scholarly journals Glutathione-S-transferase, Superoxide Dismutase (GST, SOD) Levels, Protein Content and Lipid Peroxidation in Schizothorax plagiostomus under the Infection of Pomphorhynchus in Nallah Sukhnag of Kashmir Valley

2017 ◽  
Vol 20 (9) ◽  
pp. 442-446 ◽  
Author(s):  
Shafaquat Nabi ◽  
Syed Tanveer ◽  
Showkat Ahmad Ganie
2016 ◽  
Vol 2016 ◽  
pp. 1-12 ◽  
Author(s):  
Israel Pérez-Torres ◽  
Verónica Guarner-Lans ◽  
Alejandra Zúñiga-Muñoz ◽  
Rodrigo Velázquez Espejel ◽  
Alfredo Cabrera-Orefice ◽  
...  

We report the effect of cross-sex hormonal replacement on antioxidant enzymes from rat retroperitoneal fat adipocytes. Eight rats of each gender were assigned to each of the following groups: control groups were intact female or male (F and M, resp.). Experimental groups were ovariectomized F (OvxF), castrated M (CasM), OvxF plus testosterone (OvxF + T), and CasM plus estradiol (CasM + E2) groups. After sacrifice, retroperitoneal fat was dissected and processed for histology. Adipocytes were isolated and the following enzymatic activities were determined: Cu-Zn superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GPx), glutathione-S-transferase (GST), and glutathione reductase (GR). Also, glutathione (GSH) and lipid peroxidation (LPO) were measured. In OvxF, retroperitoneal fat increased and adipocytes were enlarged, while in CasM rats a decrease in retroperitoneal fat and small adipocytes are observed. The cross-sex hormonal replacement in F rats was associated with larger adipocytes and a further decreased activity of Cu-Zn SOD, CAT, GPx, GST, GR, and GSH, in addition to an increase in LPO. CasM + E2exhibited the opposite effects showing further activation antioxidant enzymes and decreases in LPO. In conclusion, E2deficiency favors an increase in retroperitoneal fat and large adipocytes. Cross-sex hormonal replacement in F rats aggravates the condition by inhibiting antioxidant enzymes.


2010 ◽  
Vol 88 (10) ◽  
pp. 977-985 ◽  
Author(s):  
R. K. Sangeetha ◽  
V. Baskaran

Retinol (ROH) and provitamin-A carotenoids are recommended to treat ROH deficiency. Xanthophyll carotenoids, being potent antioxidants, can modulate health disorders. We hypothesize that nonprovitamin-A carotenoids may yield ROH and suppress lipid peroxidation under ROH deficiency. This study aimed to (i) study the possible bioconversion of astaxanthin and lutein to ROH similar to β-carotene and (ii) determine the antioxidant potential of these carotenoids with reference to Na+/K+-ATPase, antioxidant molecules, and lipid peroxidation (Lpx) induced by ROH deficiency in rats. ROH deficiency was induced in rats (n = 5 per group) by feeding a diet devoid of ROH. Retinol-deficient (RD) rats were gavaged with astaxanthin, lutein, β-carotene, or peanut oil alone (RD group) for 7 days. Results show that the RD group had lowered plasma ROH levels (0.3 µmol/L), whereas ROH rose in astaxanthin and β-carotene groups (4.9 and 5.7 µmol/L, respectively), which was supported by enhanced (69% and 70%) intestinal β-carotene 15,15′-monooxygenase activity. Astaxanthin, lutein, and β-carotene lowered Lpx by 45%, 41%, and 40% (plasma), respectively, and 59%, 64%, and 60% (liver), respectively, compared with the RD group. Lowered Na+/K+-ATPase and enhanced superoxide dismutase, catalase, and glutathione-S-transferase activities support the lowered Lpx. To conclude, this report confirms that astaxanthin is converted into β-carotene and ROH in ROH-deficient rats, and the antioxidant potential of carotenoids was in the order astaxanthin > lutein > β-carotene.


