scholarly journals Bcl-xL overexpression attenuates glutathione depletion in FL5.12 cells following interleukin-3 withdrawal

1997 ◽  
Vol 325 (2) ◽  
pp. 315-319 ◽  
Author(s):  
Heidi K. BOJES ◽  
Kaushik DATTA ◽  
Jie XU ◽  
Anita CHIN ◽  
Phil SIMONIAN ◽  
...  
Keyword(s):  
Cell Death ◽  
Superoxide Dismutase ◽  
Glutathione Peroxidase ◽  
Oxidative Damage ◽  
Glutathione Reductase ◽  
Cell Line ◽  
Incubation Period ◽  
Glutathione Depletion ◽  
Rapid Loss ◽  
Induction Of Apoptosis

Bcl-xL and bax are bcl-2-related genes whose protein products either inhibit or promote apoptosis. Oxidative damage, including the loss of glutathione, has been implicated in the induction of apoptosis. The ability of the Bcl proteins to affect GSH was assessed in control, bax- and bcl-xL-transfected FL5.12 cells [an interleukin (IL)-3-dependent murine prolymphocytic cell line]. Overall levels of GSH were approximately the same in control and bcl-xL transfectants during the 6 h incubation period, although levels increased in bcl-xL transfectants 24 h after replating. GSH in cells overexpressing bax was reduced by ∼ 36%. There were no consistent differences between these cell lines in the activities of superoxide dismutase, catalase, glutathione peroxidase or glutathione reductase. Following IL-3 withdrawal, a condition known to cause apoptosis in these cells, a rapid loss of intracellular GSH occurred in control and bax transfectants, which preceded the onset of apoptosis. GSH depletion could not be attributed to intracellular oxidation but rather seemed to occur due to a translocation out of the cell. Cells overexpressing bcl-xL did not lose significant amounts of GSH upon withdrawal of IL-3, and no apoptosis was evident. These results suggest a possible role for GSH in the mechanism by which bcl-xL prevents cell death.

scholarly journals Synergistic Neuroprotective Effect of Endogenously-Produced Hydroxytyrosol and Synaptic Vesicle Proteins on Pheochromocytoma Cell Line against Salsolinol

Molecules ◽  
2020 ◽  
Vol 25 (7) ◽  
pp. 1715 ◽  
Author(s):  
Robina Manzoor ◽  
Aamir Rasool ◽  
Maqbool Ahmed ◽  
Ullah Kaleem ◽  
Lucienne Nneoma Duru ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Superoxide Dismutase ◽  
Glutathione Peroxidase ◽  
Glutathione Reductase ◽  
Synaptic Vesicle ◽  
Cell Line ◽  
Pc12 Cells ◽  
Neuroprotective Effect ◽  
Pheochromocytoma Cell ◽  
Synapsin 1

Oxidative stress triggers a lethal cascade, leading to Parkinson’s disease by causing degeneration of dopaminergic neurons. In this study, eight antioxidants were screened for their neuroprotective effect on PC12 cells (pheochromocytoma cell line) under oxidative stress induced by salsolinol (OSibS). Hydroxytyrosol was found to be the strongest neuroprotective agent; it improved viability of PC12 cells by up to 81.69% under OSibS. Afterward, two synaptic vesicle proteins, synapsin-1 and septin-5, were screened for their neuroprotective role; the overexpression of synapsin-1 and the downregulation of septin-5 separately improved the viability of PC12 cells by up to 71.17% and 67.00%, respectively, compared to PC12 cells only treated with salsolinol (PoTwS) under OSibS. Subsequently, the PC12+syn++sep− cell line was constructed and pretreated with 100 µM hydroxytyrosol, which improved its cell viability by up to 99.03% and led to 14.71- and 6.37-fold reductions in the levels of MDA and H2O2, respectively, and 6.8-, 12.97-, 10.57-, and 7.57-fold increases in the activity of catalase, glutathione reductase, superoxide dismutase, and glutathione peroxidase, respectively, compared to PoTwS under OSibS. Finally, alcohol dehydrogenase-6 from Saccharomyces cerevisiae was expressed in PC12+syn++sep− cells to convert 3,4-dihydroxyphenylacetaldehyde (an endogenous neurotoxin) into hydroxytyrosol. The PC12+syn++sep−+ADH6+ cell line also led to 22.38- and 12.33-fold decreases in the production of MDA and H2O2, respectively, and 7.15-, 13.93-, 12.08-, and 8.11-fold improvements in the activity of catalase, glutathione reductase, superoxide dismutase, and glutathione peroxidase, respectively, compared to PoTwS under OSibS. Herein, we report the endogenous production of a powerful antioxidant, hydroxytyrosol, from 3,4-dihydroxyphenylacetaldehyde, and evaluate its synergistic neuroprotective effect, along with synapsin-1 and septin-5, on PC12 cells under OSibS.

