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Deficiency in the Catalase Activity of Xeroderma Pigmentosum Cell and Simian Virus 40-transformed Human Cell Extracts¹

U.A. 686 C.N.R.S., Ecole Normale Supérieure, 46, rue d'Ulm, 75230 Paris [M. V., P. T., M. H.]; Laboratoire des Membranes biologiques, Université Paris VII, 2 place Jussieu, 75005 Paris [R. C.]; U.A. 1135 C.N.R.S., Université Paris VI, 7 quai Saint Bernard, 75005 Paris [M. B. B.]; Institut Curie, 26, rue d'Ulm, 75005 Paris [Y. D.]; and Laboratory of Molecular Mutagenesis, Institut de Recherches Scientifiques sur le Cancer, B. P. No. 8, 94802 Villejuif [A. S.], France

It has been previously shown that skin biopsies isolated from various xeroderma pigmentosum (XP) patients present a permanent decline in catalase activity from the onset of the disease to the tumor formation. We report here that cultured XP cell strains are also markedly deficient in the catalase activity with about only 25% of the activity measured in normal human cells. No direct correlation between catalatic activity and excision repair ability has been found, since a XP variant line is as deficient as an XP-C strain. The exact cause of the catalase deficiency is still unknown but could be due to the synthesis of a modified enzyme or to an abnormal regulation leading to a limited enzyme synthesis. Furthermore, simian virus 40 transformation of normal and radiosensitive cells (XP, ataxia telangiectasia) provokes a decrease in catalase activity of about 80% compared to the control derivatives.

Mathematical analysis performed on our data shows a clearcut distinction between XP and normal cells while some of the XP heterozygote cells exhibit an intermediate behavior. Although most of the XP syndrome could be explained by the impairment in the excision repair ability, the decrease in catalase activity leading to a probable increase in intracellular H₂O₂ concentration and/or to a higher sensitivity to any oxygen-activated species could represent an additive effect in inducing the carcinogenic process.

¹ This research was supported by grants from the Association pour le Développement de la Recherche sur le Cancer (Villejuif, France) and from the Commission of the European Communities (Brussels, Belgium).

² To whom requests for reprints should be addressed.

Received 7/11/85. Revised 10/23/85. Accepted 10/25/85.

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