Role of oxidative stress and thiol antioxidant enzymes in nickel toxicity and resistance in strains of the green alga Scenedesmus acutus f. alternans

2001 ◽  
Vol 47 (11) ◽  
pp. 987-993 ◽  
Author(s):  
Varinder K Randhawa ◽  
Fengzhen Zhou ◽  
Xiaolei Jin ◽  
Czesia Nalewajko ◽  
Donn J Kushner
Keyword(s):  
Reactive Oxygen Species ◽  
Superoxide Dismutase ◽  
Glutathione Peroxidase ◽  
Glutathione Reductase ◽  
Resistant Strain ◽  
Sensitive Strain ◽  
The Other ◽  
Oxygen Species ◽  
Scenedesmus Acutus ◽  
Glucose 6 Phosphate Dehydrogenase

Treatment with Ni(NO3)2 leads to the formation of reactive oxygen species (ROS) in the green alga Scenedesmus acutus f. alternans, causing lipid peroxidation. This effect was stronger in a Ni-sensitive strain, UTEX72, than in a Ni-resistant strain, B4. In the resistant strain, Ni induced an increased ratio of reduced to oxidized glutathione (GSH:GSSG), whereas it caused a lowered ratio in the sensitive strain. Enzymes involved in the control of ROS were studied in these strains as well as two others that have shown different degrees of nickel resistance. The resistant strain, B4, which grows while containing large amounts of internal Ni, had much higher levels of glutathione reductase and catalase than the other strains. The sensitive strain, UTEX72, had higher levels of glutathione peroxidase, superoxide dismutase, and glucose-6-phosphate dehydrogenase than did strain B4. The resistant strains, Ni-Tol and Cu-Tol, derived from strain UTEX72, which are partly able to exclude Ni, had enzyme profiles that resembled that of UTEX72 more closely than that of B4. Treatment with 10 and 100 µM Ni for 4 or 22 h had complex effects on enzyme levels in all four strains. Ni decreased glutathione reductase in B4, slightly increased it in Ni-Tol and Cu-Tol, and did not affect the low levels of this enzyme in UTEX72. Ni lowered glutathione peroxidase in B4 and either did not affect it or slightly raised it in the other strains. Ni lowered catalase in B4 and did not affect the other strains. Superoxide dismutase was raised in B4 and Ni-Tol and lowered in Cu-Tol and UTEX72, and glucose-6-phosphate dehydrogenase was lowered in all four strains. These results suggest that one major mechanism of Ni resistance, especially in strain B4, may be the ability to combat the formation of ROS when exposed to this metal, likely by maintaining a high GSH:GSSG ratio.Key words: Scenedesmus acutus f. alternans, glutathione reductase, glutathione peroxidase, catalase, superoxide dismutase, glucose-6-phosphate dehydrogenase, lipid peroxidation, nickel, reactive oxygen species.

184 Effects of cyanidin supplementation on invitro maturation of pig oocytes

2020 ◽  
Vol 32 (2) ◽  
pp. 220
Author(s):  
E. Hicks ◽  
M. Mentler ◽  
B. D. Whitaker
Keyword(s):  
Oxidative Stress ◽  
Reactive Oxygen Species ◽  
Superoxide Dismutase ◽  
Glutathione Peroxidase ◽  
Oocyte Maturation ◽  
Catalase Activity ◽  
Reactive Oxygen ◽  
Oxygen Species ◽  
Enzyme Mechanisms ◽  
Maturation Medium

