Ultraviolet A – Induced Lipid Peroxidation and Antioxidant Defense Systems in Cultured Human Skin Fibroblasts

Moysan, A.; Marquis, Isabelle; Gaboriau, François; Santús, René; Dubertret, Louis; Morlière, Patrice

doi:10.1111/1523-1747.ep12472352

Cited by 115 publications

(68 citation statements)

References 51 publications

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“…Data were obtained with fibroblasts from four different donors. As earlier reported, TBARS in the supernatant may vary depending on the cell origin [9,14], the number of passages in culture [9], the antioxidative defense status [14], the cell growing status [10], and on other still unknown parameters. The TBARS released from sham-irradiated cells, are always very low, as already reported and discussed [9,14] and are independent of the DDC treatment (Fig.…”

Section: Effect Of Ddc On the Primary Antioxidative Defensesmentioning

confidence: 78%

“…After addition of 50 µl 0.5% aqueous Triton X100 to produce homogenous solutions, 400 µl were collected for catalase assay and 150 µl for protein determination. The spectrophotometric catalase assay [22] was carried out by a slightly modified procedure already described [14] in monitoring, at 240 nm, the consumption of 20 mM H 2 O 2 (25°C). One unit is defined as 1 µmol H 2 O 2 consumed/min.…”

Section: Methodsmentioning

confidence: 99%

“…Cells from two Petri dishes (60 mm diameter) were washed twice with DPBS (2 ml), scrapped into 800 µl 100 mM sodium phosphate, pH 7.5, containing 1 mM diethylenetriaminepentaacetic acid, collected and sonicated in ice for 30 s. After addition of 80 µl 0.5 % Triton X-100 in water, 75 µl was saved for protein determination while 250 µl was used for the GSHPx assay. GSHPx activity was assayed, as earlier reported [14], according to a slight modification of the procedure described by Flohé and Günzler [25]. The consumption rate of 0.15 mM NADPH at 37°C was monitored at 340 nm in the presence of 0.07 unit glutathione reductase, 4 mM GSH and 0.57 mM tert-BuOOH.…”

Section: Methodsmentioning

confidence: 99%

“…Cells from two Petri dishes (60 mm diameter) were washed twice with DPBS (2 ml), scrapped into 700 µl water, collected and sonicated in ice for 30 s. Then, 75 µl were saved for protein determination while 500 µl were used for total GSH (GSH t ) and GSSG assays. The assay was performed, as reported earlier [14], according to a slight modification of the procedure reported by Tietze [26]. For GSSG determinations, 2-vinylpyridine was used to ensure GSH derivatization (у 99.5%) [27,28].…”

Section: Methodsmentioning

confidence: 99%

“…1). Since basal levels of the antioxidative defenses in cells not treated with DDC depend on the fibroblasts origin [13,14], data were normalized to that from corresponding cells untreated with DDC and used as reference for each donor. The values for these reference systems were assigned to be 100%.…”

Section: Effect Of Ddc On the Primary Antioxidative Defensesmentioning

confidence: 99%

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Pro‐oxidant role of superoxide dismutase in ultraviolet‐A‐induced lipid peroxidation in cultured normal human skin fibroblasts

Morlière

Santús

1998

European Journal of Biochemistry

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Exposure of cultured normal human skin fibroblasts to ultraviolet A triggers lipid peroxidation. In sharp contrast with the tert-butylhydroperoxide-induced lipid peroxidation, the ultraviolet-A-induced lipid peroxidation is inhibited by treating cells with diethyldithiocarbamate. Diethyldithiocarbamate decreases superoxide dismutase activity and, to a lesser extent, the total glutathione level. Catalase and glutathione peroxidase, however, are unaffected. The decrease in the superoxide dismutase activity parallels an inhibition of H 2 O 2 formation in both irradiated and unirradiated cells. The protection against lipid peroxidation may thus be associated with superoxide dismutase inhibition. Membrane damage revealed by neutral red uptake is not prevented by diethyldithiocarbamate.

