Oxidoreductase Gene Expression Research Articles

Tetrahydrocurcumin protects against nonalcoholic fatty liver disease by improving lipid metabolism and redox homeostasis

• Tetrahydrocurcumin (THC) improves glucose and lipid metabolism disorders in nonalcoholic fatty liver disease (NAFLD) in mice. • THC regulates the expression of oxidoreductase genes and lipid-metabolizing enzyme genes in the liver of NAFLD mice. • THC increases the antioxidant capacity and inhibits lipid deposition in HepG2 cells by activating the NRF2 signaling pathway. Nonalcoholic fatty liver disease (NAFLD) is the most common liver metabolic disease in the world. In this study we investigated the effect of tetrahydrocurcumin (THC), a potent antioxidant, on NAFLD. We found that THC significantly reduced the body weight, serum and liver lipids, serum malondialdehyde (MDA) and fasting blood glucose (FBG) of male NAFLD mice induced by feeding a high-fat diet (HFD) for 8 weeks. A RNA-seq analysis revealed that THC also affected the expression of many genes involved in lipid metabolism in the liver of NAFLD mice, including increasing the mRNA expression of CYP51 and FOXQ1 . Moreover, THC significantly reduced sodium oleate-induced lipid accumulation, activated the NRF2 pathway, and up-regulated the mRNA expression of FGF21 in HepG2 cells. Overall, our study showed that THC can improve the antioxidant capacity of liver, which suggests that dietary THC may be used to treat NAFLD.

Influence of carbon source on wood decay-associated gene expression in sequential hyphal zones of the brown rot fungus Gloeophyllum trabeum.

Brown rot fungi show a two-step wood degradation mechanism comprising oxidative radical-based and enzymatic saccharification systems. Recent studies have demonstrated that the brown rot fungus Rhodonia placenta expresses oxidoreductase genes ahead of glycoside hydrolase genes and spatially protects the saccharification enzymes from oxidative damage of the oxidoreductase reactions. This study aimed to assess the generality of the spatial gene regulation of these genes in other brown rot fungi and examine the effects of carbon source on the gene regulation. Gene expression analysis was performed on 14 oxidoreductase and glycoside hydrolase genes in the brown rot fungus Gloeophyllum trabeum, directionally grown on wood, sawdust-agar, and glucose-agar wafers. In G. trabeum, both oxidoreductase and glycoside hydrolase genes were expressed at higher levels in sections behind the wafers. The upregulation of glycoside hydrolase genes was significantly higher in woody substrates than in glucose, whereas the oxidoreductase gene expression was not affected by substrates.

Morphological Changes and the Expression of Oxidoreductase Genes of Brassica napus in Deep Culture Media Containing PEG

The aim of this research was to investigate the expression of important oxidoreductase genes involved in drought stress tolerance in two Brassica napus cultivars. For this purpose, morphological traits and the expression of four oxidoreductase genes within 0, 3, 6, 12, 24, 48 and 72 h after culture in deep culture medium containing 0, 3, 6, 12 and 15% polyethylene glycol 6000 (PEG 6000) were investigated. Results revealed that in both sensitive and tolerant cultivars, there was a declining trend in not only the leaf weight and area but also the stem weight and length with increasing the PEG level. In both cultivars, changes in the expression of NDH were approximately the same at different PEG levels. The tolerant cultivar showed higher expression of FNR than the sensitive cultivar. The expression of GR1 and GPX1 genes was higher in Hyola 308 than SLM 046.

An effort toward molecular neuroeconomics of food deprivation induced food hoarding in mice: focus on xanthine oxidoreductase gene expression and xanthine oxidase activity.

The crucial role of xanthine oxidoreductase (XOR) gene and its active isoform, xanthine oxidase (XO), in purine metabolism and cellular oxidative status led us to investigative their fluctuations in food deprivation induced food hoarding in mice. After, 10h food deprivation, mice that hoarded lesser than 5g were considered as 'low-hoarders' while mice that hoarded higher than 20g were considered as 'high-hoarders'. Mice who hoarded between 5 to 20g of food were excluded from study. An increase (1.133-fold) in encephalic XOR expression has been found in high-hoarders compared with low-hoarders without sex consideration. An increase (~ 50-fold) in encephalic XOR in female high-hoarders vs. female low-hoarders while a decrease (0.026-fold) in encephalic XOR in male high-hoarders vs. male low-hoarders demonstrated that food deprivation is associated with sex-dependent alteration in XOR expression. The encephalic and hepatic XO activities were not different in male high-hoarders vs. male low-hoarders while encephalic XO activity has been also increased significantly in female high-hoarders (~ 4 times) compared to female low-hoarders. The plasma and hepatic XO activities tended to be increased in female high-hoarders as compared to female low-hoarders, however the uric acid levels in plasma, liver and brain tissues were not altered in female high-hoarders as compared to female low-hoarders. In sum, this study generally proposed that different gene expression space is behind of hoarding behavior in a food-deprived mouse model. Specifically, this is the first study that examined the levels of encephalic XO activity and XOR expression in hoarding behavior, although additional studies are requested.

