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Cell Biochem Biophys. 2019 Dec;77(4):343-355. doi: 10.1007/s12013-019-00884-3. Epub 2019 Sep 18.

Carnosine Prevents Different Structural Damages Induced by Methylglyoxal in Lens Crystallins.

Author information

1
Protein Chemistry Laboratory (PCL), Department of Biology, College of Sciences, Shiraz University, Shiraz, Iran.
2
Protein Chemistry Laboratory (PCL), Department of Biology, College of Sciences, Shiraz University, Shiraz, Iran. ryousefi@shirazu.ac.ir.

Abstract

The elevated lenticular level of methylglyoxal (MGO) in diabetic patients is an important risk factor for the development of age-related (senile) cataract disorders. Carnosine (β-alanyl L-histidine), a natural antioxidant dipeptide product, has been indicated to prevent the development of cataract diseases. Therefore, it is possible that the anti-cataract activity of this naturally occurring compound is mediated by its anti-glycoxidation effect. In this study, the eye lens proteins were treated with MGO in the presence of carnosine. Then, sodium dodecyl sulfate polyacrylamide gel electrophoresis (SDS-PAGE) analysis and several spectroscopic evaluations were used with the aim to investigate the possible inhibitory activity of carnosine against the MGO-induced structural damages of eye lens proteins. Our results indicated that MGO causes a substantial structural alteration in the lens proteins. The results of fluorescence assessments also suggested that MGO-induced structural changes were accompanied with the formation of additional chromophores in the protein structure. Also, in the presence of carnosine, a notable reduction in the protein structural damages was observed. Our results may highlight an important protective role of carnosine against MGO-induced structural insults in the lens proteins. This study suggests carnosine supplementation as a possible preventive strategy against development of the diabetic cataracts in human.

KEYWORDS:

Carnosine; Cataract; Diabetes; Lens crystallins; Methylglyoxal

PMID:
31535344
DOI:
10.1007/s12013-019-00884-3
[Indexed for MEDLINE]

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