2022 ◽  
Vol 20 (4) ◽  
pp. 63-70
Author(s):  
O. V. Smirnova ◽  
V. V. Tsukanov ◽  
A. A. Sinyakov ◽  
O. L. Moskalenko ◽  
N. G. Elmanova ◽  
...  

Background. The problem of gastric cancer remains unresolved throughout the world, while chronic atrophic gastritis (CAG) increases the likelihood of its development by 15 times. In the Russian Federation, the incidence of gastric cancer (GC) is among the highest, with it prevailing among males. One of the leading mechanisms in molecular pathology of membranes is lipid peroxidation (LPO). The severity of oxidative membrane damage depends on concomitant diseases, contributing to emergence and progression of pathological processes and development of cancer. Currently, the problem of LPO is unsolved in biological systems.The aim of this study was to investigate the state of LPO and antioxidant defense system in CAG and GC. Materials and methods. The parameters were studied in 45 patients with CAG and 50 patients with GC. The control group included 50 practically healthy volunteers without gastrointestinal complaints, who did not have changes in the gastric mucosa according to the fibroesophagogastroduodenoscopy (FEGDS) findings.Results. In patients with CAG, an increase in malondialdehyde, superoxide dismutase, catalase, glutathione S-transferase, and glutathione peroxidase was found in the blood plasma compared with the control group. In patients with CAG, lipid peroxidation was activated, and the malondialdehyde level increased by 3.5 times relative to normal values. At the same time, the body fought against oxidative stress by increasing the activity of antioxidant enzymes, such as superoxide dismutase, catalase, glutathione S-transferase, and glutathione peroxidase. All patients with GC showed pronounced oxidative stress in the blood plasma in the form of a 45-fold increase in malondialdehyde. The activity of the main antioxidant enzyme superoxide dismutase was reduced in GC. Catalase was activated, which indicated pronounced oxidative stress, significant damage to blood vessels, and massive cell death. Glutathione-related enzymes (glutathione S-transferase and glutathione peroxidase) and the antioxidant protein ceruloplasmin were activated, which also indicated significant oxidative stress and severe intoxication in patients with GC.Conclusion. Depending on the stage and type of cancer, an in-depth study of lipid peroxidation and factors of the antioxidant defense system can be used to correct therapy and prevent cancer and can serve as markers of progression and prognosis in gastric cancer. 


2020 ◽  
Vol 39 (7) ◽  
pp. 920-929
Author(s):  
G Eğimezer ◽  
ÜV Üstündağ ◽  
PS Ateş ◽  
İ Ünal ◽  
FD Üstündağ ◽  
...  

Cancer continues to be a major cause of mortality globally. Zebrafish present suitable models for studying the mechanisms of genotoxic carcinogens. The aim of this study was to investigate the interaction between oxidant–antioxidant status, apoptosis and immunity in zebrafish that were exposed to three different genotoxic carcinogens methylnitrosourea, dimethylbenzanthracene, benzoapyrene and methylnitrosourea + dimethylbenzanthracene starting from early embryogenesis for 30 days. Lipid peroxidation, nitric oxide levels, superoxide dismutase and glutathione- S-transferase activities and mRNA levels of apoptosis genes p53, bax, casp3a, casp2 and immunity genes fas, tnfα and ifnγ1 were evaluated. The disruption of the oxidant–antioxidant balance accompanied by altered expressions of apoptotic and immunity related genes were observed in different levels according to the carcinogen applied. Noteworthy, ifnγ expressions decreased in all carcinogen-exposed groups. Our results will provide basic data for further carcinogenesis research in zebrafish models.


