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Iodine Research

Resource Network of The Iodine Movement


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                                         Iodine and the Body

Eyes

Iodine is concentrated in certain parts of the eye and has been used therapeutically for various eye
diseases and infections.  It may be useful for dry eyes, cataracts, infections, glaucoma, and UVB
protection.

Becker suggests that iodide in the eye can be inhibited by similar substances that inhibit thyroid
iodine transport

Winkler et al found that the iodine content in the ocular tissues showed the following rank order:
cornea > retina > vitreous body > anterior chamber fluid > lens.  They discuss the possible protective,
antioxidative, and OH-scavenging efficacy of iodide. They have researched using iodide for UVB-
protection, dry eyes, and cataracts.

Elstner et al focus on iodide and cataracts, as well as the antioxidant effect of iodide.

Howenstine suggests that iodine may be implicated in glaucoma.

Mazumdar investigated lacrimal gland peroxidase and iodide in sheep.

The Paracelsus Institute for Baineology and Iodine Research at Bad Hall, Austria researches
the use of topical iodine brines for a number of eye problems including degenerative eye diseases
such as dry eyes, cataracts and macula degeneration.

More articles on lacrimal glands and tears under
exocrine glands.

BECKER
Iodide transport by the rabbit eye.
Becker B
Am J Physiol. 1961 Apr;200:804-6.
[
abstract only]
I131 is accumulated by rabbit ciliary body-iris preparations in vitro and transported out of the living
rabbit eye. The secretory system resembles the accumulation of iodide by the thiouracil-treated
thyroid gland. It is saturated by iodide and inhibited by perchlorate, thiocyanate and fluoroborate.
The mechanism for iodide transport out of the rabbit eye appears to be independent of the
analogous transport of iodopyracet and related organic anions.

The turnover of iodide in the rabbit eye.
Becker B
Arch Ophthalmol. 1961 Jun;65:832-6.
[abstract only]
Recently a transport system for iodide which resembles the thiouracil-treated thyroid gland has been
demonstrated in the rabbit eye. Iodide was accumulated in ciliary body-iris preparations in vitro and
was transported out of the rabbit eye in vivo.1 Saturation by iodide and inhibition by perchlorate,
fluoroborate, and related ions characterized the accumulation as well as the transport system. The
transport of iodide out of the vitreous humor of the rabbit eye might account for the deficit of this ion
in the aqueous humor as compared with plasma concentrations.2,3 The purpose of the present study
was to evaluate the turnover of systemically administered I131 in the rabbit eye with an intact iodide
transport system and in the animal subjected to perchlorate inhibition.
Methods  Unanesthetized 2-3 kg. male albino rabbits were used throughout. Nonlabeled sodium
iodide in doses of 3μM/kg. was administered intraperitoneally to all animals in order to


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.

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.


FLECHAS
How Does Iodine Deficiency Manifest Itself?
Flechas JD
"Iodine is concentrated in the lacrymal glands of the eye, and a lack of iodine can cause dry eyes".


GEBHARD, RIEGER
The effect of iodide iontophoresis on the antioxidative capacity of the tear fluid
Gebhard Rieger, Manfred Klieber, Wolfgang Schimetta, Werner Pölz, Sirid Griebenow, Rudolf
Winkler, Jutta Horwath-Winter, Otto Schmut, Birgit Spitzer-Sonnleitner
Graefe's Archive for Clinical and Experimental Ophthalmology
November 2010, Volume 248, Issue 11, pp 1639-1646
Date: 23 May 2010
Abstract
Background
Environmental oxidative stress changing the properties of the tear fluid can lead to
keratoconjunctivitis sicca (dry eye syndrome). The aim of this study was to determine whether iodide
iontophoresis influences the antioxidative capacity (ACW = water soluble antioxidative capacity) of the
tear fluid, and to compare iodide iontophoresis with other balneotherapeutic measures.
Methods
This prospective study evaluated 92 patients in four groups. Twenty-four patients were treated with
iodide iontophoresis, 24 with other balneotherapeutic methods. Twenty-five patients received iodide
iontophoresis combined with other balneotherapeutic methods and 21 persons received no treatment
(control). Unstimulated tear fluid, serum and urine were collected. ACW was determined
photochemically in tear fluid and serum; iodine was measured in urine photometrically.
Results
Iodide iontophoresis increases the ACW of the tear fluid but not the ACW of the serum. Other iodine
therapies increase the ACW in serum but not in tear fluid. Iodine excretion in urine was increased in
all treated groups compared to the control.
Conclusion
The increase of ACW in tear fluid after iodide iontophoresis can support the defense mechanism of
the eye against oxidative influence effects, which may alleviate the symptoms of keratoconjunctivitis
sicca.