scholarly journals Effect of Chronic Exposure to Pesticide Methomyl on Antioxidant Defense System in Testis of Tilapia (Oreochromis niloticus) and Its Recovery Pattern

2021 ◽  
Vol 11 (8) ◽  
pp. 3332
Author(s):  
Shunlong Meng ◽  
Xi Chen ◽  
Chao Song ◽  
Limin Fan ◽  
Liping Qiu ◽  
...  
Keyword(s):  
Superoxide Dismutase ◽  
Glutathione Peroxidase ◽  
Oxidative Damage ◽  
Glutathione Reductase ◽  
Oreochromis Niloticus ◽  
Reduced Glutathione ◽  
Free Water ◽  
Oxidized Glutathione ◽  
Glutathione S Transferase ◽  
Recovery Pattern

The chronic effect of environmental methomyl on the antioxidant system in testis of Nile tilapia (Oreochromis niloticus) and its recovery pattern was investigated. Tilapia were exposed to sublethal concentrations of 0.2, 2, 20 and 200 μgL−1 methomyl for 30 days and thereafter moved to methomyl-free water for 18 days. Antioxidant levels in testis, including glutathione peroxidase, catalase, glutathione-S-transferase, glutathione reductase, superoxide dismutase, reduced glutathione, oxidized glutathione were measured every 6 days during the period of exposure, and at 18 days after being transferred to methomyl-free water. The results showed that lower methomyl concentration (0.2 μgL−1) had no effect on the above antioxidants, thus 0.2 μgL−1 could be seen as NOAEL for methomyl to tilapia. However, higher methomyl concentration of 2, 20 and 200 μgL−1 could significantly influence the above antioxidants. Glutathione peroxidase and oxidized glutathione increased significantly. On the contrary, reduced glutathione decreased significantly. Catalase, superoxide dismutase, glutathione reductase, glutathione-S-transferase increased at lower methomyl (2 and 20 μgL−1), but decreased at higher methomyl (200 μgL−1). The recovery test showed that oxidative damage caused by lower methomyl of 2 and 20 μgL−1 was reversible, and oxidative damage caused by higher methomyl of 200 μgL−1 was irreversible within 18 days of recovery period.

scholarly journals Effect of Cross-Sex Hormonal Replacement on Antioxidant Enzymes in Rat Retroperitoneal Fat Adipocytes

2016 ◽  
Vol 2016 ◽  
pp. 1-12 ◽  
Author(s):  
Israel Pérez-Torres ◽  
Verónica Guarner-Lans ◽  
Alejandra Zúñiga-Muñoz ◽  
Rodrigo Velázquez Espejel ◽  
Alfredo Cabrera-Orefice ◽  
...  
Keyword(s):  
Lipid Peroxidation ◽  
Superoxide Dismutase ◽  
Antioxidant Enzymes ◽  
Glutathione Peroxidase ◽  
Glutathione Reductase ◽  
Enzymatic Activities ◽  
Glutathione S Transferase ◽  
Control Groups ◽  
Intact Female ◽  
Hormonal Replacement

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.

Response of antioxidant enzymes to intermittent and continuous hyperbaric oxygen

1990 ◽  
Vol 69 (1) ◽  
pp. 328-335 ◽  
Author(s):  
A. L. Harabin ◽  
J. C. Braisted ◽  
E. T. Flynn
Keyword(s):  
Superoxide Dismutase ◽  
Antioxidant Enzymes ◽  
Glutathione Peroxidase ◽  
Oxidative Damage ◽  
Hyperbaric Oxygen ◽  
Enzyme Activities ◽  
Guinea Pigs ◽  
Exposure Duration ◽  
Biochemical Variables ◽  
Time Required

