The ability of L-carnosine to attenuate the products of lipid peroxidation within the ocular lens was first suggested by Dr. Alan Babizhayev
and colleagues in 1987.10 Indeed, much research has since confirmed that carnosine reduces the formation of lipid peroxides within the lens.11,12,13 In addition to directly attenuating membrane structure damage through lessening peroxidation of lipids, reduction of lipid peroxides also reduces the formation of its highly reactive metabolite, malondialdehyde (MDA).
MDA interacts with amino acid moieties on crystallin proteins within the lens to cause crosslinking of these proteins, resulting in insoluble aggregate molecules.14 In cataracts, many enzymes that normally provide defense against ROS overproduction, including superoxide dismutase and catalase, are depleted.15 Exacerbating this effect, the nuclear region of the lens is normally dependent on the production and subsequent diffusion of glutathione from the cortical region, but this diffusion process becomes less efficient as we age.16 Carnosine has been shown to preserve levels of these enzymes in cataract lenses, thus improving their antioxidative capacity.17 There is also postulation that carnosine lessens ROS damage through its ability to chelate free metal ions, which are required to generate O2-.18 Separately, carnosine has been shown to act as an alternative target for glycation, a "sacrificial transglycation," that effectively binds sugars to itself rendering them unavailable to bind proteins.
No mention is given in the publication of the statistical analysis or of the results of the 2 nontreatment groups.31 Babizhayev
and colleagues have shown beneficial effects of 1.0% NAC instillation in the eyes in several small human clinical trials.
For a thorough review of carnosine's biological effects throughout the body, the reader is referred to a recent publication by Alan Hipkiss.38 Much of the clinical research demonstrating the efficacy of carnosine in preventing or treating cataracts in humans has been done by Dr. Babizhayev of Innovative Vision Products (IVP), Delaware, USA.
His group proposed the use of NAC as a prodrug for L-carnosine in 1996.39 Since then, IVP has manufactured a patented formula called Can-C (private label, Nu-Eyes) which consists of deionized water, glycerin (1.0%), NAC (1.0%), carboxymethylcellulose (0.3%), benzyl alcohol (0.3%), and potassium borate and bicarbonate buffers.40 Babizhayev's group proposes this particular formulation obtains superior absorption through the cornea and that acetylation of carnosine optimizes the delivery of carnosine into the lens in several ways: protection from degradation by carnosinase in the aqueous humor, a more lipophilic molecule that allows for easier penetration into the lens, and, due to the pharmacokinetics of deacetylation, "timed release" of the carnosine molecule.41,42 Babizhayev and colleagues reported that instillation of non-acetylated L-carnosine (1%) to rabbit eyes did not lead to an increase of L-carnosine concentration in the anterior compartment versus placebo, an effect they speculate is due to carnosinase degradation of the dipeptide.43 While this is in keeping with the assumption that carnosinases in the eye rapidly degrade L-carnosine, there is recent evidence of L-carnosine accumulation in the eyes of rabbits using a 5.0% instillation.44 Further, Babisheyev asserts that not only is L-carnosine less effective than NAC, but that there may be risk of harm to the eye due to the byproduct of histamine that ultimately results from the degradation of carnosine.