Advanced glycation end products (AGEs) are non-enzymatic interactions between reducing sugars and amino groups in proteins, lipids and nucleic acids. In numerous diseases, such as diabetes, neuropathy, atherosclerosis, aging, nephropathy, retinopathy and chronic kidney disease, the accumulation of AGEs has been proposed as a pathogenic mechanism of inflammation, oxidative stress and structural tissue damage leading to chronic vascular problems. Current studies on AGE inhibition mainly focused on food processing.
Carnosine (β-alanyl-L-histidine) has recently attracted much attention as a natural antioxidant and transition metal ion sequestering agent. It has also been shown to act as an antiglycation agent, inhibiting the formation of advanced glycation end products (AGEs). Through its distinctive combination of antioxidant and antiglucant properties, carnosine is capable of attenuating cellular oxidative stress and can inhibit the intracellular formation of reactive oxygen species and reactive nitrogen species. By controlling oxidative stress, suppressing glycation, and chelating metal ions, carnosine can reduce harmful consequences such as DNA damage. AGEs are known to contribute to cardiovascular and neurodegenerative disease pathology and therefore carnosine deserves serious attention as a potential therapeutic agent.
Evidence demonstrated that carnosine supplementation had a beneficial impact on preventing sarcopenia, fatty liver disease, preserving cognitive abilities, and improving neurodegenerative disorders and possesses anticancer actions of carnosine. Carnosine (1) inhibits the proliferation of breast, ovarian, colon and leukemia cancer cells; (2) positively regulates the expression of proinflammatory molecules; (3) modulates cytokine secretion and (4) restores normal cellular homeostasis
Carnosine capable of reducing the levels of glycosylated lens proteins, preventing the loss of protective enzymes and, ultimately, delaying lens opacity. It is also effective in the eradication treatment of Helicobacter pylori.
Advanced glycation end products (AGEs) are non-enzymatic interactions between reducing sugars and amino groups in proteins, lipids and nucleic acids. In numerous diseases, such as diabetes, neuropathy, atherosclerosis, aging, nephropathy, retinopathy and chronic kidney disease, the accumulation of AGEs has been proposed as a pathogenic mechanism of inflammation, oxidative stress and structural tissue damage leading to chronic vascular problems. Current studies on AGE inhibition mainly focused on food processing.
Carnosine (β-alanyl-L-histidine) has recently attracted much attention as a natural antioxidant and transition metal ion sequestering agent. It has also been shown to act as an antiglycation agent, inhibiting the formation of advanced glycation end products (AGEs). Through its distinctive combination of antioxidant and antiglucant properties, carnosine is capable of attenuating cellular oxidative stress and can inhibit the intracellular formation of reactive oxygen species and reactive nitrogen species. By controlling oxidative stress, suppressing glycation, and chelating metal ions, carnosine can reduce harmful consequences such as DNA damage. AGEs are known to contribute to cardiovascular and neurodegenerative disease pathology and therefore carnosine deserves serious attention as a potential therapeutic agent.
Evidence demonstrated that carnosine supplementation had a beneficial impact on preventing sarcopenia, fatty liver disease, preserving cognitive abilities, and improving neurodegenerative disorders and possesses anticancer actions of carnosine. Carnosine (1) inhibits the proliferation of breast, ovarian, colon and leukemia cancer cells; (2) positively regulates the expression of proinflammatory molecules; (3) modulates cytokine secretion and (4) restores normal cellular homeostasis
Carnosine capable of reducing the levels of glycosylated lens proteins, preventing the loss of protective enzymes and, ultimately, delaying lens opacity. It is also effective in the eradication treatment of Helicobacter pylori.
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