The role of calcium in human lymphocyte DNA repair ability

Uzi Gafter*, Tsipora Malachi, Yaacov Ori, Haim Breitbart

*Corresponding author for this work

Research output: Contribution to journalArticlepeer-review

28 Scopus citations

Abstract

DNA repair ability is reduced in a variety of pathologic conditions. In addition, in some of these diseases a disturbance in cellular Ca homeostasis occurs or cytosolic (Ca2+) responses to various stimuli are impaired. The leading environmental cause for genomal DNA damage is ultraviolet (UV) irradiation. The aims of the present study were (1) to evaluate a possible dependence of UV-induced DNA repair ability on cytosolic Ca2+ in human lymphocytes and (2) to assess the direct effect of UV irradiation on Ca2+ homeostasis in these cells. UV-induced DNA repair ability in lymphocytes was maximal at 1 mmol/L CaCl2 in the medium. Suppression of DNA repair ability occurred after elevation or reduction of cellular (Ca2+) when various methods were used, including changes in Ca2+ concentration in the medium, cellular Ca2+ depletion by ethyleneglycol-bis(βaminoethylether)-N,N,N',N'-tetraacetic acid, excessive Ca2+ concentration induced by ionophore, and shortening of Ca2+ presence time during repair synthesis. UV irradiation caused an immediate and significant rise in cytosolic (Ca2+) that was the result of both enhanced Ca2+ uptake and inhibition of plasma membrane Ca-adenosine triphosphotase activity. The tyrosine kinase inhibitor genistein inhibited both UV-induced DNA repair and UV-induced cytosolic (Ca2+) elevation. These results emphasize the importance of a precise cellular Ca2+ level regulation for the optimal DNA repair process, UV irradiation, by inducing cellular Ca2+ rise, may activate DNA repair as soon as DNA is damaged.

Original languageEnglish
Pages (from-to)33-41
Number of pages9
JournalJournal of Laboratory and Clinical Medicine
Volume130
Issue number1
DOIs
StatePublished - Jul 1997

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