Hepatic Cytosolic Non Selenium-Dependent Glutathione Peroxidase Activity: Its Nature and the Effect of Selenium Deficiency

Lawrence, Richard; Parkhill, Linda; Burk, Raymond F.

doi:10.1093/jn/108.6.981

Cited by 228 publications

(61 citation statements)

References 15 publications

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“…They have been shown to be capable of detoxifying various endogenous and exogenous substances by conjugation with glutathione, and might act as ligands for nonsubstrate compounds such as heme and bilirubin (33). They also exhibit variable levels of nonselenium-dependent GSH-Px activity against organic hydroperoxides, but not against H202 (2,33). Human red cells have been said to contain only GSTT, a form of transferase that has a relatively low sp act with cumene hydroperoxide and therefore poor glutathione peroxidase activity (33).…”

Section: Resultsmentioning

confidence: 99%

“…These antioxidant systems include both enzymatic and nonenzymatic mechanisms. Vitamin E appears to be the most significant non-enzymatic antioxidant, and CAT, SOD, and selenium-dependent GSH-Px are believed to be the primary enzymatic systems; however, a role has also been identified recently for nonselenium-dependent glutathione peroxidase activity (I), and this appears to be a function of the GST (2).…”

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confidence: 99%

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Developmental Patterns of Antioxidant Defense Mechanisms in Human Erythrocytes

Ripalda

Rudolph

1989

Pediatr Res

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ABSTRACT. To obtain a profile of erythrocyte antioxidant defense potential during late fetal development, we studied selected antioxidant parameters in blood samples from 65 neonates with birth wt between 520 and 4210 g and from 12 healthy adults. Erythrocyte superoxide dismutase activity did not change significantly with maturation and no significant differences were observed among preterm infants grouped in increasing birth wt categories, term neonates, and adults. Erythrocyte catalase and glutathione peroxidase, as well as plasma vitamin E levels, showed highly significant positive correlations ( p < 0.001) with increasing fetal wt and gestational age; by term, CAT activity reached a level similar to the adult control group, but glutathione peroxidase activity, as well as plasma vitamin E levels, were markedly lower in all the preterm and in the term groups than in adults ( p < 0.01). Erythrocyte glutathione S-transferase activity showed a negative correlation with increasing gestational age ( p < 0.01) and the adult values were considerably lower than any of the neonatal levels ( p < 0.001). The role of glutathione Stransferase in erythrocyte metabolism remains obscure. Maturational changes in the activity of the red cell enzymes that were studied and in the plasma vitamin E level were apparent from about 31-36 wk of gestation, suggesting that the stimulation for these changes may have commenced from about 28-31 wk. (Pediatr Res 26: 366-369, 1989) Abbreviations CAT, catalase SOD, superoxide dismutase GSH-Px glutathione peroxidase GSH-Px[H202], glutathione peroxidase with hydrogen peroxide as substrate GSH-Px[t-bh], glutathione peroxidase with t-butyl hydroperoxide as substrate GST, glutathione S-transferase The evolution of oxidative metabolic processes within mammalian cells has necessitated the concomitant development of mechanisms to protect vital cell components against oxygeninduced damage that could result from oxygen free-radical species produced during metabolism. These antioxidant systems include both enzymatic and nonenzymatic mechanisms. Vitamin E appears to be the most significant non-enzymatic antioxidant, and CAT, SOD, and selenium-dependent GSH-Px are believed to be the primary enzymatic systems; however, a role

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Section: Resultsmentioning

confidence: 99%

mentioning

confidence: 99%

Developmental Patterns of Antioxidant Defense Mechanisms in Human Erythrocytes

Ripalda

Rudolph

1989

Pediatr Res

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“…On the other hand, there is strong evidence for an induction of antioxidant and phase II enzymes in selenium-deficiency. Already in the late 1970s, it was reported that heme oxygenase 1 (HMOX1) [12] as well as GST activity were elevated in selenium-deficient rat liver [32]. The idea of a compensatory up-regulation of antioxidant and phase II enzymes in selenium-deficiency was further supported by findings in mice with an organ-specific targeted removal of the gene encoding for selenocysteine tRNA (Trsp).…”

