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- W1978505963 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." @default.
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- W1978505963 date "2004-01-01" @default.
- W1978505963 modified "2023-09-24" @default.
- W1978505963 title "Metallothionein-null mice exhibit reduced tolerance to ultraviolet B injury in vivo" @default.
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- W1978505963 doi "https://doi.org/10.1111/j.1365-2230.2004.01424.x" @default.
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