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Section: Effect Of Ddc On the Primary Antioxidative Defensesmentioning

confidence: 78%

Section: Methodsmentioning

confidence: 99%

Section: Methodsmentioning

confidence: 99%

Section: Methodsmentioning

confidence: 99%

Section: Effect Of Ddc On the Primary Antioxidative Defensesmentioning

confidence: 99%

See 3 more Smart Citations

Pro‐oxidant role of superoxide dismutase in ultraviolet‐A‐induced lipid peroxidation in cultured normal human skin fibroblasts

Morlière

Santús

1998

European Journal of Biochemistry

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Epidermis as a Shield from Radiation and Oxidative Stress

Valacchi

2011

Innate Immune System of Skin and Oral Mucosa

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Imbalanced secondary mucosal antioxidant response in inflammatory bowel disease

Kruidenier

Kuiper

Duijn

et al. 2003

The Journal of Pathology

198

135

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Intestinal mucosal damage in the inflammatory bowel diseases (IBD) Crohn's disease (CD) and ulcerative colitis (UC) involves reactive oxygen metabolites (ROMs). ROMs are neutralized by endogenous antioxidant enzymes in a carefully balanced two-step pathway. Superoxide dismutases (SODs) convert superoxide anion to hydrogen peroxide (H(2)O(2)), which is subsequently neutralized to water by catalase (CAT) or glutathione peroxidase (GPO). Remarkably changed expression levels of the three isoforms of SOD in paired non-inflamed and inflamed mucosae from CD and UC patients have been previously reported in comparison to normal control mucosa. Most notable was the strong up-regulation of Mn-SOD in inflamed epithelium. It was hypothesized that in order to provide optimal protection against ROM-mediated damage, these changes should be coordinately counterbalanced by an increased H(2)O(2)-neutralizing capacity. Therefore, the same tissue samples were used to assess the levels, activities, and/or localization of the most prominent mucosal H(2)O(2)-related antioxidants CAT, GPO, glutathione (GSH), myeloperoxidase (MPO), and metallothionein (MT). Quantitative measurements showed that in both CD and UC patients, intestinal inflammation was associated with increased activities of CAT, GPO, and MPO, whereas the mucosal GSH content was unaffected and the concentration of MT was decreased. Despite this overall increase in mucosal H(2)O(2)-metabolizing enzyme capacity, immunohistochemical analysis revealed a differentially disturbed antioxidant balance in IBD epithelium and lamina propria. In the lamina propria, the risk of direct H(2)O(2)-mediated damage seemed to be restrained by the increasing numbers of CAT- and MPO-positive monocytes/macrophages and neutrophils that infiltrated the inflamed areas. On the other hand, MPO overexpression might increase the lamina propria levels of hypochlorous acid, a stable ROM with multiple pro-inflammatory effects. In the epithelium, the number of cells that expressed CAT remained unchanged during inflammation and GPO was found in only a very low and constant number of epithelial cells. In addition, the inflamed epithelium displayed decreased expression of the hydroxyl radical (OH(*)) scavenger MT. In view of the high epithelial SOD levels in inflamed IBD epithelium, it is speculated that the efficient removal of excess H(2)O(2) is hampered in these cells, thereby increasing not only the risk of detrimental effects of H(2)O(2) directly, but also those of its extremely reactive derivatives such as OH(*). Taken together, the results suggest an imbalanced and inefficient endogenous antioxidant response in the intestinal mucosa of IBD patients, which may contribute to both the pathogenesis and the perpetuation of the inflammatory processes.

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Ultraviolet A – Induced Lipid Peroxidation and Antioxidant Defense Systems in Cultured Human Skin Fibroblasts

Cited by 115 publications

References 51 publications

Pro‐oxidant role of superoxide dismutase in ultraviolet‐A‐induced lipid peroxidation in cultured normal human skin fibroblasts

Pro‐oxidant role of superoxide dismutase in ultraviolet‐A‐induced lipid peroxidation in cultured normal human skin fibroblasts

Epidermis as a Shield from Radiation and Oxidative Stress

Imbalanced secondary mucosal antioxidant response in inflammatory bowel disease

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