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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.

Iodine may be useful for dry eyes, cataracts, infections, glaucoma, and UVB protection.

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.

Bolt discusses the use of povidone eye drops -- how they are used today and how they were used
historically.

Howenstine suggests that iodine may be implicated in glaucoma.

Mazumdar investigated lacrimal gland peroxidase and iodide in sheep.

nformation on iodine
eye drugs
More articles on lacrimal glands and tears under exocrine glands.

BECKER
odide 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.
[citation only]

Cerebrospinal fluid iodide.
Becker B
Am J Physiol. 1961 Dec;201:1149-51.
[abstract only]

In vitro preparations of rabbit choroid plexus accumulated I131 to a concentration 20–30 times the
media. The accumulation was temperature dependent and was blocked by metabolic inhibitors. It
could also be saturated with iodide, and was inhibited by perchlorate, fluoroborate, and related
anions. In vivo the low 4-hr steady state concentration (1.6% of plasma) of trace doses of I131 in the
rabbit cerebrospinal fluid was increased (to 40% of plasma) by the systemic administration of iodide
or perchlorate. The results resembled qualitatively those obtained in the vitreous and aqueous
humors of the same animals and suggested an active transport of iodide out of the cerebrospinal
fluid, much as postulated previously for ocular fluids.


BOLT
Povidone-Iodine Eye Drops – Uses Past and Present
Bolt AP
2004

Povidone-Iodine is a polyvinylpyrrolidone-iodine (PVP-I) complex which slowly releases iodine in
solution. Iodine is a broad-spectrum antiseptic active against bacteria, fungi, viruses, and protozoa.
In vitro work demonstrates that weaker solutions of PVP-I are more active than stronger, as there is
more free iodine. In practice, however, a 5% solution has been shown more effective than a 1% for
surgical prophylaxis. PVP-I at concentrations of 10% and above has been shown to damage corneal
epithelial cells in rabbits, whereas solutions of 5% or less do not.


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.

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.

More articles by Flechas (Clinician)
More articles by Flechas (Orthoiodosupplementation)


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.


ISENBERG
The Ocular Application of Povidone-Iodine
Sherwin J Isenberg, MD Leonard Apt MD
Community Eye Health. 2003; 16(46): 30–31.

Why was povidone-iodine chosen as an antimicrobial agent?
  • In the appropriate concentration, it is not toxic to the eye as are other iodine bearing
    compounds

  • It has a very broad antimicrobial spectrum, including bacteria, viruses, and fungi, given
    enough contact time in vitro

  • Resistance by bacteria is rare

  • The medication turns the eye brown for a few minutes proving that it has been applied

  • It is widely available as a solution or powder; and so it is available throughout the world in
    some form

Finally, especially important for use in developing areas, it is not expensive.
In summary, povidone-iodine ophthalmic solution has been proven effective before (5% solution)
and after ocular surgery (1.25%), at birth (2.5%), and for some forms of conjunctivitis (1.25%).
Investigations of its use in treating other types of ophthalmic infections are continuing. The use of
povidone-iodine in ophthalmic practice continues to reduce the incidence of blindness in children
and adults throughout the world.

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.