HOWENSTINE
Iodine Is Vital for Good Health
Howenstine J.
"Iodine is found in large quantities in the brain and the ciliary body of the eye. Lack of iodine may be
involved in production of Parkinson’s disease and glaucoma."


MAZUMDAR
Characterization of sheep lacrimal-gland peroxidase and its major physiological electron donor.
Mazumdar A, Chatterjee R, Adak S, Ghosh A, Mondal C, Banerjee RK.
Biochem J. 1996 Mar 1;314 ( Pt 2):413-9.
A soluble sheep lacrimal-gland peroxidase was purified to apparent homogeneity. It had a native
molecular mass of 75 kDa with a subunit molecular mass of 82 kDa and an isoelectric point of 6.5.
Western blotting showed that it shares some of the enzyme antigenic determinants in common with
other soluble peroxidases. The enzyme exhibits a Soret peak at 410 nm which is shifted to 431 nm by
5 equiv. of H2O2 due to the formation of compound II. The latter is, however, unstable and gradually
returns to the native state. The enzyme forms complexes with CN- and N3- and is reduced by
dithionite showing a characteristic reduced peroxidase spectrum. Although the enzyme oxidizes I-,
SCN- and Br- optimally at pH 5.5., 5.25 and 5.0 respectively, at physiological pH, it oxidizes I- and
SCN- only. Since extracellular SCN- concentration is much higher than I-, SCN- may act as the major
electron donor to the enzyme. The second-order rate constants for the reaction of the enzyme with
H2O2 (k+1) and of compound I with SCN- (k+2) were 4 X 10(7) M-1 X s-1 and 8.1 X 10(5) M-1 X s-1
respectively. A plot of log Vmax against pH yields a sigmoidal curve consistent with a single ionizable
group on the enzyme with a pK(a) value of 5.75, controlling thiocyanate oxidation. In a coupled
system with the peroxidase, H2O2, SCN-, GSH, NADPH and glutathione reductase, peroxidase-
catalysed SCN- oxidation by H2O2 could be coupled to NADPH consumption. The system is proposed
to operate in vivo for the efficient elimination of endogenous H2O2.


WINKLER, SCHMUT, RIEGER, MURANOV
Diagnosis and therapy of dry eye syndrome]
Horwath-Winter J, Nepp J, Rieger G, Schmut O.
Ophthalmologe. 2006 Aug;103(8):724; author reply 725. German.
[citation only]

Iodine brine-therapy from the ophthalmological and internal medicine viewpoint.  150th anniversary of
Landeskuranstalten, 55th anniversary of Paracelsus-Institute, 50th anniversary of Department of
Ophthalmology Bad Hall
Schmut O, Horwath-Winter J, Rieger G, Winkler R, Klieber M, Loos W, Griebenow S
Spektrum Augenheilkd (2006) 20/3: 150-7.  [article in German]
In this review the history of the spa Bad Hall, the content of ions and chemical elements in the iodine
brine, and the biological as well as the therapeutical effect of the water is discussed.  Especially the
effect of the iodine containing water for the therapy of different eye diseases is reported.  Studies
showing the improvement of visual acuity, the colour perception, the contrast sensitivity and the
capability to delay cataract development by a therapy with iodine brine are discussed.  Especially the
therapies of the sicca syndrome by iontophoresis with iodine brine and with an oil-in-water emulsion
spray are mentioned.

