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Iodine and the Body

 

Iodine and Eyes

 

Exocrine Glands

Elstner

 

Cataract induction by 1,2-naphthoquinone. II. Mechanism of hydrogenperoxide formation and inhibition by iodide.

Kroner R, Kleber E, Elstner EF.

Z Naturforsch [C]. 1991 Mar-Apr;46(3-4):285-90.

[abstract only]

 

"Naphthalene cataract is probably due to peroxide production through naphthoquinone (NQ) redox cycling and/or glutathione conjugation. Both mechanisms yield losses of essential SH-groups in cristallins and are thus probably involved in protein modification finally visible as lens opacity. 1,2-Naphthoquinone produces H2O2 in the presence of either ascorbate, glutathione, NADH or--to a lesser extend--by homogenates of lens protein preparations. In the presence of 1,2-naphthoquinone and the above reductive additions, both, oxygen uptake and H2O2 formation can be observed. Reductive oxygen activation in these systems are diminuated by iodide in a concentration-dependent manner. Since maleimide-treated proteins are less capable to activate oxygen by 1,2-naphthoquinone, a direct oxygen activation by the interactions of 1,2-naphthoquinone with protein-SH is indicated. Catalysis of "diaphorase"-type (dia) enzymes via NADH--dia--1,2-NQ--O2 seems not to operate in hydrogenperoxide production during 1,2-naphthoquinone lens toxicity."

 

 

Cataract induction by 1,2-naphthoquinone. I. Studies on the redox properties of bovine lens proteins.

Kleber E, Kroner R, Elstner EF.

Z Naturforsch [C]. 1991 Mar-Apr;46(3-4):280-4.

[abstract only]

 

"Conditions of oxidative stress may lead to cataract formation. Reaction of certain flavoproteins, the NADH: oxidoreductases, with different quinones is well known to form hydrogen-peroxide. This reaction was investigated to get more information on cataract induction by naphthalene and its quinone metabolites. Protein extracts from bovine lens cortex exhibit "diaphorase" activity, indicated as dye reduction in the presence of NADH and dichlorophenol-indophenol (DCPIP) or ferricyanide. Different redox cycling compounds are shown to be active in this "diaphorase" reaction by lens protein extract (LCE): Oxygen consumption can be detected in the presence of pyrroloquinoline quinone and juglone whereas 1,4-naphthoquinone, menadione and paraquat are no redox cyclists in this flavoprotein catalyzed reaction."

 

 

Model systems for testing anticataractic activities in rabbit eyes.

Kroner RP, Elstner EF.

Dev Ophthalmol. 1989;17:138-44.

[citation only]

 

 

Biochemical test reactions for the evaluation of the potential anticataractic function of iodide.

Heinisch HH, Hippeli S, Elstner EF.

Dev Ophthalmol. 1989;17:132-7.

[citation only]

 

 

[New biochemical models for cataract research]

Kroner R, Heinisch H, Hippeli S, Elstner EF.

Fortschr Ophthalmol. 1989;86(1):26-31. German.

[abstract only]

 

"In recent years, it has been suggested that reactive oxygen species are involved in the genesis of cataracts. To elucidate the basic reaction mechanisms underlying these processes and the influence of drugs, we developed simple biochemical model reactions. The purpose was to simulate cataractogenic processes and to document the effects of potential "anticataractous" drugs in vitro. Application tests allowed us to quantify the penetration rates and the enrichment processes of iodidecontaining drugs. Our results document the ability of KI to inhibit photodynamic reactions and related cataractogenic processes, such as lipid and sulfhydryl oxidation, as well as the structural changes of the lens proteins."

 

 

[The uptake of potassium iodide and its effect as an antioxidant in isolated rabbit eyes]

Elstner EF, Adamczyk R, Kroner R, Furch A.

Ophthalmologica. 1985;191(2):122-6. German.

[abstract only]

 

"Potassium iodide (KI) passes the cornea of isolated rabbit eyes with kinetics of approximately 0.25 mumol/h/ml aqueous humor. In photodynamic reactions, simulated as light-dependent decay of S-methyl-alpha-ketobutyric acid in the presence of riboflavin, KI acts as an antioxidant cooperating with internal scavengers such as ascorbate. With the simple model reactions applied it may be possible to study mechanism and functions in vivo of eye-protecting factors or combinations of compounds."

 

 

Biochemical model reactions for cataract research.

Elstner EF, Adamczyk R, Furch A, Kroner R.

Ophthalmic Res. 1985;17(5):302-7.

[abstract only]

 

"There are several experimental indications that cataract formation is induced and/or enhanced by activated oxygen species including hydrogen peroxide, superoxide radical anion, singlet oxygen and hydroxyl radical. These species can be generated chemically, enzymatically or photodynamically. Taking advantage of endogenous photodynamic compounds in isolated lens, aqueous humor or vitreous preparations in the presence of S-methyl-alpha-ketobutyric acid (KMB), ethylene formation can be monitored for at least 2 h of light-dependent KMB degradation. This reaction is extremely sensitive and can be inhibited by potassium iodide in low concentrations. This model reaction might be useful for studying possibly inhibiting substances or stimulating processes involved in cataract formation."

 

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