Metallothionein-null mice exhibit reduced tolerance to ultraviolet B injury in vivo.

Abstract

Events that induce expression of the metallothionein (MT) gene, such as injection of cadmium chloride, cold stress or topical application of 1,25-dihydroxyvitamin D3, can deplete the number of ultraviolet (UV) B-induced sunburn cells (SBC) in mouse skin in vivo. MT-null mouse skin explants exhibit reduced tolerance to UVB injury in vitro. However, the in vivo response of MT-null mice to UVB injury has not been investigated. In the present study, we investigated the role of the MT gene on UVB injury in vivo. MT-null mice that are deficient in MT-I and MT-II genes were studied and compared with homozygous wild-type mice. Mouse dorsal skin was irradiated with 0.05, 0.70 and 1.40 J/cm2 UVB. The thickness of the dorsal skin was measured with a spring micrometer before and 24 h after UVB irradiation. In addition, SBC were counted 24 h after UVB irradiation. No significant difference was found in the change of skin thickness between MT-null mice and control mice irradiated with low-dose UVB (0.05 J/cm2) (Student's t-test, t = 1.519, P = 0.167). At higher doses (0.70 and 1.40 J/cm2), the skin of MT-null mice became much thicker than that of control mice (Student's t-test, t = 6.576, P < 0.01 and t = 3.142, P = 0.007, respectively). More SBC were detected in MT-null mice skin irradiated with the highest dose of UVB (1.40 J/cm2) (Student's t-test, t = 4.258, P < 0.01). These results suggest that the MT gene in mice has a photoprotective role in vivo.