Rats and guinea pigs were exposed to O2 at 2.8 ATA (HBO) delivered either continuously or intermittently (repeated cycles of 10 min of 100% O2 followed by 2.5 min of air). The O2 time required to produce convulsions and death was increased significantly in both species by intermittency. To determine whether changes in brain and lung superoxide dismutase (SOD), catalase (CAT), and glutathione peroxidase (GSHPx) correlated with the observed tolerance, enzyme activities were measured after short or long HBO exposures. For each exposure duration, one group received continuous and one intermittent HBO; O2 times were matched. HBO had marked effects on these enzymes: lung SOD increased (guinea pigs 47%, rats 88%) and CAT and GSHPx activities decreased (33%) in brain and lung. No differences were seen in lung GSHPx or brain CAT in rats or brain SOD in either species. In guinea pigs, but less so in rats, the observed changes in activity were usually modulated by intermittency. Increases in hematocrit, organ protein, and lung DNA, which may also reflect ongoing oxidative damage, were also slowed with intermittency in guinea pigs. Intermittency benefited both species by postponing gross symptoms of toxicity, but its modulation of changes in enzyme activities and other biochemical variables was more pronounced in guinea pigs than in rats, suggesting that there are additional mechanisms for tolerance.

scholarly journals Comparison of oxidant and antioxidant status of seminal plasma and spermatozoa of several fish species

2013 ◽  
Vol 58 (No. 7) ◽  
pp. 313-320 ◽  
Author(s):  
A. Shaliutina-Kolešová ◽  
I. Gazo ◽  
J. Cosson ◽  
O. Linhart
Keyword(s):  
Superoxide Dismutase ◽  
Glutathione Peroxidase ◽  
Glutathione Reductase ◽  
Seminal Plasma ◽  
Brook Trout ◽  
Siberian Sturgeon ◽  
Russian Sturgeon ◽  
Thiobarbituric Acid Reactive Substance ◽  
Acipenser Baerii ◽  
Carbonyl Protein

Oxidant and antioxidant activity in seminal plasma was compared with that in spermatozoa of teleost (common carp Cyprinus carpio and brook trout Salvelinus fontinalis) and chondrostean (Russian sturgeon Acipenser gueldenstaedtii, Siberian sturgeon Acipenser baerii, and sterlet Acipenser ruthenus) fishes. No differences were found between seminal plasma and spermatozoa in the level of thiobarbituric-acid-reactive substance (0.24 ± 0.08 to 0.33 ± 0.04 nmol/mg proteins) in Russian sturgeon, Siberian sturgeon, and sterlet. Carbonyl protein concentration was significantly higher in spermatozoa than in seminal plasma of all studied species. Analyzed antioxidants included superoxide dismutase, glutathione reductase, and glutathione peroxidase activity. Significant differences (P < 0.05) were detected between seminal plasma and spermatozoa in total superoxide dismutase (SOD) and glutathione reductase (GR). Total glutathione peroxidase (GPx) activity was significantly higher in brook trout (12.56 ± 3.23 mU/mg proteins) and Russian sturgeon (11.56 ± 3.12 mU/mg proteins) spermatozoa compared to seminal plasma (6.81 ± 1.56 mU/mg proteins in brook trout and 9.56 ± 3.12 mU/mg proteins in Russian sturgeon). This study provides new data on oxidant and antioxidant balance between spermatozoa and seminal plasma that may be of value in the development of methods for artificial reproduction of teleost and chondrostean species.  

Oxidative damage and antioxidants in cervical cancer

2020 ◽  
pp. ijgc-2020-001587
Author(s):  
Daciele Paola Preci ◽  
Angélica Almeida ◽  
Anne Liss Weiler ◽  
Maria Luiza Mukai Franciosi ◽  
Andréia Machado Cardoso
Keyword(s):  
Cervical Cancer ◽  
Superoxide Dismutase ◽  
Glutathione Peroxidase ◽  
Oxidative Damage ◽  
Cancer Progression ◽  
Reduced Glutathione ◽  
Reactive Oxygen ◽  
Enzymatic Antioxidants ◽  
Glutathione S Transferase ◽  
The Impact