Similar developmental fluctuations of hepato-renal xanthine oxidoreductase gene expression and xanthine oxidase activity in layer and broiler chicken embryos

ABSTRACT1. Xanthine oxidase (XO) has many physiological functions associated with the synthesis of both antioxidant (uric acid: UA) and numerous oxidants (e.g. H2O2), which makes it an important regulator of the cellular redox potential involving organogenesis. The ontogenetic study of hepatic and renal XO makes a better understanding of the putative role of this enzyme in the development of these tissues.2. Developmental changes of gene expression of xanthine oxidoreductase (XOR), XO activity and UA content of liver and kidney tissues in both broiler and layer chicken embryos were examined during incubation d 14–21.3. In both strains, hepatic XOR gene expression peaked on d 21 while renal XOR gene expression did not change.4. The XO activity was higher in kidney than liver in both strains. Hepatic XO activity of both strains peaked on d 18 and thereafter was decreased on d 21. Renal XO activity peaked on d 18 and from then on did not show any significant changes until d 21 in both strains.5. The UA content was higher in kidney vs. liver in both strains. The hepatic and renal UA values of the both strains increased significantly from d 14 to d 21.6. The present results showed dissimilar behaviour of XOR gene expression, XO activity and UA content of liver and kidney tissues in both broiler and layer chicken embryos.

Editorial Note

The FEBS JournalVolume 283, Issue 22 p. 4208-4208 Editorial NoteFree Access Editorial Note This article corrects the following: Human Antioxidant-Response-Element-Mediated Regulation of Type 1 NAD(P)H:quinone Oxidoreductase Gene Expression Ying Li, Anil K. Jaiswal, Volume 226Issue 1European Journal of Biochemistry pages: 31-39 First Published online: June 28, 2008 First published: 05 November 2016 https://doi.org/10.1111/febs.13936AboutSectionsPDF ToolsRequest permissionExport citationAdd to favoritesTrack citation ShareShare Give accessShare full text accessShare full-text accessPlease review our Terms and Conditions of Use and check box below to share full-text version of article.I have read and accept the Wiley Online Library Terms and Conditions of UseShareable LinkUse the link below to share a full-text version of this article with your friends and colleagues. Learn more.Copy URL Share a linkShare onFacebookTwitterLinkedInRedditWechat The University of Maryland Office of Accountability and Compliance has notified The FEBS Journal of a potential issue with Figure 5 in the paper entitled “Human antioxidant-response-element-mediated regulation of type 1 NAD(P)H:quinone oxidoreductase gene expression: Effect of sulfhydrylmodifying agents” by Ying Li and Anil K. Jaiswal (Eur J. Biochem 226 (1994), 31–39; DOI: http://dx.doi.org/10.1111/j.1432-1033.1994.00t31.x) [1]. We note that the right-most four lanes in Figure 5A appear to be identical to and are superimposable on Figure 5B. At this point, it is impossible to determine conclusively whether the data have been duplicated. The corresponding author states that the data in Figure 5 are supported by other data in Figures 4, 6 and 7 and is confident that an error in Figure 5 would not affect the overall conclusions presented in this article. This Editorial Note is intended to alert our readers to the fact that questions have been raised regarding a figure in the above-mentioned manuscript [1]. It is unfortunate that we cannot state with complete certainty that the data in Figure 5 are accurate representations of the described experiments. However, we are satisfied that the key conclusions of the manuscript would not be affected by a potential error in this figure and thus will not be pursuing further action at this time. Reference 1Li Y & Jaiswal AK (1994) Human antioxidant-response-element-mediated regulation of type 1 NAD(P)H: quinone oxidoreductase gene expression: effect of sulfhydrylmodifying agents. Eur J Biochem 226, 31– 39. Volume283, Issue22November 2016Pages 4208-4208 This article also appears in:Editorials ReferencesRelatedInformation

Supportive or detrimental roles of P2Y receptors in brain pathology?--The two faces of P2Y receptors in stroke and neurodegeneration detected in neural cell and in animal model studies.

