DNA repair ability is reduced in a variety of pathologic conditions. I
n addition, in some of these diseases a disturbance in cellular Ca hom
eostasis occurs or cytosolic (Ca2+) responses to various stimuli are i
mpaired. The leading environmental cause for genomal DNA damage is ult
raviolet (UV) irradiation. The aims of the present study were (1) to e
valuate a possible dependence of UV-induced DNA repair ability on cyto
solic Ca2+ in human lymphocytes and (2) to assess the direct effect of
UV irradiation on Ca2+ homeostasis in these cells. UV-induced DNA rep
air ability in lymphocytes was maximal at 1 mmol/L CaCl2 in the medium
. Suppression of DNA repair ability occurred after elevation or reduct
ion of cellular (Ca2+) when various methods were used, including chang
es in Ca2+ concentration in the medium, cellular Ca2+ depletion by eth
yleneglycol-bis-(beta aminoethylether)-N,N,N',N'-tetraacetic acid, exc
essive Ca2+ concentration induced by ionophore, and shortening of Ca2 presence time during repair synthesis. UV irradiation caused an immed
iate and significant rise in cytosolic (Ca2+) that was the result of b
oth enhanced Ca2+ uptake and inhibition of plasma membrane Ca-adenosin
e triphosphatase activity. The tyrosine kinase inhibitor genistein inh
ibited both UV-induced DNA repair and UV-induced cytosolic (Ca2+) elev
ation. These results emphasize the importance of a precise cellular Ca
2+ level regulation for the optimal DNA repair process. UV irradiation
, by inducing cellular Ca2+ rise, may activate DNA repair as soon as D
NA is damaged.