How does Can‑C™ work in the eye?

As you can imagine this is a complex subject. Essentially, the prime ingredient in Can-C™ is N-acetylcarnosine.


This is a “carrier” for the di-peptide, L-carnosine into the aqueous humor of the eye, (this is the fluid area surrounding the lens). It is here, that the substance becomes most active in its ability to basically act, as a natural and comprehensive anti-oxidant. Once N-acetylcarnosine has delivered L-carnosine safely through into the aqueous humor, the L-carnosine itself is flushed out of the eye via the canal of schlemm, and once into the bloodstream, it is broken down by carnosinase and excreted.

N-acetylcarnosine is acting as a time release version of L-carnosine, but it is resistant to hydrolysis with carnosinases. (Please note that some carnosines, such as L-carnosine, must not be used directly as an eye-drop. That subject is covered in the question: What makes N-acetylcarnosine different from L-carnosine?

Cataract is caused by the nuclear matter of the elderly human lens hardening and taking on a yellowish/ brown color. Hence, once this occurs the obvious vision impairment and deterioration.

This hardening and discoloration of the lens is the result of lifelong cross-linking (or glycosylation), of the lens proteins with ascorbate. This persists in the aqueous humor at high concentrations, due to the kynurenine derivatives, and takes place due to the low availability of natural defenses in the form of anti-oxidants, (which decline with advancing age).

N-acetylcarnosine and intraocular released carnosine can effectively act as anti-glycators, helping to cleave these formed links and scavenge the radicals of tryptophan/ kynurenine and ascorbate radicals. This can be measured by the intensity of fluorescence becoming decreased.

It is further believed, that N-acetylcarnosine can prevent and reverse the cross-linking of the lens proteins, including crystallins induced by lipid hydroperoxides and their secondary breakdown molecular products, like aldehydes. This mechanism is believed to be the prominent factor in reversing and preventing lens opacification, (i.e. cataract) and it is related to the glycation reactions of the lens proteins.

In addition, N-acetylcarnosine and L-carnosine act in the biological system as universal antioxidants. They possess the ability to protect cells from oxidative stress, both in the lipid phase of cellular membranes and in the aqueous environment. L-carnosine is able to reduce the content of lipid peroxidation products in the peroxidized lens fiber cells plasma membranes, and to repair their structure accordingly. It is the only known antioxidant able to protect structural proteins of the lens/ alpha-crystalline, from the free-radical induced oxidation process.

Another advantage is the capability of L-carnosine to stimulate the activity of antioxidant enzymes like SOD in the lens. SOD activity is diminished in the ageing and cataractogenesis processes.

Furthermore, there is published material about the reactivity of carnosine and its derivatives, to quench the potent free radicals- singlet oxygen species.

Carnosine expert, Dr. Hipkiss is convinced that carnosine protects protein carbonyls via the carnosylation process. In studies, it has been indicated that carnosine has the ability to block the glycosylation process, being induced by ascorbate and transition metal ions in the aqueous humor.

However it is very important that correct purity and formulas are used, so that efficacy and safety can be confirmed.