Sustainability of the increased watersoluble anti-oxitave status (ACW) in tear fluid taken without
stimulation after iodide-iontophoresis in Bad Hall
Griebenow S, Rieger G, Horwath-Winter J, Schmut O
Spektrum Augenheilkd (2006) 20/1:7-8.  [article in German]
Background.  
The tear fluid contains antioxidative protective mechanisms.  By the attack of free radicals, arising by
influence of ozone, UV light, smog, smoking, etc., these antioxidative protective mechanisms can be
destroyed.  The so-called environmental induced dry eye can arise by the damage of the tear-fluid
compounds by oxidative stress.
In earlier studies, we pointed out that the antioxidative status can be positively influenced by the
supply of the oxygen radical scavenger iodide taken up in the course of a cure in Bad Hall.  The
sustainability of the increased antioxidative capacity was examined after ophthalmo-iodine-
iontophoresis-treatments had been carried out.
Method.  
For the investigation of sustainability, 21 patients after 6 months and 18 patients after 9 months were
measured out of a group of 23 patients.  The analysis of the ACW value was carried out by
photochemoluminescence.
Results.  
It is evident that ACW values in the tear fluid were still increased significantly 6 months after therapy
for patients with a three-week eye treatment duration.
Conclusion.  
The more than 6 month improvement of the antioxidative capacity in the tear liquid underlines the
important value of this ophthalmo-iodide-iontophoresis treatment for patients with a dry eye condition.

Iodide iontophoresis as a treatment for dry eye syndrome.
Horwath-Winter J, Schmut O, Haller-Schober EM, Gruber A, Rieger G.
Br J Ophthalmol. 2005 Jan;89(1):40-4.
BACKGROUND/AIMS:
Among the causes related to the development or perpetuation and aggravation of dry eye disease,
oxidative reactions may have a role in the pathogenesis of this disorder. Antioxidants, such as iodide,
have shown a strong effect in preventing the oxidative damage to constituents of the anterior part of
the eye. In this clinical trial the effectiveness of iodide iontophoresis and iodide application without
current in moderate to severe dry eye patients was compared.
METHODS:
16 patients were treated with iodide iontophoresis and 12 patients with iodide application without
current for 10 days. Subjective improvement, frequency of artificial tear application, tear function
parameters (break up time, Schirmer test without local anaesthesia), vital staining (fluorescein and
rose bengal staining) as well as impression cytology of the bulbar conjunctiva were evaluated before
treatment, 1 week, 1 month, and 3 months after treatment.
RESULTS:
A reduction in subjective symptoms, frequency of artificial tear substitute application, and an
improvement in certain tear film and ocular surface factors could be observed in both groups. A
stronger positive influence was seen after application of iodide with current (iontophoresis), as
observed in a distinct improvement in break up time, fluorescein and rose bengal staining, and in a
longer duration of this effect compared with the non-current group. No significant change in Schirmer
test results and impression cytology were observed in both groups.
CONCLUSIONS:
Iodide iontophoresis has been demonstrated to be a safe and well tolerated method of improving
subjective and objective dry eye factors in patients with ocular surface disease.

Iodide protects hyaluronate from oxidative stress
Schmut O, Rieger G, Winkler R, Griebenow S, Wachswender C, Horwath-Winter J
Spektrum Augenheilkd (2004) 18/6: 294-7  [article in German]
Background:
H2O2 and free radicals are responsible for damaging reactions by oxidative stress.  It was
investigated whether iodide can destroy H2O2 and a protection against oxidative stress can be
obtained by this reaction.
Materials and methods:  
The decrease of H2O2 concentrations in physiological buffer solutions by addition of iodide was
determined by titration with KMnO4.  By viscometry the protecting activity of iodide on hyaluronate
solutions against oxidative degradation by H2O2 was measured.
Results:
Micromolar amounts of iodide can decrease the H2O2 concentration in physiological solutions within
a short time.  Iodide has the capability to protect hyaluronate from depolymerization by H2O2.
Conclusions:
The protecting activity of iodide from H2O2-induced oxidative stress may be responsible for the
positive effect on the anterior part of the eye by sprays and iontophoresis with iodide brine as
performed in Bad Hall (Upper Austria).

