Carnosine, glycation and your skin
glycation, antioxidant, anti-ageing, cellulite
Carnosine is one of the most important and most widely used anti-ageing actives. It is widely researched for it's action against glycation. Glycation is the main cause of collagen damage (caused by sugar consumption) and thereby skin ageing, blood vessel wall damage and also a major contributor to the formation of cellulite.
For all those reasons, carnosine is of great importance as active ingredient in anti-ageing, anti-cellulite, leg wellness, skin firming and under-eye creams [the Celluence® cellulite creams are the only creams in the world to contain pure, highly bioavailable carnosine PLUS 39 more natural actives, for maximum results with cellulite and skin tightening].
5+ ways carnosine...
...helps fight glycation, free radical damage and overall ageing
Both carnosine and exercise induce adipocyte browning...
...boost fat burning and reduce oxidative damage and inflammation, with the combination predictably offering the best results. Specifically, both exercise and carnosine improved dyslipidemia, reduced the thiobarbituric acid reactive species (TBARS) and TNF-alpha and increased total antioxidant capacity, IL-10, irisin, UCP1, adipose CD137 and FNDC5, the precursor of irisin gene expression. [Source: Synergistic effect of Carnosine on Browning of Adipose Tissue in Exercised Obese Rats ; A Focus on Circulating Irisin Levels]
Antiglycation and anti-oxidant efficiency of carnosine in the plasma and liver of aged rats.
Abstract: AIM: Increases in oxidative stress and advanced glycation end-products (AGE) formation play an important role in the pathogenesis of aging. Carnosine (CAR; β-alanyl-L-histidine) has anti-oxidant and antiglycating properties. We investigated the effect of CAR supplementation on AGE levels, and protein and lipid oxidation products in the serum and liver tissue in aged rats. METHODS: Young (3 months-of-age) and aged (20 months-of-age) rats were injected with CAR (250 mg/kg/daily; i.p.; 5 days per week) for 2 months. At the end of this period, AGE, protein carbonyl, advanced oxidized protein products, and malondialdehyde levels were determined in the serum and liver tissue. Furthermore, reactive oxygen species formation and ferric reducing anti-oxidant power values were measured. RESULTS: AGE, malondialdehyde, protein carbonyl and advanced oxidized protein products levels, and reactive oxygen species formation were higher in the serum and liver tissue of aged rats compared with young rats. CAR treatment was observed to significantly decrease AGE, malondialdehyde, protein carbonyl and advanced oxidized protein products levels, and reactive oxygen species formation in the serum and liver of aged rats. CONCLUSIONS:
These results clearly show that CAR might be useful for decreasing glycoxidant stress in aged rats.
Carcinine and acetyl-L-carnosine REVERSE glycation and fine lines, improving skin appearance
Abstract: Skin beautification with oral non-hydrolized versions of carnosine and carcinine: Effective therapeutic management and cosmetic skincare solutions against oxidative glycation and free-radical production as a causal mechanism of diabetic complications and skin aging.
