Effects of Se, Cu and Se + vitamin E deficiency on the activities of CuZnSOD, GSH‐Px, CAT and LPO levels in chicken erythrocytes

Bozkaya, Lütfiye Arzu; Öztürk-Ürek, Raziye; Aydemir, Tülin; Tarhan, Leman

doi:10.1002/cbf.906

Cited by 31 publications

(21 citation statements)

References 17 publications

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“…MDA content was measured in exponentially growing yeast cultures by a modified method of Bozkaya et al (2001). We found that P. guilliermondii cells ex-creted a major part of thiobarbituric acid reactive species (TBA-RS), apparently MDA, into culture media.…”

Section: Methodsmentioning

confidence: 99%

Mutations and environmental factors affecting regulation of riboflavin synthesis and iron assimilation also cause oxidative stress in the yeast Pichia guilliermondii

Boretsky

Protchenko

Prokopiv

et al. 2007

J. Basic Microbiol.

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Iron deficiency causes oversynthesis of riboflavin in several yeast species, known as flavinogenic yeasts. However, the mechanisms of such regulation are not known. We found that mutations causing riboflavin overproduction and iron hyperaccumulation (rib80, rib81 and hit1), as well as cobalt excess or iron deficiency all provoke oxidative stress in the Pichia guilliermondii yeast. Iron content in the cells, production both of riboflavin and malondialdehyde by P. guilliermondii wild type and hit1 mutant strains depend on a type of carbon source used in cultivation media. The data suggest that the regulation of riboflavin biosynthesis and iron assimilation in P. guilliermondii are linked with cellular oxidative state.

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Section: Methodsmentioning

confidence: 99%

Mutations and environmental factors affecting regulation of riboflavin synthesis and iron assimilation also cause oxidative stress in the yeast Pichia guilliermondii

Boretsky

Protchenko

Prokopiv

et al. 2007

J. Basic Microbiol.

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“…In studies of mitochondrial diseases, the increase in reactive oxygen species required a concurrent increase in the expression of the antioxidative enzymes superoxide dismutase and glutathione peroxidase to scavenge these reactive oxygen species and protect the cells from damage (3,11). In this context, dietary copper restriction reducing the activity of these enzymes is likely to reduce antioxidant defense (2). Consequently, we propose that the inborn reduction of COX activity in CDs rats may produce an initial state of oxidative stress that is potentiated by the HSD due to the further reduction in activity of COX and of the antioxidative enzymes.…”

Section: Cohen-diabetes Sensitive Ratmentioning

confidence: 99%

IL-1β hampers glucose-stimulated insulin secretion in Cohen diabetic rat islets through mitochondrial cytochromecoxidase inhibition by nitric oxide