This review describing the role of P2Y receptors in neuropathological conditions focuses on obvious differences between results demonstrating either a role in neuroprotection or in neurodegeneration, depending on in vitro and in vivo models. Such critical juxtaposition puts special emphasis on discussions of beneficial and detrimental effects of P2Y receptor agonists and antagonists in these models. The mechanisms reported to underlie the protection in vitro include increased expression of oxidoreductase genes, like carbonyl reductase and thioredoxin reductase; increased expression of inhibitor of apoptosis protein-2; extracellular signal-regulated kinase- and Akt-mediated antiapoptotic signaling; increased expression of Bcl-2 proteins, neurotrophins, neuropeptides, and growth factors; decreased Bax expression; non-amyloidogenic APP shedding; and increased neurite outgrowth in neuronal cells. Animal studies investigating the influence of P2Y receptors in middle cerebral artery occlusion (MCAO) models for stroke prove beneficial effects of P2Y receptor antagonists. In MCAO mice and rats, the application of broad-range P2 receptor antagonists decreased the infarct volume and improved neurological outcome. Moreover, antagonists of the P2Y1 receptor, one of the most abundant P2Y receptor subtypes in brain tissue, decreased neuronal loss and improved spatial memory in rats after traumatic brain injury (TBI). Currently available data show a discrepancy between in vitro and in vivo models concerning the benefits of P2Y receptor activation in pathological conditions. In vitro models demonstrate protection by P2Y receptor agonists, but in vivo P2Y receptor activation deteriorates the outcome after MCAO and controlled cortical impact brain injury, a TBI model. To broaden the scope of the review, we additionally discuss publications that demonstrate detrimental effects of P2Y receptor agonists in vitro and publications showing protective effects of agonists in vivo. All these studies help to better understand the significant role of P2Y receptors especially in stroke models and to develop pharmacological strategies for the treatment of stroke.

Hepatocyte circadian clock controls acetaminophen bioactivation through NADPH-cytochrome P450 oxidoreductase.

The diurnal variation in acetaminophen (APAP) hepatotoxicity (chronotoxicity) reportedly is driven by oscillations in metabolism that are influenced by the circadian phases of feeding and fasting. To determine the relative contributions of the central clock and the hepatocyte circadian clock in modulating the chronotoxicity of APAP, we used a conditional null allele of brain and muscle Arnt-like 1 (Bmal1, aka Mop3 or Arntl) allowing deletion of the clock from hepatocytes while keeping the central and other peripheral clocks (e.g., the clocks controlling food intake) intact. We show that deletion of the hepatocyte clock dramatically reduces APAP bioactivation and toxicity in vivo and in vitro because of a reduction in NADPH-cytochrome P450 oxidoreductase gene expression, protein, and activity.

Effect of Allopurinol and Inosine Administration on Xanthine Oxidoreductase Gene Expression in Selected Tissues of Broiler Chickens

Effect of Allopurinol and Inosine Administration on Xanthine Oxidoreductase Gene Expression in Selected Tissues of Broiler Chickens

The effect of inosine and allopurinol on xanthine oxidoreductase gene expression and mitochondrial function in liver and kidney tissues of broiler chickens (693.16)

Uric acid is generated in the xanthine/hypoxanthine reactions catalyzed by xanthine oxiodreductase (XOR) as the end‐product of purine degradation. The purpose of the first study was to determine the effects of allopurinol and inosine on XOR activity and gene expression in liver and kidney tissue. In the first study, Cobb x Cobb (n=15; 5weeks old) were separated into three treatments (n=5); control (CON), INO (inosine at .6M/kg feed), or INOAL (inosine and allopurinol 50mg/kgBW). Liver uric acid concentrations were reduced (p< 0.05). There was a significant (p 蠄 0.05) increase in XOR gene expression in the liver tissue of INOAL birds compared to CON and INO groups. There was no difference in XOR expression between treatments in kidney tissue. The purpose of the second study was to assess mitochondrial function. Cobb x Cobb broilers (n=12; 4 weeks old) were separated into two treatments (n=6); control (CON) and AL (allopurinol 35mg/kg BW). Mitochondria were freshly isolated from liver tissue and assessed for State III and State IV respiration using polarography. There was a reduction in State III respiration (p=0.01) and State IV respiration (p=0.007) in allopurinol‐treated birds compared to the control. Lowered uric acid in the liver can increase oxidative stress within this tissue subsequently resulting in mitochondrial dysfunction and an upregulation of XOR gene expression.

