
positive foci; nodules showed universally lower levels of catalase and
GSH
. In the DEN/PB and BZ/PB groups the parenchyma showed increases (even before PB treatment started) in G-6PD and in gamma-glutamyl transpeptidase (gamma-GT) and decreases in
GSH
. DEN raised and BZ lowered 5'-Nu. Neither initiator affected alpha-GPD. Both initiators caused a high incidence of foci positive for G-6PD and for gamma-GT; nodules induced by DEN/PB were mainly positive for gamma-GT and showed an erratic response to the other parameters. Carcinomas, found only after DEN/PB, were all positive for G-6PD and, with one exception, all were negative for alpha-GPD, 5'-Nu, AP and
GSH
. All changes regressed within 3 months of withdrawal of CLOF but not after withdrawal of PB from DEN-initiated animals. In conclusion G-6PD, alpha-GPD and 5'-Nu may be useful histocytochemical parameters for studying the precarcinogenic hepatic changes and nodules induced by peroxisome proliferators and by genotoxic hepatocarcinogens.
...
PMID:A cytochemical study of the livers of rats treated with diethylnitrosamine/phenobarbital, with benzidine/phenobarbital, with phenobarbital, or with clofibrate. 282 19
In an effort to examine cellular responses to cadmium insult a bovine kidney cell line was used to monitor select cell functions for toxicity related alterations. Cadmium concentrations used ranged between 0.2 and 2.5 microM CdCl2 and elicited 0-85% cytotoxicity (cell attachment); 24-h incubations were used for all studies. Toxicity related inhibition of leucine incorporation into cellular protein and thymidine incorporation into DNA was noted. Decreases in protein synthesis activity closely paralleled the cytotoxicity profile; DNA synthesis was a less sensitive indicator to toxicity. K+-dependent phosphatase (KP),
acid phosphatase
(AP) and succinate dehydrogenase (SDH) were monitored in surviving cells and in a cell-free system. Significant inhibitions were detected for all enzyme activities following a 24 h culture with cadmium. KP and AP were most sensitive. In the cell-free system KP was significantly inhibited with 0.1 microM cadmium; AP and SDH were either unchanged or sensitive only at concentrations of 100 microM cadmium or greater. Reduced glutathione (
GSH
) concentration in surviving cells was elevated up to 7-fold over control cultures. The elevation occurred in a progressive toxicity-related manner.
...
PMID:Cytotoxicity related changes in biochemical cell function following in vitro cadmium treatment. 298 56
The effect of selenium (SeO2) and glutathione (
GSH
) on the bioaccumulation of mercury (HgCl2) and on the activities of lysosomal enzymes in four species of tropical estuarine lamellibranchs is reported. A definite correlation between mercury levels in the external medium and tissue uptake and physiological behaviour--opening and closing of shell valves, response to mechanical stimulus, mucus secretion, and incidence of bleeding--was evident. In the clams exposed to Hg (range 0.1-5.0 mg l-1), bioaccumulation was dependent on the ambient concentration of Hg. The highest bioaccumulation of Hg occurred during the initial 24 h exposure period. Further exposure of up to 7 days did not increase the body burden of Hg. Of the four bivalve species exposed to 0.1 mg Hg l-1, Perna viridis showed the highest levels of Hg (approximately 47 ppm) followed by Anadara granosa, A. rhombea (approximately 25 ppm) and Meretrix casta (approximately 9 ppm). The uptake of Hg by A. granosa was greatly reduced by
GSH
, whereas Se enhanced it by 50% when administered in combination with Hg. However, the presence of Hg did not influence the uptake of Se. Exposure to combined
GSH
and Hg resulted in almost complete inhibition of Hg uptake in all four bivalve species. Prior exposure to
GSH
, however, did not have the same influence on their uptake of Hg. Nevertheless, exposure of clams to
GSH
following initial exposure to Hg resulted in complete depuration of accumulated Hg. The activities of lysosomal enzymes--arylsulfatase,
acid phosphatase
, beta-galactosidase and beta-glucuronidase--varied considerably. Treatment with Hg and
GSH
, separately and in combination, significantly enhanced the levels of beta-galactosidase (P less than 0.05) and beta-glucuronidase (P less than 0.001) in the digestive gland after 96 h exposure. Although Se increased beta-glucuronidase activity (P less than 0.001), it had no effect on beta-galactosidase. On exposure to Hg + Se the activity of both enzymes decreased, except in P. viridis where it increased by 39%. The results show unequivocally that Se does not offer any protection against the toxic effects of mercury in marine lamellibranchs, whereas in many marine vertebrates it does.
GSH
, a thiol-rich tripeptide, on the other hand, completely nullifies the toxic effects of Hg, both in vivo and in vitro.
...
PMID:Do selenium and glutathione inhibit the toxic effects of mercury in marine lamellibranchs? 323 22
Glutathion (
GSH
) plays an important role in maintenance of the redox state of the myocardium and acts as the membrane stabilizer. Seventeen patients who underwent cardiac surgery were subjected to cardiopulmonary bypass (CPB) and ischemic cardioplegia. The effect of
GSH
on ischemic myocardium was evaluated by serum lysosomal enzymes (
acid phosphatase
, beta-glucuronidase), isoenzymes of creatine phosphokinase (MB-CPK) and aspartate aminotransferase (m-GOT). standard CPB was instituted and systemic hypothermia was employed.
