Expression of Glucose-6-Phosphate Dehydrogenase and 6-Phosphogluconate Dehydrogenase in Oxidative Stress Induced by Long-Term Iron Toxicity in Rat Liver

2014 ◽  
Vol 28 (5) ◽  
pp. 217-223 ◽  
Author(s):  
Harun Budak ◽  
Hamid Ceylan ◽  
Enver Fehim Kocpinar ◽  
Nurdan Gonul ◽  
Orhan Erdogan
Keyword(s):  
Oxidative Stress ◽  
Rat Liver ◽  
Iron Toxicity ◽  
Phosphogluconate Dehydrogenase ◽  
Glucose 6 Phosphate Dehydrogenase

scholarly journals Eugenol attenuates concanavalin A-induced hepatitis through modulation of cytokine levels and inhibition of mitochondrial oxidative stress

2019 ◽  
Vol 71 (2) ◽  
pp. 339-346
Author(s):  
Jing Liu ◽  
Yidong Mao
Keyword(s):  
Oxidative Stress ◽  
Concanavalin A ◽  
Hepatoprotective Activity ◽  
Antioxidant Enzyme Activities ◽  
Mitochondrial Oxidative Stress ◽  
Immune Mediated ◽  
Wide Range ◽  
Cytokine Levels ◽  
Glucose 6 Phosphate Dehydrogenase

Therapeutic management of hepatitis with conventional drugs alone worsens hepatic functioning in the long term because of sustained oxidative stress. Active compounds from several plant sources have been investigated to counteract this. Eugenol, a phytochemical abundant in various plants, is known for its wide range of pharmacological effects. There is a lacuna in the deeper understanding of its hepatoprotective activity at the molecular level. Our present study aimed to determine the effects of eugenol on the changes in antioxidant components, inflammatory cytokines and modulation of mitochondrial oxidative stress in immune-mediated hepatitis. We employed a model that mimics viral hepatitis using concanavalin A (ConA) to induce T-cell-mediated acute hepatitis. Eugenol increased (P<0.01) antioxidant enzyme activities, including reduced glutathione (GSH)-regenerating enzyme, glutathione reductase, and glucose-6-phosphate dehydrogenase. Its antiinflammatory and antifibrogenic effects were evident from the reduction (P<0.01) in interleukin and tumor necrosis factor levels. Eugenol was found to decrease mitochondrial oxidative stress, which was elevated in hepatitis. The hepatoprotective effects of eugenol were confirmed by histological findings. The current investigation shows that eugenol exerts a hepatoprotective effect through the modulation of different pathways which include restoration of mitochondrial oxidative stress. Eugenol could be a promising candidate for human hepatitis management, warranting preclinical studies.

scholarly journals Changes in activity of some enzymes involved in glucose utilization and formation in developing rat liver

1968 ◽  
Vol 106 (2) ◽  
pp. 321-329 ◽  
Author(s):  
R. G. Vernon ◽  
D G Walker
Keyword(s):  
Malate Dehydrogenase ◽  
Rat Liver ◽  
Postnatal Period ◽  
Supernatant Fraction ◽  
Atp Citrate Lyase ◽  
Carboxylase Activity ◽  
Phosphogluconate Dehydrogenase ◽  
Citrate Lyase ◽  
Glucose 6 Phosphate Dehydrogenase ◽  
Developing Rat

1. The activities of some enzymes involved in both the utilization of glucose (pyruvate kinase, ATP citrate lyase, NADP-specific malate dehydrogenase, glucose 6-phosphate dehydrogenase, 6-phosphogluconate dehydrogenase and NADP-specific isocitrate dehydrogenase, all present in the supernatant fraction of liver homogenates) and the formation of glucose by gluconeogenesis (glucose 6-phosphatase in the whole homogenate and fructose 1,6-diphosphatase, phosphopyruvate carboxylase, NAD-specific malate dehydrogenase and fumarase in the supernatant fraction) have been determined in rat liver around birth and in the postnatal period until the end of weaning. 2. The activities of those enzymes involved in the conversion of glucose into lipid are low during the neonatal period and increase with weaning. NADP-specific malate dehydrogenase first appears and develops at the beginning of the weaning period. 3. The marked increase in cytoplasmic phosphopyruvate carboxylase activity at birth is probably the major factor initiating gluconeogenesis at that time. 4. The results are discussed against the known changes in dietary supplies and the known metabolic patterns during the period of development.

Long-term fructose-enriched diet introduced immediately after weaning does not induce oxidative stress in the rat liver

2014 ◽  
Vol 34 (7) ◽  
pp. 646-652 ◽  
Author(s):  
Jelena Nestorov ◽  
Alhadi M. Glban ◽  
Ana Mijušković ◽  
Aleksandra Nikolić-Kokić ◽  
Ivana Elaković ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Rat Liver

scholarly journals NADP-Dependent Isocitrate Dehydrogenase fromArabidopsisRoots Contributes in the Mechanism of Defence against the Nitro-Oxidative Stress Induced by Salinity

