Note to users. If you're seeing this message, it means that your browser cannot find this page's style/presentation instructions -- or possibly that you are using a browser that does not support current Web standards. Find out more about why this message is appearing, and what you can do to make your experience of our site the best it can be.


Sci. Aging Knowl. Environ., 4 May 2005
Vol. 2005, Issue 18, p. pe12
[DOI: 10.1126/sageke.2005.18.pe12]


Carnosine: A Versatile Antioxidant and Antiglycating Agent

V. Prakash Reddy, Matthew R. Garrett, George Perry, and Mark A. Smith

The authors are in the Department of Chemistry, University of Missouri-Rolla, Rolla, MO 65409, USA (V.P.R.), and the Institute of Pathology, Case Western Reserve University, Cleveland, OH 44106, USA (M.R.G., G.P., and M.A.S.). E-mail: preddy{at} (V.P.R.); mark.smith{at} (M.A.S.)

Key Words: advanced glycation end products • Alzheimer's disease • antioxidant • carnosine • DNA damage • oxidative stress

Abstract: Carnosine ({beta}-alanyl-L-histidine) has recently attracted much attention as a naturally occurring antioxidant and transition-metal ion sequestering agent. It has also been shown to act as an anti-glycating agent, inhibiting the formation of advanced glycation end products (AGEs). Through its distinctive combination of antioxidant and antiglycating properties, carnosine is able to attenuate 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 is able to reduce harmful sequelae such as DNA damage. AGEs are known contributors to the pathology of Alzheimer's disease, and carnosine therefore merits serious attention as a possible therapeutic agent.

Citation: V. P. Reddy, M. R. Garrett, G. Perry, M. A. Smith, Carnosine: A Versatile Antioxidant and Antiglycating Agent. Sci. Aging Knowl. Environ. 2005 (18), pe12 (2005).

Read the Full Text

Plasma metabolic profile delineates roles for neurodegeneration, pro-inflammatory damage and mitochondrial dysfunction in the FMR1 premutation.
C. Giulivi, E. Napoli, F. Tassone, J. Halmai, and R. Hagerman (2016)
Biochem. J. 473, 3871-3888
   Abstract »    Full Text »    PDF »

To Advertise     Find Products

Science of Aging Knowledge Environment. ISSN 1539-6150