GSH
was administered to 8 patients in a dose of 200 mg/kg i.v. prior to institution of CPB. Mixed venous blood was sampled before administration of
GSH
, 10 min after institution of CPB and 0, 1, 6, 24 and 48 hr of reperfusion period following cardioplegia. Activity of
acid phosphatase
and beta-glucuronidase were significantly suppressed in the
GSH
-treated group compared to the non-treated group at 24 hours of reperfusion and immediately after aortic unclamping, respectively. Serum MB-CPK levels remained stable during reperfusion, but in the non-treated group, the level increased significantly at 6 hours of reperfusion. Increment of serum m-GOT levels was significantly suppressed at 1, 6 and 24 hours of reperfusion, compared to the non-treated group. These data suggest that pretreatment of
GSH
can protect the myocardium subjected to CPB from ischemic insult.
...
PMID:Effect of glutathion pretreatment on hypothermic ischemic cardioplegia. 710 61
We investigated whether intraportal injection of 150 mg/kg N-acetylcysteine (NAC) into rats reduced hepatic ischemia-reperfusion injury after 48 hours of cold storage and 2 hours of reperfusion. The organ was isolated and perfused to evaluate liver function. The control group received an intraportal injection of 5% dextrose. NAC increased L-cysteine concentrations 15 minutes after injection (1.29 +/- 0.11 mumol/g vs. 2.68 +/- 0.4 mumol/g, P < .05). However, neither treatment modified glutathione liver concentrations relative to preinjection values. After 48 hours of cold storage and 2 hours of reperfusion, livers from NAC-treated rats produced larger amounts of bile than those in the control group (5.04 +/- 1.92 vs. 0.72 +/- 0.37 microL/g liver; P < .05), and showed a significant reduction in liver injury, as indicated by reduced release of lactate dehydrogenase (679.4 +/- 174.4 vs. 1891.3 +/- 268.3 IU/L/g; P < .01), aspartate transaminase (AST) (13.94 +/- 3.5 vs. 38.75 IU/L/g; P < .01), alanine transaminase ALT) (14.92 +/- 4.09 vs. 45.91 +/- 10.58 IU/L/g; P < .05), and
acid phosphatase
, a marker of Kupffer cell injury (344.4 +/- 89.6 vs. 927.3 +/- 150.8 IU/L/g; P < .01) in the perfusate. Reduced glutathione concentrations in the perfusate were similar in the two groups (805 +/- 69 vs. 798 +/- 252 nmol/L/g), whereas oxidized glutathione (GSSG) concentrations were higher in the control group (967 +/- 137 vs. 525 +/- 126 nmol/L/g; P < .05). Reduced glutathione (
GSH
) concentrations in liver tissue collected at the end of perfusion were significantly higher in the NAC group (7.3 +/- 0.9 vs. 4.1 +/- 1.0 mumol/g; P < .05).(ABSTRACT TRUNCATED AT 250 WORDS)
...
PMID:Protective effects of N-acetylcysteine on hypothermic ischemia-reperfusion injury of rat liver. 763 22
Cyclophosphamide causes lung injury in rats through its ability to generate free radicals with subsequent endothelial and epithelial cell damage. In order to observe the protective effects of a potent anti-inflammatory antioxidant, curcumin (diferuloyl methane) on cyclophosphamide-induced early lung injury, healthy, pathogen free male Wistar rats were exposed to 20 mg/100 g body weight of cyclophosphamide, intraperitoneally as a single injection. Prior to cyclophosphamide intoxication oral administration of curcumin was performed daily for 7 days. At various time intervals (2, 3, 5 and 7 days post insult) serum and lung samples were analyzed for angiotensin converting enzyme, lipid peroxidation, reduced glutathione and ascorbic acid. Bronchoalveolar lavage fluid was analyzed for biochemical constituents. The lavage cells were examined for lipid peroxidation and glutathione content. Excised lungs were analyzed for antioxidant enzyme levels. Biochemical analyses revealed time course increases in lavage fluid total protein, albumin, angiotensin converting enzyme (ACE), lactate dehydrogenase, N-acetyl-beta-D-glucosaminidase, alkaline phosphatase,
acid phosphatase
, lipid peroxide levels and decreased levels of glutathione (
GSH
) and ascorbic acid 2, 3, 5 and 7 days after cyclophosphamide intoxication. Increased levels of lipid peroxidation and decreased levels of glutathione and ascorbic acid were seen in serum, lung tissue and lavage cells of cyclophosphamide groups. Serum angiotensin converting enzyme activity increased which coincided with the decrease in lung tissue levels. Activities of antioxidant enzymes were reduced with time in the lungs of cyclophosphamide groups.(ABSTRACT TRUNCATED AT 250 WORDS)
...
PMID:Modulation of cyclophosphamide-induced early lung injury by curcumin, an anti-inflammatory antioxidant. 775 45
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