Protection by iodide of lens from selenite-induced cataract.
Muranov K, Poliansky N, Winkler R, Rieger G, Schmut O, Horwath-Winter J.
Graefes Arch Clin Exp Ophthalmol. 2004 Feb;242(2):146-51.
BACKGROUND:
Iodide has been used empirically against different age-related eye diseases, including cataract. The
purpose of the present study was to investigate the effect of iodide on selenite-induced cataract in rat
lens.
METHODS:
Young white rats received subcutaneously sodium selenite (20 and 30 nmol/g b.w.) on day 13 post
partum (p.p.). Cataract development was measured by expert estimation and image data analysis.
Potassium iodide (1.5 nmol/g b.w.) was given (1-5 times) i.p. at different times with respect to the
selenite administration. Lens opacification was analyzed in selenite, selenite-iodide, iodide and
control groups on day 7 after selenite administration.
RESULTS:
Iodide showed a significant protective effect against selenite cataract when injected 2 days (2 times)
before selenite injection, i.e., on days 11 and 12 p.p. No significant effects on lens opacity were
found: (1) after only one iodide injection (on day 12 p.p.), (2) after an initial iodide administration 1 h
before selenite and (3) after injections of iodide once a day for 5 consecutive days. The protective
effect of iodide was the same (about 50%) for both selenite doses used.
CONCLUSIONS:
There is a time-dependent protective influence of iodide against selenite cataract development. It is
supposed that the anticataract effect of iodide could be based on direct or indirect antioxidant
mechanisms.

Iodide protection from UVB irradiation-induced degradation of hyaluronate and against UVB-damage
of human conjunctival fibroblasts.
Schmut O, Horwath-Winter J, Rieger G, Winkler R, Trummer G, Spitzenberger H, Wachswender C.
Graefes Arch Clin Exp Ophthalmol. 2004 Apr;242(4):279-83. Epub 2003 Dec 16.
BACKGROUND:
To determine whether iodide protects from UVB irradiation-induced destruction of hyaluronate and
against UVB injury of cultured human conjunctival fibroblasts.
METHODS:
Hyaluronate and primary cultured human conjunctival fibroblasts were incubated with various
concentrations of iodide and then exposed to UV light irradiation of 312 nm. Hyaluronate destruction
was determined by viscosity measurements. Cell viability was assessed with MTT assay.
RESULTS:
Iodide protects hyaluronate from UVB light-induced degradation of this macromolecule in a
concentration-dependent manner. Incubation of human conjunctival fibroblasts with iodide inhibited
cells from damage by UVB light.
CONCLUSION:
Iodide protects hyaluronate, a component of tear fluid and tissues of the anterior part of the eye,
against UVB light-induced degradation. Also, injury of human conjunctival cells can be prevented by
incubation with iodide before UVB irradiation. The mechanism of protection is likely to include an
antioxidative reaction. To support the natural defence mechanisms of the eyes, the administration of
an antioxidant such as iodide to artificial tears, for example, may help to prevent the damage of the
eye provoked by oxidative stress.

