Queuine promotes antioxidant defence system by activating cellular antioxidant enzyme activities in cancer

Constant generation of ROS (reactive oxygen species) during normal cellular metabolism of an organism is generally balanced by a similar rate of consumption by antioxidants. Imbalance between ROS production and antioxidant defence results in an increased level of ROS, causing oxidative stress, which leads to promotion of malignancy. Queuine is a hyper-modified base analogue of guanine, found at the first anticodon position of the Q-family of tRNAs. These tRNAs are completely modified with respect to queuosine in terminally differentiated somatic cells; however, hypo-modification of Q-tRNAs is closely associated with cell proliferation. Q-tRNA modification is essential for normal development, differentiation and cellular function. Queuine is a nutrient factor for eukaryotes. It is found to promote the cellular antioxidant defence system and inhibit tumorigenesis. The activities of antioxidant enzymes such as catalase, superoxide dismutase, glutathione peroxidase and glutathione reductase are found to be low in the DLAT (Dalton's lymphoma ascites transplanted) mouse liver compared with normal mouse liver. However, exogenous administration of queuine to the DLAT cancerous mouse improves the activities of antioxidant enzymes. These results suggest that queuine promotes the antioxidant defence system by increasing antioxidant enzyme activities and in turn inhibits oxidative stress and tumorigenesis.

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Anti-carcinogenic action of curcumin by activation of antioxidant defence system and inhibition of NF-κB signalling in lymphoma-bearing mice

Bioscience Reports ◽

10.1042/bsr20110043 ◽

2011 ◽

Vol 32 (2) ◽

pp. 161-170 ◽

Cited By ~ 51

Author(s):

Laxmidhar Das ◽

Manjula Vinayak

Keyword(s):

Oxidative Stress ◽

Cell Proliferation ◽

Antioxidant Enzymes ◽

Morphological Changes ◽

Nuclear Factor Κb ◽

Antioxidant Defence ◽

Defence System ◽

Antioxidant Defence System ◽

Endogenous Antioxidant ◽

Endogenous Antioxidant Defence

NF-κB (nuclear factor κB) plays a significant role in inflammation, immunity, cell proliferation, apoptosis and malignancy. ROS (reactive oxygen species) are among the most important regulating factors of NF-κB. Intracellular ROS are mainly regulated by an endogenous antioxidant defence system. Any disruption of redox balance leads to oxidative stress, which causes a number of pathological conditions including inflammation and malignancy. Increased metabolic activity in cancerous cells leads to oxidative stress, which is further enhanced due to depletion of the endogenous antioxidant defence system. However, the activation and signalling of NF-κB are reported to be inhibited by overexpression and induced activity of antioxidant enzymes. Therefore the present study focuses on the correlation between the endogenous antioxidant defence system, ROS and NF-κB activation during lymphoma growth in mice. The study highlights the anti-carcinogenic role of curcumin by modulation of NF-κB activation and oxidative stress via the endogenous antioxidant defence system. Oxidative stress was monitored by lipid peroxidation, protein carbonylation and antioxidant enzyme activity. NF-κB-mediated signalling was tested by DNA-binding activity. The results reflect that intracellular production of H2O2 in oxidative tumour micro-environment regulates NF-κB activation. Curcumin inhibits oxidative state in the liver of lymphoma-bearing mice by enhancing the transcription and activities of antioxidant enzymes, which in turn modulate activation of NF-κB, leading to a decrease in lymphoma growth. Morphological changes as well as cell proliferation and cell survival assays confirmed reduced lymphoma growth. Thus curcumin contributes to cancer prevention by disrupting the vicious cycle of constant ROS production, responsible for a high oxidative micro-environment for tumour growth.

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Physiological responses of peanut (Arachis hypogaea L.) cultivars to water deficit stress: status of oxidative stress and antioxidant enzyme activities

Acta Botanica Croatica ◽

10.1515/botcro-2015-0011 ◽

2015 ◽

Vol 74 (1) ◽

pp. 123-142 ◽

Cited By ~ 11

Author(s):

Koushik Chakraborty ◽

Amrit L. Singh ◽

Kuldeep A. Kalariya ◽

Nisha Goswami ◽

Pratap V. Zala

Keyword(s):

