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Iodine Research

Resource Network of The Iodine Movement


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                                      Iodine Special Topics

Antioxidant
    Iodine has many functions.  One of those functions appears to be as a powerful antioxidant.  
    In fact, iodine seems to function as both an oxidant and an antioxidant depending on the
    circumstances.

    The function of both oxidants and antioxidants is to transfer electrons.  An oxidant takes on
    electrons.  An antioxidant gives up electrons.

    A "free radical" is any molecule which has an "unpaired electron".  An antioxidant can give
    one of its electrons to the free radical, thus neutralizing it.

    Iodine appears to function as a powerful antioxidant, neutralizing free radicals.

Iodine and Evolution
Venturi S
Published in Italian on-line: February 8, 2004,

The link is to the English summary, as well as the Italian article complete with pictures and diagrams.

The authors report their hypothesis on the antioxidant role of iodine in the evolution of life on the
earth. Iodine is the most electron rich of the essential elements in the animal diet, and as iodide (I-)
enters in the cells by an iodide transporter. Iodide, which acts as primitive electron donor by
peroxidase enzymes, seems to have an ancestral antioxidant function in all iodide-concentrating
cells from primitive marine algae to more recent terrestrial vertebrates. Thyroxine and
iodothyronines seem also to have an antioxidant activity, by deiodinase enzymes, which are donors
of iodides and indirectly of electrons. Thyroid cells phylogenetically derived from primitive
gastroenteric cells, which during evolution, migrated and specialized in uptake and storage iodine-
compounds in the new follicle, as reservoir of iodine, for a better adaptation of modern vertebrates
to iodine deficient terrestrial environment.

Evolution of dietary antioxidants: role of iodine
Venturi S, Venturi M
Lecture.  Feb 6, 2007

The authors review the role of inorganic and organic forms of iodine as an antioxidant in evolution
of plants and animals. Iodine is one of the most abundant electron-rich essential element in the diet
of marine and terrestrial organisms. It is transported from the diet to the cells via iodide
transporters. Iodide, which acts as a primitive electron-donor through peroxidase enzymes, seems
to have an ancestral antioxidant function in all iodide-concentrating cells from primitive marine algae
to more recent terrestrial vertebrates. Thyroxine and iodothyronines have an antioxidant activity too  
and, through deiodinase enzymes, are donors of iodides and indirectly of electrons. Thyroid cells
phylogenetically derived from primitive gastroenteric cells, which during evolution of vertebrates
migrated and specialized in uptake and storage of iodo-compounds in a new follicular “thyroidal”
structure, for a better adaptation to iodine-deficient terrestrial environment. Finally, some animal
and human chronic diseases, such as cancer and cardiovascular diseases, favored by dietary
antioxidant deficiency, are briefly discussed.

Iodide, thyroid and stomach carcinogenesis: evolutionary story of a primitive antioxidant?
Venturi S
Eur J Endocinol. 1999 Apr;140(4):371-2

The thyroid gland is, embryogenetically and phylogenetically, derived from the primitive gut, and we
may consider the thyroid cells as primitive gastroenteric cells which, during evolution, migrated and
specialized in the uptake of iodide and in the storage and elaboration of iodine compounds…. In
conclusion, we believe that the evolutionary story of iodide and the thyroid might suggest and
explain a primitive antioxidant activity of this trace element.

Selenium and iodide: ancient antioxidants of cellular membrane lipids?
Cocchi M, Venturi, S
7th International Symposium on Selenium in Biology and Medicine, Italy, Oct 2000, Abstract Book P-
88:134.

Recently, we have hypothesized that iodide might have an ancestral antioxidant function in all iodide-
concentrating cells from primitive algae to more recent vertebrates.

Role of iodine in antioxidant defense in thyroid and breast disease.
Smyth PP.
Biofactors. 2003;19(3-4):121-30. Review.