Oxidative stress can have a negative effect on oocyte maturation during invitro production of pig embryos. Imbalance of reactive oxygen species and antioxidant levels can affect the progression of oocyte maturation up to the point of fertilization. Antioxidants are effective in maintaining more ideal reactive oxygen species levels, which help to protect oocytes from potential harmful effects of oxidative stress. Berries from the elder plant (Sambucus sp.) contain high levels of a broad spectrum of antioxidants. One of these antioxidants, cyanidin, when supplemented to maturation medium at 100μM concentrations, reduces reactive oxygen species formation and improves IVF and early embryonic development in pigs. However, changes in the enzyme mechanisms of action during oocyte maturation due to cyanidin supplementation are unknown. Therefore, the objective of this study was to characterise the intracellular oocyte enzyme mechanisms between oocytes supplemented with 100μM cyanidin during 40 to 44h of maturation (n=600) and oocytes without supplementation of cyanidin during maturation (n=558). At the end of maturation, oocytes were evaluated for either glutathione peroxidase (n=300), catalase (n=564), or superoxide dismutase (n=294) activities. Glutathione peroxidase activity was determined by following the rate of NADPH oxidation, catalase activity was determined by following the rate of hydrogen peroxide decomposition, and superoxide dismutase activity was determined by following the reduction rate of cytochrome c, utilising the xanthine-xanthine oxidase system. Data were analysed using ANOVA and Tukey's test. There were no significant differences between oocytes matured with 100μM cyanidin and those that were not when comparing glutathione peroxidase and superoxide dismutase activities. Supplementation of 100μM cyanidin to maturation medium increased (P<0.05) catalase activity in oocytes (0.78±0.15 units/oocyte) compared with no cyanidin supplementation (0.14±0.11 units/oocyte). These results indicate that supplementing 100μM cyanidin to the maturation medium of pig oocytes could reduce the negative effects of oxidative stress by increasing intracellular catalase activity during oocyte maturation.

scholarly journals Cytoplasmic superoxide dismutase activity is a sensitive indicator of the antioxidant status of the rat liver and brain

2014 ◽  
Vol 60 (1) ◽  
pp. 63-71 ◽  
Author(s):  
T.V. Sirota ◽  
M.V. Zakharchenko ◽  
M.N. Kondrashova
Keyword(s):  
Reactive Oxygen Species ◽  
Superoxide Dismutase ◽  
Glutathione Reductase ◽  
Rat Liver ◽  
Antioxidant System ◽  
Antioxidant Status ◽  
Immobilization Stress ◽  
Oxygen Species ◽  
Nadph Oxidation ◽  
The Brain

Several parameters of the cytoplasmic enzymatic antioxidant system of the liver and brain of the rat have been investigated under conditions of immobilization stress and of an antioxidant preparation in the diet of animals. These included superoxide dismutase (SOD) and glutathione reductase (GR) activities and nonspecific NADPH oxidation. Only changes in the activity of SOD both in the liver and brain were revealed. In the liver of animals that receive no preparation, a decrease in the activity of SOD after 30-min immobilization and its restoration after a 360-min immobilization were observed. In the brain, the activity of SOD decreased only in preconditioned animals after 30 and 360 min of exposure to stress. In addition, the activity of SOD in the brain of preconditioned animals, both stressed and unstressed, was lower than in the corresponding groups of control animals. It is probable that, under the conditions of immobilization stress, the level of reactive oxygen species (ROS) and as a consequence the activity of SOD decrease. The intake of an antioxidant preparation under these conditions seems to be not correct.

scholarly journals PENGARUH PAPARAN GELOMBANG ELEKTROMAGNETIK PONSEL TERHADAP OTAK

2020 ◽  
Vol 8 (1) ◽  
pp. 89-95
Author(s):  
Ahmad Rizki Dwi Prasetia ◽  
Waluyo Rudiyanto
Keyword(s):  
Reactive Oxygen Species ◽  
Superoxide Dismutase ◽  
Glutathione Peroxidase ◽  
Electromagnetic Radiation ◽  
Electromagnetic Waves ◽  
Absorption Rate ◽  
Specific Absorption Rate ◽  
Oxygen Species ◽  
Cornu Ammonis ◽  
Negative Effect