Evaluation of the clinical course of dry eye syndrome.
Horwath-Winter J, Berghold A, Schmut O, Floegel I, Solhdju V, Bodner E, Schwantzer G, Haller-
Schober EM.
Arch Ophthalmol. 2003 Oct;121(10):1364-8.
[abstract only]
OBJECTIVE:
To assess subjective symptoms, tear function factors, and ocular surface morphology in the clinical
course of patients with dry eye syndrome under treatment within an observation period of up to 8
years.
METHODS:
In 97 patients (78 women and 19 men) with ocular discomfort, a clinical diagnosis of dry eye
syndrome was made based on typical symptoms and a reduced tear film breakup time of less than 10
seconds. Subsequent evaluations revealed a diagnosis of aqueous tear deficiency in 9 patients,
meibomian gland dysfunction in 32 patients, and aqueous tear deficiency combined with meibomian
gland dysfunction in 30 patients, aqueous tear deficiency associated with Sjogren syndrome in 12
patients, and aqueous tear deficiency and meibomian gland dysfunction associated with Sjogren
syndrome in 14 patients. Follow-up assessments were performed 12 to 94 months (mean follow-up,
40 months) after the initial diagnosis.
MAIN OUTCOME MEASURES:
In different subgroups of dry eye tear film breakup time, Schirmer test without local anesthesia
(Schirmer I), fluorescein and rose bengal staining, impression cytology, as well as subjective dry eye
symptoms and frequency of tear substitute application were compared at baseline and after a follow-
up of 1 to 8 years (mean, 3.3 years).
RESULTS:
At baseline, tear film function and ocular surface test results found more pathologic abnormalities and
more severe subjective symptoms in patients with aqueous tear deficiency associated with Sjogren
syndrome and aqueous tear deficiency and meibomian gland dysfunction associated with Sjogren
syndrome compared with the other groups who had dry eye syndrome. No differences in frequency of
tear substitute application were observed. At follow-up, tear breakup time, Schirmer I test results, and
corneal fluorescein staining improved compared with baseline values, whereas rose bengal staining
and impression cytology of the conjunctival surface remained almost unchanged. Subjective
symptoms and frequency of artificial tear application were reduced.
CONCLUSIONS:
Within the observation period of up to 8 years, the dry eye syndrome improved or stabilized under
appropriate treatment. Although no patient was completely cured, subjective reports as well as
frequency of artificial tear application were reduced.


Iodide iontophoresis as a treatment for dry eye syndrome
J Horwath-Winter1, O Schmut1, E-M Haller-Schober1, A Gruber1 and G Rieger2
+ Author Affiliations
Br J Ophthalmol 2005;89:40-44 doi:10.1136/bjo.2004.048314
Clinical science
1Department of Ophthalmology, Medical University, Graz, Austria
2Paracelsus Society for Balneology and Iodine Research, Bad Hall, Austria
Correspondence to: Jutta Horwath-Winter Department of Ophthalmology, Auenbruggerplatz 4, A-
8036 Graz, Austria; jutta.horwath@meduni-graz.at
Accepted 29 June 2004
Abstract
Background/aims:
Among the causes related to the development or perpetuation and aggravation of dry eye disease,
oxidative reactions may have a role in the pathogenesis of this disorder. Antioxidants, such as iodide,
have shown a strong effect in preventing the oxidative damage to constituents of the anterior part of
the eye. In this clinical trial the effectiveness of iodide iontophoresis and iodide application without
current in moderate to severe dry eye patients was compared.
Methods:
16 patients were treated with iodide iontophoresis and 12 patients with iodide application without
current for 10 days. Subjective improvement, frequency of artificial tear application, tear function
parameters (break up time, Schirmer test without local anaesthesia), vital staining (fluorescein and
rose bengal staining) as well as impression cytology of the bulbar conjunctiva were evaluated before
treatment, 1 week, 1 month, and 3 months after treatment.
Results:
A reduction in subjective symptoms, frequency of artificial tear substitute application, and an
improvement in certain tear film and ocular surface factors could be observed in both groups. A
stronger positive influence was seen after application of iodide with current (iontophoresis), as
observed in a distinct improvement in break up time, fluorescein and rose bengal staining, and in a
longer duration of this effect compared with the non-current group. No significant change in Schirmer
test results and impression cytology were observed in both groups.
Conclusions:
Iodide iontophoresis has been demonstrated to be a safe and well tolerated method of improving
subjective and objective dry eye factors in patients with ocular surface disease.