Vitamin A (retinol) is an essential nutrient for the visual system. An enzymatic oxidation reaction converts it into trans-retinal. trans-Retinal exists in the photoreceptor cells of the human eye, but before it can perform its biological functions, it must first undergo isomerization to form cis-retinal under the catalysis of an enzyme called retinal isomerase. This molecule binds very tightly to an active site called opsin (relative molecular mass approximately 38,000). cis-Retinal reacts with an amino group of opsin to form the imine rhodopsin, the light-sensitive chemical unit in the eye. The absorption at 506 nm (e=40,000) in the electronic spectrum of rhodopsin indicates the presence of protonated imine.

When a photon strikes rhodopsin, the cis-retinal moiety isomerizes to the trans isomer at an extremely rapid rate, within picoseconds. This isomerization causes a significant change in geometry, thereby disrupting the original tight binding of the molecule within the active cavity of the protein. This photoreaction product generates a series of new intermediates within nanoseconds, accompanied by conformational changes in the protein. Then, retinaldehyde units incompatible with the active cavity are hydrolyzed. This process triggers a nerve impulse, and we perceive light. Then, trans-retinal isomerizes under the catalysis of retinal isomerase to reform cis-retinal, regenerating rhodopsin and preparing for the next photon attack. The most remarkable aspect of this mechanism is its sensitivity; even a single photon impact on the retina can be recorded by the eye. Remarkably, all known visual systems in nature, despite potentially vastly different evolutionary histories, stimulate vision using the retinaldehyde system. Clearly, this molecule provides an optimal method for organisms to see.

Vitamin A supplementation is crucial for vision. Rod cells are responsible for vision in low-light conditions. When light enters the eye, rhodopsin breaks down and triggers nerve signals transmitted to the brain, forming night vision. Vitamin A deficiency slows rhodopsin regeneration, leading to decreased dark adaptation. Vitamin A maintains the integrity of the ocular surface mucosa and promotes tear secretion. Long-term deficiency can cause conjunctival dryness, corneal softening, and even ulceration, and in severe cases, blindness. Vitamin A deficiency in children is one of the leading causes of blindness. The antioxidant properties of vitamin A can reduce oxidative damage to the macula from blue light, indirectly protecting vision; it also participates in regulating gene expression and supports normal retinal cell metabolism.