Oxidative Stress ◽

Antioxidant Enzymes ◽

Antioxidant Enzyme ◽

Water Deficit ◽

Chlorophyll A ◽

Enzyme Activities ◽

Carotenoid Content ◽

Water Deficit Stress ◽

Antioxidant Enzyme Activities ◽

Pod Development

AbstractFrom a field experiment, the changes in oxidative stress and antioxidant enzyme activities were studied in six Spanish peanut cultivars subjected to 25−30 days of water deficit stress at two different stages: pegging and pod development stages. Imposition of water deficit stress significantly reduced relative water content, membrane stability and total carotenoid content in all the cultivars, whereas total chlorophyll content increased at pegging stage but decreased at pod developmental stage. Chlorophyll a/b ratio increased under water deficit stress in most of the cultivars suggesting a greater damage to chlorophyll b rather than an increase in chlorophyll a content. Oxidative stress measured in terms of H2O2, superoxide radical content and lipid peroxidation increased under water deficit stress, especially in susceptible cultivars such as DRG 1, AK 159 and ICGV 86031. Relationship among different physiological parameters showed that the level of oxidative stress, in terms of production of reactive oxygen species, was negatively correlated with activities of different antioxidant enzymes such as superoxide dismutase, catalase, peroxidase, ascorbate peroxidase and glutathione reductase. In conclusion, the study shows that water deficit stress at pod development stage proved to be more detrimental than at pegging stage. The higher activities of antioxidant enzymes in the tolerant cultivars like ICGS 44 and TAG 24 were responsible for protection of oxidative damage and thus provide better tolerance to water deficit stress.

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Downregulation of FeSOD-A expression in Leishmania infantum alters trivalent antimony and miltefosine susceptibility

Parasites & Vectors ◽

10.1186/s13071-021-04838-8 ◽

2021 ◽

Vol 14 (1) ◽

Author(s):

Ana Maria Murta Santi ◽

Paula Alves Silva ◽

Isabella Fernandes Martins Santos ◽

Silvane Maria Fonseca Murta

Keyword(s):

Oxidative Stress ◽

Western Blot ◽

Leishmania Infantum ◽

Transcript Level ◽

Drug Susceptibility ◽

Central Component ◽

Multiplication Rate ◽

Antioxidant Defence ◽

Defence System ◽

Antioxidant Defence System

Abstract Background Superoxide dismutase (SOD), a central component of the antioxidant defence system of most organisms, removes excess superoxide anions by converting them to oxygen and hydrogen peroxide. As iron (Fe) SOD is absent in the human host, this enzyme is a promising molecular target for drug development against trypanosomatids. Results We obtained Leishmania infantum mutant clones with lower FeSOD-A expression and investigated their phenotypes. Our attempts to delete this enzyme-coding gene using three different methodologies (conventional allelic replacement or two different CRISPR/methods) failed, as FeSOD-A gene copies were probably retained by aneuploidy or gene amplification. Promastigote forms of WT and mutant parasites were used in quantitative reverse-transcription polymerase chain reaction (RT-qPCR) and western blot analyses, and these parasite forms were also used to assess drug susceptibility. RT-qPCR and western blot analyses revealed that FeSOD-A transcript and protein levels were lower in FeSOD-A−/−/+L. infantum mutant clones than in the wild-type (WT) parasite. The decrease in FeSOD-A expression in L. infantum did not interfere with the parasite growth or susceptibility to amphotericin B. Surprisingly, FeSOD-A−/−/+L. infantum mutant clones were 1.5- to 2.0-fold more resistant to trivalent antimony and 2.4- to 2.7-fold more resistant to miltefosine. To investigate whether the decrease in FeSOD-A expression was compensated by other enzymes, the transcript levels of five FeSODs and six enzymes from the antioxidant defence system were assessed by RT-qPCR. The transcript level of the enzyme ascorbate peroxidase increased in both the FeSOD-A−/−/+ mutants tested. The FeSOD-A−/−/+ mutant parasites were 1.4- to 1.75-fold less tolerant to oxidative stress generated by menadione. Infection analysis using THP-1 macrophages showed that 72 h post-infection, the number of infected macrophages and their intracellular multiplication rate were lower in the FeSOD-A−/−/+ mutant clones than in the WT parasite. Conclusions The unsuccessful attempts to delete FeSOD-A suggest that this gene is essential in L. infantum. This enzyme plays an important role in the defence against oxidative stress and infectivity in THP-1 macrophages. FeSOD-A-deficient L. infantum parasites deregulate their metabolic pathways related to antimony and miltefosine resistance. Graphic Abstract

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Effects of prolonged stanozolol treatment on antioxidant enzyme activities, oxidative stress markers, and heat shock protein HSP72 levels in rat liver

The Journal of Steroid Biochemistry and Molecular Biology ◽

10.1016/j.jsbmb.2003.09.001 ◽

2003 ◽

Vol 87 (4-5) ◽

pp. 269-277 ◽

Cited By ~ 40

Author(s):

Angel Pey ◽

Ana Saborido ◽

Isabel Blázquez ◽

Jerónimo Delgado ◽

Alicia Megı́as

Keyword(s):

Oxidative Stress ◽

Heat Shock ◽

Heat Shock Protein ◽

Antioxidant Enzyme ◽

Rat Liver ◽

Enzyme Activities ◽

Antioxidant Enzyme Activities ◽

Oxidative Stress Markers ◽

Stress Markers

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Cytokines increase rat lung antioxidant enzymes during exposure to hyperoxia