Correlation between Oxidative Stress and L-type Calcium Channel Expression in the Ventricular Myocardia of Selenium-deficient Mice

Expression of the Cacna1c (calcium channel, voltage-dependent, L-type, α1C subunit) gene was studied to investigate the relationship between oxidative stress and L-type calcium channels in the myocardium of selenium-deficient mice. Selenium levels in liver and heart tissue samples from mice fed normal or selenium-deficient diets were evaluated by fluorometry. In the same mice, glutathione peroxidase (GPx) and Cacna1c gene expression were analysed, malondialdehyde (MDA) content and superoxide dismutase (SOD) activity were measured, oxidoreductase gene expression profiles were analysed (by DNA microarray), and myocardial structural changes were studied. In selenium-deficient versus control mice, GPx expression and SOD activity were decreased, and Cacna1c expression and MDA concentration were increased. Selenoprotein oxidoreductase and nonselenoprotein oxidoreductase gene expression differed significantly between selenium-deficient and control mice. In selenium-deficient mice, myocardial fibres were separated by loose collagenous tissue; electron microscopy showed shortened sarcomeres, dilated sarcoplasmic reticulum, scattered myofibril lysis and increased mitochondria with amorphous matrix densities. L-type calcium channels were involved in selenium deficiency-induced cardiomyocyte injury, which was positively related to oxidative stress.

Inhibition of pyruvate-ferredoxin oxidoreductase gene expression in Giardia lamblia by a virus-mediated hammerhead ribozyme.

Giardia lamblia is a primitive eukaryotic microorganism that derives its metabolic energy primarily from anaerobic glycolysis. In trophozoites, pyruvate-ferredoxin oxidoreductase (PFOR) converts pyruvate to acetyl-CoA with the transfer of a pair of electrons to ferredoxin, which can then reduce metronidazole and activate it into a potent antigiardiasis agent. It is unclear, however, whether this anaerobic disposal of electrons is essential for the energy metabolism in Giardia. In the present study, cDNAs encoding hammerhead ribozyme flanked with various lengths of antisense PFOR RNA were cloned into a viral vector pC631pac derived from the genome of giardiavirus (GLV). RNA transcripts of the plasmids showed high cleavage activities on PFOR mRNA in vitro. They were introduced into GLV-infected G. lamblia trophozoites by electroporation and stablized in the transfected cells via serial passages under puromycin selection. PFOR mRNA and enzyme activity in the transfected cells were decreased by 46-60% with the ribozyme PRzS flanked with 20 nt PFOR antisense RNA on each arm and by 69-80% with the ribozyme PRzL flanked with 600 and 1500 nt PFOR antisense RNA. PRzS without the inserted ribozyme or ribozyme flanked with alcohol dehydrogenase E antisense RNA showed no effect on PFOR mRNA and activity. The ribozyme-transfected cells demonstrated significantly enhanced resistance to metronidazole and grew equally well under anaerobic and aerobic conditions. In contrast, the wild-type cells grew slightly better anaerobically than the transfectants but did not grow at all in aerobic conditions. Thus, the reduced PFOR expression enables Giardia to grow under molecular oxygen and the presence of PFOR enhances the anaerobic growth of Giardia with an increased susceptibility towards metronidazole. In addition, this study demonstrated for the first time the feasibility of using a viral RNA vector to express a ribozyme targeted at a specific mRNA in G. lamblia to reduce the expression of a specific gene.

Xanthine Oxidoreductase Gene Expression and Enzyme Activity in Developing Human Tissues

Xanthine oxidoreductase (XOR) has been implicated in tissue injury following ischemia-reperfusion because of its ability to generate reactive oxygen species under these conditions. In order to elucidate its role in various organs, we quantified the levels of XOR mRNA expression and activity in developing human tissues. XOR gene expression was highest in the intestine and in the liver, which also showed the highest enzyme activities. By a sensitive RNA-PCR assay, low levels of the transcript were detected in the kidney, lung, cardiac muscle, and brain of all subjects studied. XOR activities followed the mRNA distribution, being low or undetectable in tissues other than the liver and the intestine.