The Replacement of Vitamin A1 by Vitamin

It is now well established that vision in dim light is due to the photochemical decomposition of “visual purple,” a pigment present in the rods of the retina (1). Visual purple is believed to be a conjugated protein in which vitamin A or one of its derivatives is a prosthetic group (2). As might be expected, the spectral sensitivity curve of the eye parallels the absorption spectrum of visual purple with a maximum at 500 rnp, except for a slight shift toward the red due mainly to light absorption of the intraocular media. In 1937, Wald (3) found that certain fresh water fish have a visual purple system which differs from that found in man and most other animals. The absorption of this pigment occurs at about 522 rnp, and the entire absorption spectrum is shifted somewhat toward longer wave-lengths. It is reasonable to assume that in dim light these fish are comparatively more sensitive to red light and less sensitive to blue than animals with the normal type of visual purple. To avoid confusion, the visual purple of humans and salt water fish was named rhodopsin, while the visual purple ,f fresh water fish was named porphyropsin. At about this same time, other investigators (4, 5) found that the livers of these fresh water fish contained, instead of vitamin A, a closely related substance having an absorption maximum in the ultraviolet at about 350 rnp instead of 328 mp and that the antimony trichloride reaction product had an absorption maximum at G93 rnp instead of 620 rnp. This material was named vitamin A*, and shortly t,hereafter Wald (6) showed this substance to be the prosthetic group in porphyropsin, as vitamin A is in rhodopsin. It has subsequently been found (7, 8) that vitamin At has biological activity for rats and occasionally occurs in small amounts in the livers of animals that eat fresh water fish (9). It, would be of considerable interest to find out whether the spectral