Journal of Applied Physiology ◽

10.1152/jappl.1989.66.2.1003 ◽

1989 ◽

Vol 66 (2) ◽

pp. 1003-1007 ◽

Cited By ~ 35

Author(s):

C. W. White ◽

P. Ghezzi ◽

S. McMahon ◽

C. A. Dinarello ◽

J. E. Repine

Keyword(s):

Superoxide Dismutase ◽

Antioxidant Enzymes ◽

Antioxidant Enzyme ◽

Enzyme Activities ◽

Tumor Necrosis ◽

Interleukin 1 ◽

Antioxidant Enzyme Activities ◽

Rat Lung ◽

Glucose 6 Phosphate Dehydrogenase ◽

Necrosis Factor

Pretreatment with the combination of tumor necrosis factor/cachectin (TNF/C) and interleukin 1 (IL-1) increased glucose-6-phosphate dehydrogenase (G6PDH), glutathione reductase (GR), glutathione peroxidase (GPX), catalase (CAT), and superoxide dismutase (SOD) activities in lungs of rats continuously exposed to hyperoxia for 72 h, a time when all untreated rats had already died. Pretreatment with TNF/C and IL-1 also increased, albeit slightly, lung G6PDH and GR activities of rats exposed to hyperoxia for 4 or 16 h. By comparison, no differences occurred in lung antioxidant enzyme activities of TNF/C and IL-1- or saline-pretreated rats exposed to hyperoxia for 36 or 52 h; the latter is a time just before untreated rats began to succumb during exposure to hyperoxia. The results raise the possibility that TNF/C and IL-1 treatment can increase lung antioxidant enzyme activities and that increased lung antioxidant enzymes may contribute to the increased survival of TNF/C and IL-1-pretreated rats in hyperoxia for greater than 72 h.

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Effects of Cadmium on Growth, Oxidative Stress and Antioxidant Enzyme Activities in Peanut (Arachis hypogaea L.) Seedlings

Journal of Agricultural Science ◽

10.5539/jas.v4n6p142 ◽

2012 ◽

Vol 4 (6) ◽

Cited By ~ 1

Author(s):

Shihua Shan ◽

Feng Liu ◽

Chunjuan Chunjuan Li ◽

Shubo Wan

Keyword(s):

Oxidative Stress ◽

Antioxidant Enzyme ◽

Arachis Hypogaea ◽

Enzyme Activities ◽

Antioxidant Enzyme Activities ◽

Arachis Hypogaea L

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Antioxidants and selenocompounds inhibit 3,5-dimethylaminophenol toxicity to human urothelial cells

Archives of Industrial Hygiene and Toxicology ◽

10.2478/aiht-2019-70-3159 ◽

2019 ◽

Vol 70 (1) ◽

pp. 18-29 ◽

Cited By ~ 4

Author(s):

Pinar Erkekoglu ◽

Ming-Wei Chao ◽

Chia-Yi Tseng ◽

Bevin P. Engelward ◽

Ozge Kose ◽

...

Keyword(s):

Oxidative Stress ◽

Bladder Cancer ◽

Antioxidant Enzyme ◽

Enzyme Activities ◽

Mammalian Cells ◽

Antioxidant Enzyme Activities ◽

Urothelial Cells ◽

Dna Breaks ◽

Primary Metabolite ◽

Stress Changes

AbstractExposure to alkyl anilines may lead to bladder cancer, which is the second most frequent cancer of the urogenital tract. 3,5-dimethylaniline is highly used in industry. Studies on its primary metabolite 3,5-dimethylaminophenol (3,5-DMAP) showed that this compound causes oxidative stress, changes antioxidant enzyme activities, and leads to death of different mammalian cells. However, there is no in vitro study to show the direct effects of 3,5-DMAP on human bladder and urothelial cells. Selenocompounds are suggested to decrease oxidative stress caused by some chemicals, and selenium supplementation was shown to reduce the risk of bladder cancer. The main aim of this study was to investigate whether selenocompounds organic selenomethionine (SM, 10 µmol/L) or inorganic sodium selenite (SS, 30 nmol/L) could reduce oxidative stress, DNA damage, and apoptosis in UROtsa cells exposed to 3,5-DMAP. 3,5-DMAP caused a dose-dependent increase in intracellular generation of reactive oxygen species, and its dose of 50 µmol/L caused lipid peroxidation, protein oxidation, and changes in antioxidant enzyme activities in different cellular fractions. The comet assay also showed single-strand DNA breaks induced by the 3,5-DMAP dose of 50 µmol/L, but no changes in double-strand DNA breaks. Apoptosis was also triggered. Both selenocompounds provided partial protection against the cellular toxicity of 3,5-DMAP. Low selenium status along with exposure to alkyl anilines can be a major factor in the development of bladder cancer. More mechanistic studies are needed to specify the role of selenium in bladder cancer.

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