ABSTRAK Ponsel merupakan alat komunikasi yang banyak dimiliki oleh manusia. Hal ini dikarenakan keefektifan oleh ponsel itu sendiri. Dalam satu ponsel, penggunanya tidak hanya dapat berkomunikasi akan tetapi juga bisa melakukan berbagai aktivitas seperti mencari suatu informasi ataupun mendengarkan musik. Di balik kehebatan ponsel tersebut sebenarnya mengandung efek negatif berupa pancaran gelombang elektromagnetiknya yang berbahaya bagi otak, terlebih bila digunakan untuk menelepon dalam jangka waktu yang lama. Radiasi elektromagnetik yang berupa non-ionisasi ini baru akan menimbulkan efek negatif bila tubuh terpajan Specific Absorption Rate (SAR) >4 watt/kg. Saat menelepon efek yang langsung ditimbulkan berupa nyeri kepala karena adanya peningkatan tekanan darah, namun untuk waktu yang lebih lama lagi dapat menimbulkan kanker otak karena adanya penurunan produksi serotonin dan melatonin yang mana kerjanya untuk menekan timbulnya tumor. Mungkin Radiasi tidak berperan secara langsung dalam terbentuknya tumor, namun dalam studi lebih lanjut, paparan radiasi yang banyak juga dapat menaikkan malondialdehyde (MDA) serta pengurangan yang signifikan pada antioksidan seperti glutathione (GSH), superoxide dismutase (SOD), dan glutathione peroxidase (GPX). Hal ini dapat mengakibatkan peningkatan Reactive Oxygen Species (ROS) dan penurunan melatonin dalam serum sehingga terjadinya kerusakan oksidatif pada jaringan otak. Pada bagian hipokampus sendiri, didapatkan bahwa radiasi elektromagnetik dapat menghambat frekuensi pelepasan neuron pada Cornu Ammonis area 1 (CA1) hipokampus yang nantinya dapat menyebabkan penurunan kemampuan belajar dan memori.   Kata Kunci:  otak, paparan  gelombang elektromagnetik, ponsel  ABSTRACT Cell phones are a communication tool that is widely owned by humans. This is because of the effectiveness of the cellphone itself. In one cellphone, users can not only communicate but also can do various activities such as searching for information or listening to music. Behind this cellphone, it actually contains a negative effect consisting of the emission of electromagnetic waves which are harmful to the brain, before being used to move for a long time. Electromagnetic radiation which consists of non-recent ionization will have a negative effect if the body is exposed to Specific Absorption Rate (SAR)> 4 watts / kg. When calling the effects directly caused by blood pressure, but for a longer time can cause brain cancer due to a decrease in the production of serotonin and melatonin which is Tinjauan Pustaka  JIMKI Volume 8 No.1 | November 2019 – Februari 2020           90 needed to increase the incidence of tumors. Radiation may not directly support tumor formation, but in further studies, greater radiation exposure can also increase malondialdehyde (MDA) and also present significant antioxidants such as glutathione (GSH), superoxide dismutase (SOD), and glutathione peroxidase (GPX). This can increase Reactive Oxygen Species (ROS) and decrease melatonin in the serum thereby preventing oxidative damage to brain tissue. In the hippocampus itself, electromagnetic radiation can be obtained which can release the frequency of the release of neurons in the Cornu Ammonis area 1 (CA1) hippocampus that can be used can cause a decrease in learning ability and memory.      Keywords:  brain, cellphone, electromagnetic waves' exposure

scholarly journals Oxymatrine Ameliorates Doxorubicin-Induced Cardiotoxicity in Rats

2017 ◽  
Vol 43 (2) ◽  
pp. 626-635 ◽  
Author(s):  
Yan-Yan Zhang ◽  
Minhan Yi ◽  
Yong-Pan Huang
Keyword(s):  
Oxidative Stress ◽  
Reactive Oxygen Species ◽  
Superoxide Dismutase ◽  
Glutathione Peroxidase ◽  
Reactive Oxygen ◽  
Oxygen Species ◽  
H9c2 Cells ◽  
Western Blots ◽  
Creatine Kinase Mb ◽  
Commercial Kits