Weksler-Zangen

Aharon-Hananel

Mantzur

et al. 2014

American Journal of Physiology-Endocrinology and Metabolism

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induces inhibition of glucose-sensitive rats (CDs) but not Cohen diabetes-resistant rats (CDr). Coppersupplemented HSD increased activity of the copper-dependent mitochondrial respiratory chain enzyme cytochrome c oxidase (COX) and reversed hyperglycemia. This study examined the mechanism by which interleukin-1␤ modulates GSIS and the role of COX in this process. We measured COX activity, ATP content, GSIS, iNOS expression, and nitrite production with and without IL-1␤, N -nitro-L-arginine, copper, or potassium cyanide in isolated islets of CDs and CDr fed different diets. We found reduced COX activity, ATP content, and GSIS in isolated islets of CDs rats fed a regular diet. These were severely reduced following HSD and were restored to regular diet levels on copper-supplemented HSD (P Ͻ 0.01 vs. CDr islets). Potassium cyanide chemically reduced COX activity, decreasing GSIS and thus reinforcing the link between islet COX activity and GSIS. Interleukin-1␤ (2.5 U/ml) reduced GSIS and COX activity in CDs islets. Exposure to 10 U/ml interleukin-1␤ decreased GSIS and COX activity in both CDs and CDr islets, inducing a similar nitrite production. Nevertheless, the effect on GSIS was more marked in CDs islets. A significant iNOS expression was detected in CDs on the HSD diet, which was reduced by copper supplementation. N -nitro-L-arginine and copper prevented the deleterious effect of interleukin-1␤ on COX activity and GSIS. We conclude that reduced islet COX activity renders vulnerability to GSIS inhibition on low-copper HSD through two interrelated pathways: 1) by further reducing the activity of COX that is essential for ␤-cell ATP-production and insulin secretion and 2) by inducing the expression of iNOS and nitric oxide-mediated COX inhibition. We suggest that islet COX activity must be maintained above a critical threshold to sustain adequate GSIS with exposure to low-copper HSD.interleukin-1␤; pancreatic ␤-cell; copper; cytochrome c oxidase; inducible nitrix oxide synthase ELEVATED PLASMA GLUCOSE LEVELS will cause a rise in pancreatic ␤-cell ATP/ADP ratio, triggering insulin secretion by oxidative phosphorylation (OXPHOS), a process elicited by the mitochondrial respiratory chain (20, 51). Therefore, mitochondrial dysfunction could lead to impaired glucose-stimulated insulin secretion (GSIS) and an increased risk of diabetes (25,27). The mitochondrial respiratory chain, situated in the inner mitochondrial membrane, consists of five multisubunit complexes (I-V). Complex IV [cytochrome c oxidase (COX)] is the terminal electron transport chain complex that catalyzes the transfer of electrons from cytochrome c to molecular oxygen. The electrochemical proton gradient formed by complexes I, III, and IV (COX) is utilized by complex V (ATP synthase) to generate ATP (25). COX activity is regulated and inhibited by numerous molecules, including potassium cyanide (KCN) and nitric oxide (NO), which reversibly competes with oxygen at the heme copper active site (8). Studies in diabetic animal models suggest that interleuki...

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“…Recently, hemolytic anemia has been found in rats with Se deficiency [4] that is closely related to glutathione peroxidase (GSH-Px) activity. It was shown that Se deficiency increased the activity of GSH-Px in Se-deficient chicken erythrocytes [5]. In Se-supplemented rats, osmotic hemolysis resistance was shown to be significantly increased compared with the control [6].…”

Section: Introductionmentioning

confidence: 99%

Effect of Selenium Deficiency on Nitric Oxide and Heat Shock Proteins in Chicken Erythrocytes

Zhao

Xing

Liu

et al. 2015

Biol Trace Elem Res

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Selenium (Se) deficiency induces various types of diseases, including hemolytic anemia, which is one of the basic pathologies of erythrocyte damage. To investigate the effect of Se deficiency on chicken erythrocytes, we detected the effects of Se deficiency on the nitric oxide (NO) content and the levels of heat shock proteins (Hsps) in chicken erythrocytes, including Hsp27, Hsp40, Hsp60, Hsp70, and Hsp90. One-day-old chickens (180) were randomly divided into two groups, a low-Se group (L group, fed with a 0.008 mg/kg Se diet) and a control group (C group, fed with a 0.2 mg/kg Se diet). Next, erythrocytes were collected at 35 days old, and the NO content, activity of inducible nitric oxide synthase (iNOS), and levels of Hsps (27, 40, 60, 70, and 90) were examined. Compared with the C group, the NO and iNOS levels were significantly higher (P < 0.05), and the Hsps in the mRNA and protein levels were generally higher (P < 0.05) in the L group. Meanwhile, the correlation analysis showed that there were positive correlations between Hsps and NO. Thus, as typical damage biomarkers, NO and Hsps may play special roles in chicken erythrocyte injury by Se deficiency.

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Effects of Se, Cu and Se + vitamin E deficiency on the activities of CuZnSOD, GSH‐Px, CAT and LPO levels in chicken erythrocytes

Cited by 31 publications

References 17 publications

Mutations and environmental factors affecting regulation of riboflavin synthesis and iron assimilation also cause oxidative stress in the yeast Pichia guilliermondii

Mutations and environmental factors affecting regulation of riboflavin synthesis and iron assimilation also cause oxidative stress in the yeast Pichia guilliermondii

IL-1β hampers glucose-stimulated insulin secretion in Cohen diabetic rat islets through mitochondrial cytochromecoxidase inhibition by nitric oxide

Effect of Selenium Deficiency on Nitric Oxide and Heat Shock Proteins in Chicken Erythrocytes

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