Section: Introductionmentioning

confidence: 99%

Nrf2 target genes are induced under marginal selenium-deficiency

et al. 2010

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A suboptimal selenium supply appears to prevail in Europe. The current study, therefore, was focused on the changes in gene expression under a suboptimal selenium intake. Previous microarray analyses in the colon of mice fed either a selenium-adequate or a moderately deficient diet revealed a change in genes of several pathways. Severe selenium-deficiency has been found previously to influence Nrf2-regulated genes of the adaptive response. Since the previous pathway analyses were done with a program not searching for Nrf2 target genes, respective genes were manually selected and confirmed by qPCR. qPCR revealed an induction of phase II (Nqo1, Gsts, Sult1b1 and Ugt1a6) and antioxidant enzymes (Hmox1, Mt2, Prdx1, Srxn1, Sod1 and Gclc) under the selenium-poor diet, which is considered to compensate for the loss of selenoproteins. The strongest effects were observed in the duodenum where preferentially genes for antioxidant enzymes were up-regulated. These also include the mRNA of the selenoproteins TrxR1 and GPx2 that would enable their immediate translation upon selenium refeeding. The down-regulation of Gsk3b in moderate selenium-deficiency observed in the previous paper provides a possible explanation for the activation of the Nrf2 pathway, because inhibition of GSK3b results in the nuclear accumulation of Nrf2.

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“…In selenium-deficient animals a huge number of nonselenoproteins, now overwhelmingly known as Nrf2 targets, were found elevated since the late seventies (78,79,270,(395)(396)(397). The unexpected phenomenon could not be convincingly explained by GPx1 deficiency alone (396).…”

Section: Fig 6 Distinct Roles Of Redoxdependent Ubiquitination In Tmentioning

confidence: 99%

Basic Principles and Emerging Concepts in the Redox Control of Transcription Factors

Brigelius‐Flohé

Flohé

2011

Antioxidants & Redox Signaling

513

442

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Convincing concepts of redox control of gene transcription have been worked out for prokaryotes and lower eukaryotes, whereas the knowledge on complex mammalian systems still resembles a patchwork of poorly connected findings. The article, therefore, reviews principles of redox regulation with special emphasis on chemical feasibility, kinetic requirements, specificity, and physiological context, taking well investigated mammalian transcription factor systems, nuclear transcription factor of bone marrow-derived lymphocytes (NFjB), and kelch-like ECH-associated protein-1 (Keap1)/Nrf2, as paradigms. Major conclusions are that (i) direct signaling by free radicals is restricted to O 2 -and NO and can be excluded for fast reacting radicals such as OH, OR, or Cl ; (ii) oxidant signals are H 2 O 2 , enzymatically generated lipid hydroperoxides, and peroxynitrite; (iii) free radical damage is sensed via generation of Michael acceptors; (iv) protein thiol oxidation/alkylation is the prominent mechanism to modulate function; (v) redox sensors must be thiol peroxidases by themselves or proteins with similarly reactive cysteine or selenocysteine (Sec) residues to kinetically compete with glutathione peroxidase (GPx)-and peroxiredoxin (Prx)-type peroxidases or glutathione-S-transferases, respectively, a postulate that still has to be verified for putative mammalian sensors. S-transferases and Prxs are considered for system complementation. The impact of NF-jB and Nrf2 on hormesis, management of inflammatory diseases, and cancer prevention is critically discussed. Antioxid. Redox Signal. 15, 2335-2381.

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Hepatic Cytosolic Non Selenium-Dependent Glutathione Peroxidase Activity: Its Nature and the Effect of Selenium Deficiency

Cited by 228 publications

References 15 publications

Developmental Patterns of Antioxidant Defense Mechanisms in Human Erythrocytes

Developmental Patterns of Antioxidant Defense Mechanisms in Human Erythrocytes

Nrf2 target genes are induced under marginal selenium-deficiency

Basic Principles and Emerging Concepts in the Redox Control of Transcription Factors

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