Background/Aims: Doxorubicin-induced cardiac toxicity has been a major concern of oncologists and is considered the main restriction on its clinical application. Oxymatrine has shown potent anti-cancer, anti-fibrosis, and anti-oxidative effects. Recently, it has been reported that oxymatrine is protective against some cardiovascular diseases. In this study, we aimed to investigate the effects of oxymatrine on doxorubicin-induced cardiotoxicity in rat hearts and H9c2 cells. Methods: Creatine Kinase - MB (CK-MB) and Lactate Dehydrogenase (LDH) levels were determined using commercial kits. Biochemical indices reflecting oxidative stress, such as catalase (CAT), malonyldialdehyde (MDA), superoxide dismutase (SOD), and glutathione peroxidase (GSH-Px) were also analyzed with commercial kits. Mitochondrial reactive oxygen species (ROS) 2’,7’-dichlorofluorescin diacetate (DCFH-DA) was measured by fluorescence microscopy. Histological analyses were conducted to observe morphological changes, and apoptosis was measured using a commercial kit. Western blots were used to detect the level of expression of cleaved caspase-3. Results: Doxorubicin treatment significantly increased oxidative stress levels, as indicated by catalase, malonyldialdehyde, superoxide dismutase, glutathione peroxidase and reactive oxygen species. Doxorubicin also increased pathological damage in myocardial tissue, myocardial ROS levels, and malonyldialdehyde levels, and induced apoptosis in myocardial tissues and H9c2 cells. All of these doxorubicin-induced effects were attenuated by oxymatrine. Conclusion: These in vitro and in vivo findings indicate that oxymatrine may be a promising cardioprotective agent against doxorubicin-induced cardiotoxicity, at least in part mediated through oxymatrine’s inhibition of cardiac apoptosis and oxidative stress.

scholarly journals The activities of superoxide dismutase, catalase, glutathione peroxidase and glutathione reductase in erythrocytes of rats with experimental neoplastic disease.

1996 ◽  
Vol 43 (2) ◽  
pp. 403-405 ◽  
Author(s):  
J Batko ◽  
T Warchoł ◽  
H Karoń
Keyword(s):  
Superoxide Dismutase ◽  
Glutathione Peroxidase ◽  
Tumor Growth ◽  
Glutathione Reductase ◽  
Reduced Glutathione ◽  
The Other ◽  
Second Phase ◽  
Neoplastic Disease ◽  
Experimental Animals ◽  
Morris Hepatoma

In erythrocytes of rats bearing Morris hepatoma 5123 the activities of superoxide dismutase, glutathione peroxidase and glutathione reductase as well as the level of reduced glutathione increased on the 10th day after transplantation of the tumor. In the second phase of the tumor growth (20 days after transplantation), the activities of glutathione peroxidase, glutathione reductase and the level of reduced glutathione in erythrocytes of the experimental animals were lower than in controls, whereas the activity of superoxide dismutase was at that time higher than in controls. On the other hand, the activity of catalase did not significantly differ from that found in healthy rats.

scholarly journals SESAMOL ANTAGONIZES ROTENONE-INDUCED CELL DEATH IN SH-SY5Y NEURONAL CELLS

2016 ◽  
Vol 8 (12) ◽  
pp. 72
Author(s):  
Rohini D. ◽  
Vijayalakshmi K.
Keyword(s):  
Reactive Oxygen Species ◽  
Cell Death ◽  
Superoxide Dismutase ◽  
Membrane Potential ◽  
Glutathione Peroxidase ◽  
Cell Viability ◽  
Mitochondrial Membrane ◽  
Thiobarbituric Acid ◽  
Oxygen Species ◽  
Thiobarbituric Acid Reactive Substances

<p><strong>Objective: </strong>To investigate the neuroprotective effect of sesamol against rotenone-induced cell death in SH-SY5Y cells associated with Parkinsonism.</p><p><strong>Methods: </strong>SH-SY5Y cells were maintained in Dulbecco’s modified Eagle’s medium. After differentiation, the cells were incubated with rotenone (20 μM) and sesamol at different concentrations (10-100 μM). Cell viability was determined by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyl-tetrazolium bromide assay. The reactive oxygen species, mitochondrial membrane potential and nuclear morphology were determined by dichlorofluorescein diacetate, rhodamine 123 and 4’, 6-diamidino-2-phenylindole, respectively. Thiobarbituric acid reactive substances, activities of catalase, superoxide dismutase, and glutathione peroxidase and glutathione level were determined by standard assays.</p><p><strong>Results: </strong>Sesamol significantly increased the cell viability and decreased the rotenone-induced cell death in SH-SY5Y cells. Sesamol antagonized rotenone-induced reactive oxygen species generation, loss of mitochondrial membrane potential and nuclear damage. Sesamol also decreased thiobarbituric acid reactive substances level, increased the activities of catalase, superoxide dismutase, glutathione peroxidase and increased the level of glutathione in rotenone-induced cells.</p><p><strong>Conclusion: </strong>The results obtained strongly indicate the promising neuroprotective role of sesamol against rotenone-induced death in SH-SY5Y cells.</p>

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