The big surprise from all of our studies, was the observation of
the lethal effect of 24 h exposure of vitamin D-deficient trout to
visible light from a 60 W incandescent bulb. These
fish were in
water with a high concentration of dissolved calcium carbonate, so
if they had been producing toxic levels of 1,25(OH)2D3 in blood,
their death may have been caused by increased uptake of calcium
from water with consequent fatal hypercalcemia. However, in
terrestrial vertebrates, visible light is not capable of converting
7-dehydrocholesterol in skin to cholecalciferol. We clearly
demonstrated that shaved rat skin did not form vitamin D when
exposed to visible light with the wavelength range of 380–480 nm.
Nevertheless, cholecalciferol was indeed produced in the skin of
both live and dead vitamin D-deficient rainbow trout exposed to
visible light in the 380–480 nm wavelength range. This observation
seems to defy the known energy requirement, (provided by UV
light at 290–320 nm), to rupture the 9–10 bond of the B ring of
7-dehydrocholesterol to form pre-cholecalciferol. One possibility
is that the structure of
fish skin, with its metallic sheen caused by
thin bony scales associated with intracellular anhydrous guanine