The pathogenesis of cervical cancer is related to oxidative damage caused by persistent infection by one of the oncogenic types of human papillomavirus (HPV). This damage comes from oxidative stress, which is the imbalance caused by the increase in reactive oxygen and nitrogen species and impaired antioxidant mechanisms, promoting tumor progression through metabolic processes. The incorporation of HPV into the cellular genome leads to the expression of oncoproteins, which are associated with chronic inflammation and increased production of reactive oxygen species, oxidizing proteins, lipids and DNA. The increase in these parameters is related, in general, to the reduction of circulating levels of enzymatic antioxidants—superoxide dismutase, catalase, glutathione peroxidase and glutathione-S-transferase; and non-enzymatic antioxidants—reduced glutathione, coenzyme Q10 and vitamins A, C and E, according to tumor staging. In contrast, some enzymatic antioxidants suffer upregulation in the tumor tissue as a way of adapting to the oxidative environment generated by themselves, such as glutathione-S-transferase, reduced glutathione, glutathione peroxidase, superoxide dismutase 2, induced nitric oxide synthase, peroxiredoxins 1, 3 and 6, and thioredoxin reductase 2. The decrease in the expression and activity of certain circulatory antioxidants and increasing the redox status of the tumor cells are thus key to cervical carcinoma prognosis. In addition, vitamin deficit is considered a possible modifiable risk factor by supplementation, since the cellular functions can have a protective effect on the development of cervical cancer. In this review, we will discuss the impact of oxidative damage on cervical cancer progression, as well as the main oxidative markers and therapeutic potentialities of antioxidants.

Dietary supplementation with magnesium citrate may improve pancreatic metabolic indices in an alloxan-induced diabetes rat model

10.5219/1375 ◽  
2020 ◽  
Vol 14 ◽  
pp. 836-846
Author(s):  
Olena Shatynska ◽  
Oleksandr Tokarskyy ◽  
Petro Lykhatskyi ◽  
Olha Yaremchuk ◽  
Iryna Bandas ◽  
...  
Keyword(s):  
Lipid Peroxidation ◽  
Superoxide Dismutase ◽  
Glutathione Peroxidase ◽  
Glutathione Reductase ◽  
Fasting Glucose ◽  
Reduced Glutathione ◽  
Pancreatic Tissue ◽  
Magnesium Supplementation ◽  
Metabolism Enzymes ◽  
Peroxidation Index

The purpose of the current study was to evaluate the protective properties of dietary magnesium supplementation on pancreatic tissue of rats with alloxan-induced diabetes mellitus. Twenty-five male Wistar rats were split into five groups (control, diabetes, diabetes with 100 mg Mg daily, diabetes with 250 mg Mg daily, diabetes with 500 mg Mg daily) with feeding supplementation starting on day 1, diabetes induction on day 21, and animal sacrifice on day 30. Fasting glucose in blood serum was measured on days 21, 25, 27, and day 30. Glucose metabolism enzymes, namely, lactate dehydrogenase and glucose-6-phosphate dehydrogenase, were measured in pancreatic tissue upon the sacrifice, as well as lipid peroxidation, antioxidant system protective enzymes (catalase and superoxide dismutase), and glutathione system components (glutathione reductase, glutathione peroxidase, and glutathione reduced). Pearson correlation coefficients showed strong negative correlation between serum glucose (control and diabetic animals) and glucose metabolism enzymes, catalase, superoxide dismutase, glutathione peroxidase in pancreatic tissue (r >-0.9, p <0.05), moderate negative correlation with reduced glutathione (r = -0.79, p <0.05), moderate positive correlation with lipid peroxidation index (r = +0.67, p <0.05), weak correlation with glutathione reductase (r = -0.57, p <0.05). Magnesium supplementation slowed down diabetes onset considering fasting glucose levels in rats (p <0.05), as well as partially restored investigated dehydrogenase levels in the pancreas of rats comparing to diabetes group (p <0.05). The lipid peroxidation index varied between treatments showing the dose-dependent influence of Mg2+. Magnesium supplementation partially restored catalase and superoxide dismutase activities in pancreatic tissue, as well as glutathione peroxidase and reduced glutathione levels (p <0.05), while glutathione reductase levels remained unaffected (p >0.05). The obtained results suggested a model, where magnesium ions may have a possible protective effect on pancreatic tissue against the negative influence of alloxan inside β cells of the pancreas.

Activity of Superoxide Dismutase, Catalase, Glutathione Peroxidase, and Glutathione Reductase in Different Stages of Colorectal Carcinoma

2013 ◽  
Vol 58 (9) ◽  
pp. 2646-2652 ◽  
Author(s):  
Kristina R. Gopčević ◽  
Branislav R. Rovčanin ◽  
Svetislav B. Tatić ◽  
Zoran V. Krivokapić ◽  
Milan M. Gajić ◽  
...  
Keyword(s):  
Superoxide Dismutase ◽  
Colorectal Carcinoma ◽  
Glutathione Peroxidase ◽  
Glutathione Reductase
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