Variation in Cellular Glutathione Peroxidase Activity in Lens Epithelial Cells, Transgenics and Knockouts Does Not Significantly Change the Response to H2O2Stress

Spector, Abraham; Yang, Yanling; Ho, Ye-Shih; Magnenat, Jean-Luc; Wang, Ren-Rong; Ma, Wu; Li, Wancheng

doi:10.1006/exer.1996.0063

Cited by 63 publications

(43 citation statements)

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“…Exposure of Lens to Oxidative Stress Generated by Photochemical Reaction-The method for quantifying damage in animal lens following exposure to photochemically induced oxidative stress has been previously described (41)(42)(43). Briefly, lenses were removed from the eyes of Cat ϩ/ϩ and Cat Ϫ/Ϫ mice immediately following sacrifice.…”

Section: Methodsmentioning

confidence: 99%

Mice Lacking Catalase Develop Normally but Show Differential Sensitivity to Oxidant Tissue Injury

Xiong

et al. 2004

Journal of Biological Chemistry

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362

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Catalase plays a major role in cellular antioxidant defense by decomposing hydrogen peroxide, thereby preventing the generation of hydroxyl radical by the Fenton reaction. The degree of catalase deficiency in acatalasemic and hypocatalasemic mice varies from tissue to tissue. They therefore may not be suitable for studying the function of this enzyme in certain models of oxidant-mediated tissue injury. We sought to generate a new line of catalase null mice by the gene targeting technique. The mouse catalase (Cat or Cas1) gene was disrupted by replacing parts of intron 4 and exon 5 with a neomycin resistance cassette. Homozygous Cat knockout mice, which are completely deficient in catalase expression, develop normally and show no gross abnormalities. Slices of liver and lung and lenses from the knockout mice exhibited a retarded rate in decomposing extracellular hydrogen peroxide compared with those of wild-type mice. However, mice deficient in catalase were not more vulnerable to hyperoxia-induced lung injury; nor did their lenses show any increased susceptibility to oxidative stress generated by photochemical reaction, suggesting that the antioxidant function of catalase in these two models of oxidant injury is negligible. Further studies showed that cortical injury from physical impact caused a significant decrease in NAD-linked electron transfer activities and energy coupling capacities in brain mitochondria of Cat knockout mice but not wild-type mice. The observed decrease in efficiency of mitochondrial respiration may be a direct result of an increase in mitochondrion-associated calcium, which is secondary to the increased oxidative stress. These studies suggest that the role of catalase in antioxidant defense is dependent on the type of tissue and the model of oxidant-mediated tissue injury.

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Section: Methodsmentioning

confidence: 99%

Mice Lacking Catalase Develop Normally but Show Differential Sensitivity to Oxidant Tissue Injury

Xiong

et al. 2004

Journal of Biological Chemistry

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362

220

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“…Glutathione peroxidase is considered to be essential for ocular lens transparency. The knockout mice, however, showed no sign of opacity development in the lens (34). Since GPX expression in the lung is pronounced, it is of interest to produce a mouse mutant in which GPX is deficient and investigate whether the mutant is highly susceptible to hyperoxia-induced pulmonary injury.…”

Section: Discussionmentioning

confidence: 99%

A Novel Glutathione Peroxidase in Bovine Eye

Singh

Shichi

1998

Journal of Biological Chemistry

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Bovine ciliary body contains a selenium-independent glutathione peroxidase (GPX) with a molecular mass of about 100 kDa that is composed of four identical subunits and exhibits no glutathione S-transferase activity. In this study, we isolated cDNA clones and determined the nucleotide sequence to deduce the primary structure of the enzyme. The cDNA contained 672 base pairs encoding a polypeptide with an estimated molecular mass of 25,064 Da. Translation of bovine ciliary mRNA produced a protein which was immunologically indistinguishable from GPX and showed high enzyme activity. The encoded amino acid sequence of the protein was 95% identical with that of a human keratinocyte gene product expressed in response to keratinocyte growth factor. It also showed sequence identity to bacterial alkyl hydroperoxide reductases and thiol specific antioxidant enzymes. GPX mRNA level was highest in the ciliary body, followed by the retina and iris. In various rat organs, the level of GPX mRNA was highest in the lung, followed by the muscle, liver, eye, heart, testis, thymus, kidney, and spleen. A very low level of mRNA was detected in the brain. Enzyme-linked immunosorbent assay with an antibody raised against the NH 2 -terminal sequence of GPX detected GPX protein in all rat tissues examined.

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“…Indeed, many components of the redox system (including SOD, catalase, GSSG reductase, NADPH oxidase, peroxiredoxin 6, thioltransferase, thioredoxin reductase, ascorbate free radical reductase, methionine sulfoxide reductase) have much higher activities/levels in the epithelial/surface cells than in the rest of the lens (Fig. 4) (7,15,63,65,124,126,143,153,154,177). Two enzymes that do not follow this pattern are GSHPx-1 (whose activity is comparable in the epithelium and in the rest of the mouse lens; 154) and peroxiredoxin 3 (a mitochondrial peroxidase with higher abundance in fiber cells than in epithelial cells; 72).…”

Section: Figmentioning

confidence: 99%

Oxidative Stress, Lens Gap Junctions, and Cataracts

Berthoud

Beyer

2009

Antioxidants & Redox Signaling

217

141

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The eye lens is constantly subjected to oxidative stress from radiation and other sources. The lens has several mechanisms to protect its components from oxidative stress and to maintain its redox state, including enzymatic pathways and high concentrations of ascorbate and reduced glutathione. With aging, accumulation of oxidized lens components and decreased efficiency of repair mechanisms can contribute to the development of lens opacities or cataracts. Maintenance of transparency and homeostasis of the avascular lens depend on an extensive network of gap junctions. Communication through gap junction channels allows intercellular passage of molecules (up to 1 kDa) including antioxidants. Lens gap junctions and their constituent proteins, connexins (Cx43, Cx46, and Cx50), are also subject to the effects of oxidative stress. These observations suggest that oxidative stress-induced damage to connexins (and consequent altered intercellular communication) may contribute to cataract formation. Antioxid. Redox Signal. 11, 339-353. 339The Eye Lens

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Variation in Cellular Glutathione Peroxidase Activity in Lens Epithelial Cells, Transgenics and Knockouts Does Not Significantly Change the Response to H2O2Stress

Cited by 63 publications

References 0 publications

Mice Lacking Catalase Develop Normally but Show Differential Sensitivity to Oxidant Tissue Injury

Mice Lacking Catalase Develop Normally but Show Differential Sensitivity to Oxidant Tissue Injury

A Novel Glutathione Peroxidase in Bovine Eye

Oxidative Stress, Lens Gap Junctions, and Cataracts

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