Carnosine combats cataracts

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July 21, 2009

Carnosine combats cataracts

 

In the July 28, 2009 issue of the journal Biochemistry, Italian

researchers report that the dipeptide carnosine shows promise not only

in preventing cataracts but also in helping to treat the condition.

Cataracts, which are characterized by a clouding of the eye's lens, are

a major cause of visual impairment among older men and women, and

surgery is currently the only effective treatment.

 

Enrico Rizzarelli of the University of Catania and his colleagues tested

the effects of D- and L-carnosine on bovine cultured alpha-crystallin,

the major structural protein in the lens of the eye. The cultures were

treated with guanidine, a compound that is known to cause cataracts via

the formation of alpha-crystallin fibrils. Co-incubation of the cultures

with carnosine helped inhibit fibrillation, and the addition of

carnosine to pre-existing fibrils was found to almost completely

dissolve them.

 

In another experiment, cultured rat lenses were exposed to two

concentrations of guanidine with or without pretreatment with

L-carnosine. While guanidine alone caused significant lens opacification

after 24 hours, with further loss occurring after 72 hours, pretreatment

with L-carnosine prevented lens opacification by 50 to 60 percent in

cultures that received either guanidine concentration.

 

http://www.lef.org/newsletter/2009/0721_Carnosine-Combats-Cataract.htm?source=eN\

ewsLetter2009Wk30-2 & key=Article & l=0

 

Cataracts

 

Treatment for cataracts is reactive: when cataracts adversely impact

vision, they are surgically removed and replaced with an implanted lens.

Cataract surgery is very effective and has a high success rate.

Nutritional therapy can prevent the onset of cataracts, particularly

because proven anti-cataract drugs are not available.

Intervention strategies should address the underlying causes of

cataracts: oxidative stress, free radical production, the breakdown and

aggregation of lens proteins, dysfunction of metabolism in the lens, and

inability to maintain a healthy ocular environment. Nutritional therapy

is available for each of these underlying causes.

Proteins deep in the lens are generated during embryogenesis and must

retain functionality for many decades. The inability to maintain protein

stability over time leads to formation of a nuclear cataract (the

predominant form). Once the lens forms (embryologically), proteins are

only synthesized in the outermost fiber cells close to the lens surface.

Accumulated damage to the proteins causes loss of enzymatic activity and

increases the likelihood of protein aggregation, a component of cataract

formation.

The glycation (glycosylation) process can change (denature) lens

proteins and significantly contribute to diabetic cataract formation and

retinopathy. Glycation occurs when proteins react with sugars and form

advanced glycation end products (AGEs), essentially, proteins strongly

(covalently) bind to sugars, compromising the function of that protein.

AGEs are biochemically altered proteins, DNA, and lipids with altered

physiological properties.

 

Continue Reading:

http://www.lef.org/newsletter/2009/0721_Carnosine-Combats-Cataract.htm?source=eN\

ewsLetter2009Wk30-2 & key=Body+Health+Concern & l=0

 

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