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Vitamin D and Cancer<br />
7-Dehydrocholesterol<br />
7-Dehydrocholesterol<br />
UVB<br />
7-Dehydrocholesterol Previtamin D3<br />
Cholesterol<br />
DBP<br />
DBP-D3<br />
DBP<br />
T<br />
Vitamin D3<br />
Vitamin D3<br />
DBP-D3<br />
DBP<br />
UVB<br />
UVB<br />
OH<br />
Tachysterol Tachysterol<br />
HO<br />
Skin surface<br />
Lumisterol<br />
DBP-D3<br />
Lumisterol<br />
Inactive sterols:<br />
Suprasterol I, II<br />
5,6-trans-vitamin D3<br />
Basal membrane<br />
Dermis<br />
Figure 4.2 - Photochemical synthesis of vitamin D3 in human skin (from Bodo Lehmann, personal collection). The<br />
provitamin D3 7-dehydrocholesterol (7-DHC) is formed in the skin from circulating cholesterol. The 7-DHC absorbs<br />
UVB radiation causing it to isomerise, resulting in the previtamin D3. Previtamin D3 then undergoes nonenzymatic<br />
isomerisation to form vitamin D3. The vitamin D3 formed in the skin is then swept out into the blood stream by the<br />
Vitamin D Binding protein (DBP), and α-globulin that has a high affinity to vitamin D and its metabolites. The constant<br />
extraction of vitamin D from the skin by DBP avoids the local accumulation of vitamin D3 and allows perpetuation of<br />
the isomerisation of previtamin D3 into vitamin D3. UVB-triggered conversion of 7-DHC to previtamin D3 is a rapid<br />
reaction which needs only a few seconds. In contrast, the half life (τ1/2) of the isomerisation of previtamin D3 to<br />
vitamin D3 in human skin is approximately 2.5 hours. The circulating concentrations of vitamin D3 are at their<br />
maximum levels within 12-24 hours after UVB exposure. A few minutes after start of UVB exposure, the previtamin<br />
D3 also transforms in inter tachysterol and lumisterol, and the UVB further promotes degradation of vitamin D3 in<br />
inactive suprasterol and other inert compounds.<br />
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