Antioxidant enzymes in xeroderma pigmentosum fibroblasts

In light of recent studies implicating low catalase activities in the pathogenesis of the cancer-prone disease xeroderma pigmentosum (XP) we have measured catalase activity, protein levels, and mRNA concentrations in six XP fibroblast strains and three normal controls. Only one XP strain of compleme...

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Bibliographic Details
Published inCancer research (Chicago, Ill.) Vol. 48; no. 8; pp. 2132 - 2134
Main Authors CRAWFORD, D, ZBINDEN, I, MORET, R, CERUTTI, P
Format Journal Article
LanguageEnglish
Published Philadelphia, PA American Association for Cancer Research 15.04.1988
Subjects
Antioxidants - analysis
Biological and medical sciences
Catalase - analysis
Dermatology
Fibroblasts - enzymology
Glutathione Peroxidase - analysis
Hereditary diseases of the skin. Congenital diseases of the skin. Haemangioma of the skin, of mucosae and of soft tissue
Humans
Medical sciences
RNA, Messenger - analysis
Superoxide Dismutase - analysis
Xeroderma Pigmentosum - enzymology
Human
Cell culture
Photodermatosis
Skin disease
Enzymatic activity
Physical agent
Catalase
Xeroderma pigmentosum
Tumor
Fibroblast
Genetic disease
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Summary:In light of recent studies implicating low catalase activities in the pathogenesis of the cancer-prone disease xeroderma pigmentosum (XP) we have measured catalase activity, protein levels, and mRNA concentrations in six XP fibroblast strains and three normal controls. Only one XP strain of complementation group A (XP1223) possessed significantly lower catalase by all three criteria. The other five XP strains (two XP variants, two strains of complementation group D, and one strain of complementation group C) possessed catalase levels which fell into the range of the interindividual variations of normal controls. We further assessed the total enzymatic antioxidant defense status by measuring the levels of copper, zinc, and manganese superoxide dismutase and glutathione peroxidase. None of these enzymes showed significant deviations from controls in XP cells. Our results do not support the notion that a deficient enzymatic antioxidant defense facilitates the establishment of a prooxidant state in XP upon exposure to near-UV. However, they do not argue against the participation of active oxygen in near-UV-induced carcinogenesis in XP.
ISSN:0008-5472
1538-7445