Full-text resources of PSJD and other databases are now available in the new Library of Science.
Visit https://bibliotekanauki.pl
Preferences help
Polish version English version Language
enabled [disable] Abstract
Number of results

Results found: 4

Number of results on page
first rewind previous Page / 1 next fast forward last

Search results

Search:
in the keywords:  Glutathione
help Sort By:

help Limit search:
first rewind previous Page / 1 next fast forward last
1
Content available remote

Effect of selenium in organic and inorganic form on liver, kidney, brain and muscle of Wistar rats

100%
Sochor J., Pohanka M., Ruttkay-Nedecky B., Zitka O., Hynek D., Mares P., Zeman L., Adam V., Kizek R.
Open Chemistry
|
2012
|
vol. 10
|
issue 5
1442-1451
EN
Selenium is a micronutrient, localized in the active sites of enzymes such as glutathione peroxidase and thioredoxin reductase, and participating together with these enzymes in an antioxidant defence system of organisms against free radicals. Administration of selenium is necessary for maintaining oxidative homeostasis. The present experiment is aimed at investigation of selenium impact on basal metabolic processes and selected antioxidants in a Wistar rat model, fed selenium in organic and inorganic forms. Liver, kidney, brain and muscle were sampled during a month-long feeding with four different doses of selenium (0.075 mg or 1.5 mg of inorganic and/or organic selenium per kg of feed). We found a significant reduction in glutathione level in liver tissue regardless of the form of the administered selenium. On the other hand, selenium caused a decreased glutathione reductase level in the liver and metallothionein level in the liver, kidney and muscle. [...]
2
Content available remote

The effect of vitamin C on amiodarone-induced toxicity in rat thymocytes

100%
Cekic S., Pavlovic D., Sarac M., Kamenov B., Dimic A., Pavlovic V.
Open Medicine
|
2011
|
vol. 6
|
issue 1
58-63
EN
Although, the antiarrhythmic effect of amiodarone (AMD) is well characterized, the mechanism of its toxicity on extracardiac tissues is still poorly understood. Several antioxidants have been shown to prevent AMD-induced toxicity by antioxidant and/or non-antioxidant mechanisms. In the current study, we evaluated the possible protective effect, in vitro, of vitamin C on AMD-induced toxicity in rat thymocytes. Rat thymocytes were cultured with increasing AMD concentrations (1–20 μM) with or without vitamin C (1000 μg/ml), for 24 hours. Cells treatment with AMD resulted in a concentration-dependent increase of hypodiploid cells and a significant decrease in cellular glutathione content. Vitamin C combined with AMD significantly decreased the proportion of hypodiploid cells and markedly increased the cellular glutathione content, compared with AMD treatment alone. These results suggest that treatment with vitamin C may prevent AMD-induced toxicity in rat thymocytes by restoring cellular glutathione content.
3
Content available remote

First synthesis of important secondary oxidative metabolites of morphine and codeine with the Michael addition

100%
Garadnay S., Gyulai Z., Makleit S., Sipos A.
Open Chemistry
|
2013
|
vol. 11
|
issue 3
430-437
EN
Abstract Morphine (1) and codeine (2) are two representatives of medically important, frequently used natural opiates, therefore the exploration of their metabolic pathways and the exact characterization of the metabolites are main targets of their pharmacological studies. These morphinans also play a crucial role in drug abuse; therefore, the analysis and preparation of the metabolites for identification and quantitation in human samples are considered important aims. In order to allow the in-depth analysis of metabolites derived from the oxidative pathways through morphinone (3) and codeinone (4), synthetic procedures have been elaborated for the gram-scale preparation of glutathione and N-acetylcysteine adducts. Primary pharmacological studies revealed the inactive nature of these metabolites in opioid receptor binding tests. Graphical abstract [...]
4
Publication available in full text mode
Content available

Amentoflavone prevents sepsis-associated acute lung injury through Nrf2-GCLc-mediated upregulation of glutathione

100%
Zong Y., Zhang H.
|
2017
|
vol. 64
|
issue 1
93-98
EN
Sepsis is a serious medical problem and is one of the main causes of high mortality in intensive care units. Fifty percent of patients with severe sepsis will develop acute lung injury (ALI). Amentoflavone (AMF) is a polyphenolic compound possessing potent anti-inflammatory activities. The study aimed to explore the protective effects of AMF against ALI in cecal ligation and puncture (CLP)-induced septic rats. The results showed that AMF administration protected against septic ALI, as reflected by marked amelioration of histological injury of lung tissues and decrease of pulmonary edema in CLP-treated rats. AMF ameliorated CLP-induced increase of systemic and lung TNFα and IL-1β and binding activity of p65 NF-κB, indicating the inhibition of inflammation. Moreover, AMF prevented CLP-induced oxidative stress, as evidenced by increase of oxygen consumption rate, decrease of TBARS content, increase of SOD activity and GSH level in lung tissue of CLP-treated rats. CLP resulted in significant decrease of mRNA expression of Nrf2 and GCLc, which was inhibited by AMF. AMF-induced protective effects on ALI, inflammation, and oxidative stress were inhibited by lentivirus shRNA-mediated silence of Nrf2 and buthionine sulphoximine (BSO), an inhibitor of GSH synthesis. AMF increased Nrf2-binding activity in GCLc promoters in lung tissue of CLP-treated rats. The results suggested that AMF protected against ALI in septic rats through upregulation of Nrf2-GCLc signaling, enhancement of GSH antioxidant defense, reduction of oxidative stress and final amelioration of inflammation and histological injury of lung. The data provide new therapeutic options for the treatment of sepsis-associated ALI.
first rewind previous Page / 1 next fast forward last
JavaScript is turned off in your web browser. Turn it on to take full advantage of this site, then refresh the page.