Abstract: Advanced glycation Maillard reaction end products (AGEs) are causing the complications of diabetes and skin aging, primarily via adventitious and cross-linking of proteins. Long-lived proteins such as structural collagen are particularly implicated as pathogenic targets of AGE processes. The formation of α-dicarbonyl compounds represents an important step for cross-linking proteins in the glycation or Maillard reaction. The purpose of this study was to investigate the contribution of glycation coupled to the glycation free-radical oxidation reactions as markers of protein damage in the aging of skin tissue proteins and diabetes. To elucidate the mechanism for the cross-linking reaction, we studied the reaction between a three-carbon α-dicarbonyl compound, methylglyoxal, and amino acids using EPR spectroscopy, a spectrophotometric kinetic assay of superoxide anion production at the site of glycation and a chemiluminescence technique. The transglycating activity, inhibition of transition metal ions peroxidative catalysts, resistance to hydrolysis of carnosine mimetic peptide-based compounds with carnosinase and the protective effects of carnosine, carcinine and related compounds against the oxidative damage of proteins and lipid membranes were assessed in a number of biochemical and model systems. A 4-month randomized, double-blind, controlled study was undertaken including 42 subjects where the oral supplement of non-hydrolized carnosine (Can-C Plus® formulation) was tested against placebo for 3 months followed by a 1-month supplement-free period for both groups to assess lasting effects. Assessment of the age-related skin parameters and oral treatment efficacy measurements included objective skin surface evaluation with Visioscan® VC 98 and visual assessment of skin appearance parameters. The results together confirm that a direct one-electron transfer between a Schiff base methylglyoxal dialkylimine (or its protonated form) and methylglyoxal is responsible for the generation of the cross-linked radical cation and the radical counteranion of methylglyoxal. Under aerobic conditions, molecular oxygen can then accept an electron from the methylglyoxal anion to generate the superoxide radical anion causing the propagation of oxidative stress chain reactions in the presence of transition metal ions. Carnosine stabilized from enzymatic hydrolysis, carcinine and leucyl-histidylhydrazide in patented formulations thereof, demonstrate the Schiff bases' transglycating activities concomitant with glycation site specific antioxidant activities and protection of proprietary antioxidant enzymes in the skin during aging and with diabetes lesions. During oral supplementation with stabilized from enzymatic hydrolysis carnosine (Can-C Plus® formulation), the skin parameters investigated showed a continuous and significant improvement in the active group during the 3 months of supplementation as compared to placebo. Visual investigation showed improvement of the overall skin appearance and a reduction of fine lines. No treatment-related side effects were reported. The finding that already-formed AGE cross-links can be pharmacologically severed and attendant pathology thereby reversed by non-hydrolized carnosine or carcinine in patented oral formulations thereof has broad implications for the skin beautification and therapeutics of the complications of diabetes and skin diseases associated with ageing.
Carnosine and carcinine have potent antioxidant action, especially against lipid peroxidation
Abstract: L-carnosine (beta-alanyl-L-histidine) and carcinine (beta-alanylhistamine) act as natural antioxidants with hydroxyl-radical-scavenging and lipid-peroxidase activities.
Abstract: Carnosine (beta-alanyl-L-histidine) and carcinine (beta-alanylhistamine) are natural imidazole-containing compounds found in the non-protein fraction of mammalian tissues. Carcinine was synthesized by an original procedure and characterized. Both carnosine and carcinine (10-25 mM) are capable of inhibiting the catalysis of linoleic acid and phosphatidylcholine liposomal peroxidation (LPO) by the O2(-.)-dependent iron-ascorbate and lipid-peroxyl-radical-generating linoleic acid 13-monohydroperoxide (LOOH)-activated haemoglobin systems, as measured by thiobarbituric-acid-reactive substance. Carcinine and carnosine are good scavengers of OH. radicals, as detected by iron-dependent radical damage to the sugar deoxyribose. This suggests that carnosine and carcinine are able to scavenge free radicals or donate hydrogen ions. The iodometric, conjugated diene and t.l.c. assessments of lipid hydroperoxides (13-monohydroperoxide linoleic acid and phosphatidylcholine hydroperoxide) showed their efficient reduction and deactivation by carnosine and carcinine (10-25 mM) in the liberated and bound-to-artificial-bilayer states. This suggests that the peroxidase activity exceeded that susceptible to direct reduction with glutathione peroxidase. Imidazole, solutions of beta-alanine, or their mixtures with peptide moieties did not show antioxidant potential. Free L-histidine and especially histamine stimulated iron (II) salt-dependent LPO. Due to the combination of weak metal chelating (abolished by EDTA), OH. and lipid peroxyl radicals scavenging, reducing activities to liberated fatty acid and phospholipid hydroperoxides, carnosine and carcinine appear to be physiological antioxidants able to efficiently protect the lipid phase of biological membranes and aqueous environments.
Carnosine fights ageing by inhibiting MTOR and by carbonyl scavenging
Source: Carnosine and the processes of ageing.
Abstract: The causes of ageing are usually regarded as multifactorial; thus effective regulation might be achieved by intervention at multiple sites. It has been suggested that the endogenous dipeptide carnosine, also available as a food supplement, possesses anti-ageing activity and may achieve its reported age-alleviating effects via a number of mechanisms. Carnosine's possible anti-ageing mechanisms are therefore discussed; the evidence suggests that inhibition of the mechanistic target of rapamycin and carbonyl scavenging may be involved.