Author(s):  
Daniele Silva ◽  
Lenard Serrano ◽  
Eduardo Alves de Almeida

Nile tilapias (Oreochromis niloticus) of three groups with different weights (juvenile, adults of lower and higher weight) were exposed to benzo[a]pyrene (0.5 mg.L-1), cupper (0.5 mg.L-1), cadmium (0.5 mg.L-1) and diazinon (1.0 mg.L-1), for 72 h. In order to determine how animals of the same species respond to such contaminants over weight gain, biochemical biomarkers (glutathione S-transferase, superoxide dismutase, catalase, glutathione peroxidase, acetylcholinesterase, carboxylesterase and lipid peroxidation levels) were analyzed in liver and in gills. In the juvenile group the catalase was induced by exposure to cupper in gills, while lipid peroxidation levels were low. In the same group the glutathione S-transferase was induced in gills, likewise glutathione peroxidase was induced by diazinon in liver. In gills of the group of adults of lower weight the low lipid peroxidation levels, in exposure to diazinon treatment, may be related to inhibition of carboxylesterase. In the group of adults of higher weight was not observed adverse effect of contaminants, except for exposure to diazinon in esterases. Thus, this study prove clear evidence that it is necessary to take into account in biomonitoring programs, the weight, the tissue and the development, when using tilapia as tested organism.


2021 ◽  
Author(s):  
Joanna Maria Drozdz-Afelt ◽  
Beata Barbara Koim-Puchowska ◽  
Piotr Kaminski

Abstract Aims: The aim of the study was to analyze the activity of antioxidant enzymes (glutathione S-transferase, catalase, superoxide dismutase) in order to determine the role of detoxification mechanisms in prostate cancer. The concentration of malondialdehyde, which is an indicator of lipid peroxidation in cancer patients, was also tested.Methods: The activities of superoxide dismutase (SOD), catalase CAT and glutathione S-transferase (GST ) were measured using ready-made kits; lipid peroxidation intensity was determined by the thiobarbituric acid method.Results: Superoxide dismutase was the only enzyme among antioxidant and detoxification enzymes for which a statistically significant difference in activity was found between the studied groups [1.4 U * ml-1 in patients vs. 1.6 U * ml-1 in control]. No statistically significant differences were found for two other biomarkers of antioxidant activity (GST, CAT). There were also no statistically significant differences in the concentration of MDA between the group of men with prostate cancer and the control group.Conclusion: The lower SOD activity in men with prostate cancer may be due to a deficiency in their antioxidant defense system.


1992 ◽  
Vol 262 (6) ◽  
pp. L748-L756 ◽  
Author(s):  
S. J. Sullivan ◽  
T. D. Oberley ◽  
R. J. Roberts ◽  
D. R. Spitz

HA-1 hamster fibroblasts receiving fresh media every 24 h were continuously passaged in progressively increasing O2 concentrations for 18 mo (designated O2R95). These cells were significantly more resistant than parental HA-1 to clonogenic inactivation mediated by 95% O2 without media replacement. The O2R95 cell line exhibited increases in the activities of catalase (CAT), Mn superoxide dismutase (MnSOD), Cu,Zn superoxide dismutase (Cu,Zn SOD), and glutathione peroxidase (GPx). O2R95 cells demonstrated uniformly distributed increased staining for CAT, MnSOD, Cu,Zn SOD, and GPx proteins, as determined by immunohistochemistry. Cellular resistance to and metabolism of 4-hydroxy-2-nonenal (4HNE), a toxic byproduct of lipid peroxidation implicated in mechanisms of O2 toxicity, was examined in HA-1 and O2R95 cell lines. O2R95 cells were significantly more resistant to 4HNE cytotoxicity, which was accompanied by a significant increase in 4HNE metabolism. O2R95 cells also demonstrated an increase in total glutathione (GSH) and glutathione S-transferase (GST) activity, an enzymatic system believed to be involved with 4HNE metabolism. Furthermore, homogenates from O2R95 cells consumed greater quantities of 4HNE in the presence of NADPH (but not NADH, NAD+, or NADP+), suggesting that an enzyme(s) utilizing NADPH contributes to 4HNE metabolism, resistance to 95% O2 and 4HNE as well as increased total GSH, antioxidant enzyme activities, and NADPH-dependent metabolism of 4HNE, persisted in O2R95 cells for 75 days of growth in 21% O2. These findings are compatible with the hypothesis that aldehydic byproducts of lipid peroxidation contribute to mechanisms of O2 toxicity and the selective pressure exerted by exposure of cells to hyperoxia.(ABSTRACT TRUNCATED AT 250 WORDS).


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