2012 ◽  
Vol 2012 ◽  
pp. 1-9 ◽  
Author(s):  
Marina Leterrier ◽  
Juan B. Barroso ◽  
Raquel Valderrama ◽  
José M. Palma ◽  
Francisco J. Corpas
Keyword(s):  
Oxidative Stress ◽  
Nitric Oxide ◽  
Isocitrate Dehydrogenase ◽  
Malic Enzyme ◽  
Superoxide Radical ◽  
Plant Defence ◽  
Maximum Activity ◽  
Nadph Regeneration ◽  
Phosphogluconate Dehydrogenase ◽  
Glucose 6 Phosphate Dehydrogenase

NADPH regeneration appears to be essential in the mechanism of plant defence against oxidative stress. Plants contain several NADPH-generating dehydrogenases including isocitrate dehydrogenase (NADP-ICDH), glucose-6-phosphate dehydrogenase (G6PDH), 6-phosphogluconate dehydrogenase (6PGDH), and malic enzyme (ME). InArabidopsisseedlings grown under salinity conditions (100 mM NaCl) the analysis of physiological parameters, antioxidant enzymes (catalase and superoxide dismutase) and content of superoxide radical (O2  ∙−), nitric oxide (NO), and peroxynitrite (ONOO-) indicates a process of nitro-oxidative stress induced by NaCl. Among the analysed NADPH-generating dehydrogenases under salinity conditions, the NADP-ICDH showed the maximum activity mainly attributable to the root NADP-ICDH. Thus, these data provide new insights on the relevance of the NADP-ICDH which could be considered as a second barrier in the mechanism of response against the nitro-oxidative stress generated by salinity.

The effects of pregnancy, lactation and involution on the metabolism of glucose and acetate by rat liver tissue

1973 ◽  
Vol 40 (3) ◽  
pp. 339-351 ◽  
Author(s):  
R. W. Smith
Keyword(s):  
Fatty Acids ◽  
Rat Liver ◽  
Milk Fat ◽  
Late Pregnancy ◽  
Acetyl Coa Carboxylase ◽  
Atp Citrate Lyase ◽  
Phosphogluconate Dehydrogenase ◽  
Citrate Lyase ◽  
Pregnancy And Lactation ◽  
Glucose 6 Phosphate Dehydrogenase

SummaryThe incorporation of 14C from [1-14C] and [6-14C]glucose and [2-14C]acetate into CO2 and fatty acids by rat liver slices was measured at intervals during pregnancy, lactation and involution.During late pregnancy, the rates of oxidation of the C-1 and C-6 atoms of glucose were respectively 65 and 40 % higher than those for unmated animals. These increases were maintained during lactation, but the highest values were observed 3 days after weaning. Pregnancy and lactation had little effect on the oxidation of [2-14C]acetate.The incorporation of14C from all 3 labelled substrates into fatty acids was increased by a factor of 3–4 during late pregnancy. There were further increases during lactation, and 3 days after weaning the values were as much as 10 times as high as those for unmated animals.The incorporation of both [14C]glucose and [14C]acetate into cholesterol was increased by a factor of 6–7 during lactation.The activities of the enzymes glucose 6-phosphate dehydrogenase, 6-phosphogluconate dehydrogenase, ATP citrate lyase and acetyl-CoA carboxylase were also increased during lactation and involution.The similarity between the changes summarized above and those brought about by changes in the pattern of food intake is discussed, and the idea that fatty acids synthesized from non-lipid precursors in the liver may make some contribution to the formation of milk fat is also considered.

scholarly journals Impact of starvation-refeeding on kinetics and protein expression of trout liver NADPH-production systems

1998 ◽  
Vol 274 (6) ◽  
pp. R1578-R1587 ◽  
Author(s):  
Juan B. Barroso ◽  
Juan Peragón ◽  
Constanza Contreras-Jurado ◽  
Leticia García-Salguero ◽  
Francisco J. Corpas ◽  
...  
Keyword(s):  
Protein Expression ◽  
Production Systems ◽  
Specific Protein ◽  
Activity Levels ◽  
Phosphogluconate Dehydrogenase ◽  
Nutritional Conditions ◽  
Normal Enzyme ◽  
Glucose 6 Phosphate Dehydrogenase ◽  
Kinetics Of

Herein we report on the kinetic and protein expression of glucose-6-phosphate dehydrogenase (G6PDH), 6-phosphogluconate dehydrogenase, and malic enzyme (ME) in the liver of the trout ( Oncorhynchus mykiss) during a long-term starvation-refeeding cycle. Starvation significantly depressed the activity of these enzymes by almost 60%, without changing the Michaelis constant. The time response to this nutritional stimulus increased with fish weight. The sharp decline in G6PDH and ME activities was due to a specific protein-repression phenomenon, as demonstrated by molecular and immunohistochemical analyses. Also, the dimeric banding pattern of liver G6PDH shifted from the fully reduced and partially oxidized forms, predominant in control, to a fully oxidized form, more sensitive to proteolytic inactivation. Refeeding caused opposite effects in both protein concentration and enzyme activities of about twice the control values in the first stages, later reaching the normal enzyme activity levels. Additionally, the partially oxidized form of G6PDH increased. The kinetics of these enzymes were examined in relation to the various metabolic roles of NADPH. These results clearly indicate that trout liver undergoes protein repression-induction processes under these two contrasting nutritional conditions.

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