Zinc and DNA fragmentation in keratinocyte apoptosis: its inhibitory effect in UVB irradiated cells

Parat, Marie-Odile; Richard, Marie‐Jeanne; Pollet, Ségolène; Hadjur, Christophe; Favier, Alain; Béani, J.-C.

doi:10.1016/s1011-1344(96)07334-4

Cited by 61 publications

(55 citation statements)

References 18 publications

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“…The activities of antioxidant enzymes (catalase and manganese-dependent and copper/zincdependent superoxide dismutases) and the levels of reduced versus oxidized glutathione were measured as described previously (38). For the determination of zinc, copper, and iron, cells were trypsinized, washed three times with 400 mM isotonic Tris (pH 7.3, treated with chelex resin to minimize contamination by exogenous metals), and resuspended in hypotonic Tris (10 mM).…”

Section: Methodsmentioning

confidence: 99%

“…After removal of aliquots for protein determination, copper, iron, and zinc concentrations were determined by electrothermal atomic absorption spectrophotometry with a Perkin-Elmer 3030 spectrophotometer for determination of zinc and a Hitachi 28270 spectrophotometer for determination of iron and copper. Strand breaks were determined by the alkaline unwinding technique as described previously (38).…”

Section: Methodsmentioning

confidence: 99%

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Regulation of p53 by Metal Ions and by Antioxidants: Dithiocarbamate Down-Regulates p53 DNA-Binding Activity by Increasing the Intracellular Level of Copper

Verhaegh

Richard

Hainaut

1997

Molecular and Cellular Biology

165

127

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Section: Methodsmentioning

confidence: 99%

Section: Methodsmentioning

confidence: 99%

Regulation of p53 by Metal Ions and by Antioxidants: Dithiocarbamate Down-Regulates p53 DNA-Binding Activity by Increasing the Intracellular Level of Copper

Verhaegh

Richard

Hainaut

1997

Molecular and Cellular Biology

165

127

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“…6D) 2 ) in the presence of 10 mM glucose and then incubated for 15 h. DNA was extracted and separated on 1.5% agarose gel. B, cells were irradiated with 25 J/cm 2 UVA and incubated for different times (3,6,12,15,18, and 24 h). Extracted DNA was subjected to 1.5% agarose gel electrophoresis.…”

Section: Figmentioning

confidence: 99%

Role of Reduced Glutathione Efflux in Apoptosis of Immortalized Human Keratinocytes Induced by UVA

Huang

Ramirez

et al. 2003

Journal of Biological Chemistry

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We have investigated the role played by GSH efflux in apoptosis of human HaCaT keratinocytes induced by UVA irradiation. UVA irradiation of HaCaT cells caused a rapid rise in GSH efflux across the intact cell membrane, followed by an increase in apoptosis. GSH efflux was stimulated by glucose and was reduced by the addition of exogenous GSH and intracellular GSH depletion by buthionine sulfoximine, suggesting that GSH transport is active and is influenced by the GSH concentration gradient across the cell membrane. Verapamil and cyclosporin A, blockers of the multidrug resistanceassociated protein, decreased UVA-induced GSH efflux. GSH efflux occurred within 2 h of UVA irradiation, suggesting that the stimulation of GSH efflux is due to an increase in the activity of pre-existing multidrug resistance-associated protein transporter carrier. Although inhibition of GSH efflux did not affect caspase activation and DNA fragmentation, it delayed the gradual increase in plasma membrane permeability and reduced phosphatidylserine translocation in HaCaT cells. It is therefore likely that upon UVA irradiation, GSH efflux increased the intracellular oxidative stress without intervention of reactive oxygen species, thus resulting in more phosphatidylserine externalization and membrane rearrangement. These provide targets for macrophage recognition and phagocytosis and thus minimize the potential to invoke inflammation or neoplastic transformation.

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“…Similarly, Zalewski et al (1993Zalewski et al ( , 1994 reported that the concentration of readily soluble Zn compounds in the cytosol plays a determining role in preventing DNA fragmentation, and thus apoptosis. According to Parat et al (1997), inhibitory action of Zn on apoptosis seems to be related to its role in protecting cell membranes and DNA from damaging attack by toxic O # species. In view of the inhibitory effect of Zn on NADPH oxidase, it is logical to assume that prevention of apoptosis by Zn can be attributed to a reduced activity of NADPH oxidases involved in ROS-mediated apoptotic cell death.…”

Section: Superoxide-generating Nadph Oxidasementioning

confidence: 99%

Tansley Review No. 111

2000

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Zinc deficiency is one of the most widespread micronutrient deficiencies in plants and causes severe reductions in crop production. There are a number of physiological impairments in Zn-deficient cells causing inhibition of the growth, differentiation and development of plants. Increasing evidence indicates that oxidative damage to critical cell compounds resulting from attack by reactive O # species (ROS) is the basis of disturbances in plant growth caused by Zn deficiency. Zinc interferes with membrane-bound NADPH oxidase producing ROS. In Zn-deficient plants the iron concentration increases, which potentiates the production of free radicals. The Zn nutritional status of plants influences photooxidative damage to chloroplasts, catalysed by ROS. Zinc-deficient leaves are highly light-sensitive, rapidly becoming chlorotic and necrotic when exposed to high light intensity. Zinc plays critical roles in the defence system of cells against ROS, and thus represents an excellent protective agent against the oxidation of several vital cell components such as membrane lipids and proteins, chlorophyll, SH-containing enzymes and DNA. The cysteine, histidine and glutamate or aspartate residues represent the most critical Znbinding sites in enzymes, DNA-binding proteins (Zn-finger proteins) and membrane proteins. In addition, animal studies have shown that Zn is involved in inhibition of apoptosis (programmed cell death) which is preceded by DNA and membrane damage through reactions with ROS.

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Zinc and DNA fragmentation in keratinocyte apoptosis: its inhibitory effect in UVB irradiated cells

Cited by 61 publications

References 18 publications

Regulation of p53 by Metal Ions and by Antioxidants: Dithiocarbamate Down-Regulates p53 DNA-Binding Activity by Increasing the Intracellular Level of Copper

Regulation of p53 by Metal Ions and by Antioxidants: Dithiocarbamate Down-Regulates p53 DNA-Binding Activity by Increasing the Intracellular Level of Copper

Role of Reduced Glutathione Efflux in Apoptosis of Immortalized Human Keratinocytes Induced by UVA

Tansley Review No. 111

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