The role played in thyroid hormonogenesis by iodide oxidation to iodine (organification) is well
established. Iodine deficiency may produce conditions of oxidative stress with high TSH producing a
level of H2O2, which because of lack of iodide is not being used to form thyroid hormones. The
cytotoxic actions of excess iodide in thyroid cells may depend on the formation of free radicals and
can be attributed to both necrotic and apoptotic mechanisms with necrosis predominating in goiter
development and apoptosis during iodide induced involution. These cytotoxic effects appear to
depend on the status of antioxidative enzymes and may only be evident in conditions of selenium
deficiency where the activity of selenium containing antioxidative enzymes is impaired. Less
compelling evidence exists of a role for iodide as an antioxidant in the breast. However the
Japanese experience may indicate a protective effect against breast cancer for an iodine rich
seaweed containing diet. Similarly thyroid autoimmunity may also be associated with improved
prognosis. Whether this phenomenon is breast specific and its possible relationship to iodine or
selenium status awaits resolution.”

Iodine can react with double bonds on lipids such as polyunsaturated fatty acids rendering them
less reactive to ROS. Polyunsaturated fatty acids such as arachidonic acid which is known to play a
role in intracellular signalling in the thyroid contains four double bonds and can be easily oxidised
and thus contribute to increased lipid peroxidation [32]. It has been postulated that formation of
iodolipids such as iodolactones or iodoaldehydes represents a form of thyroidal autoregulation [33]
which may be the mode of action of iodide inhibition of thyroidal function in the Wolff-Chaikoff effect
[6,34,35]. While lower doses of iodide are necessary substrates for TPO mediated conversion into
I2, iodinated compounds (so called XI) at high doses may exert inhibitory effects on adenylate-
cyclase, NADPH-oxidase and TPO activities [6,35]. This effect seems to require oxidation of I− to I2
as inhibitors of TPO or I− trapping can reverse the inhibitory effect [35].

A role for iodide as an antioxidant possibly through a protective action of iodolipids as described for
the thyroid has been suggested [64–66]. This is on the basis of a shared iodide concentrating
mechanism in both thyroid and breast as well as a requirement for an iodide oxidation system to
provide for the formation of iodoamino acids leading to thyroid hormone formation in the thyroid and
to iodinated milk proteins by the breast necessary for neonatal nutrition [50–52]. Figure 3 shows in
cartoon form the uptake of I− by the breast and its incorporation into iodoproteins. When taken into
the breast I− is incorporated into lactoproteins presumably as a result of organification into I2 by
lactoperoxidases [57,66]. These iodoproteins together with free I− are secreted in breast milk. As
mentioned elsewhere in this communication, I− may also be incorporated into iodolipids such as
iodolactones or iodoaldehydes which in the thyroid have been shown to possess antiproliferative
properties. To date there is no evidence that a similar effect is produced in the breast.

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 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.

Effect of iodide on total antioxidant status of human serum.
Winkler R, Griebenow S, Wonisch W.
Cell Biochem Funct. 2000 Jun;18(2):143-6.

Free radicals and subsequent lipid peroxidation have been implicated in the pathogenesis of
several degenerative and chronic diseases which are also treated frequently in spas. There are
some data arising from previous studies which support an antioxidant or scavenging effect of iodide,
being the essential ingredient of a therapeutically used local brine. The aim of the study was to test
the antioxidant capacity of iodide in human serum. For this reason we measured the so-called Total
Antioxidant Status determined by a colorimetric method, which reflects the protection against the
attack of reactive oxygen species, including enzymic and non-enzymic antioxidants. Exogenous
iodide applied as NaI, shows a significantly increased antioxidant capacity in comparison with NaCl
at a concentration of 15 microM, which is quite comparable to the upper range of serum iodide
levels achieved through balneo-therapeutical intervention. This result is in accordance with previous
results from in vitro depolymerization experiments with hyaluronic acid. The antioxidant effect of 15
microM NaI has been found to be approaching the physiologically relevant concentration of ascorbic
acid (50 microM).

Alterations of antioxidant tissue defense enzymes and related metabolic parameters in
streptozotocin-diabetic rats--effects of iodine treatment.
Winkler R, Moser M.
Wien Klin Wochenschr. 1992;104(14):409-13.

This study reports on the effect of streptozotocin (STZ) induced diabetes on water soluble-SH and -
SS, as well as on hepatic glutathione peroxidase (GSH-Px), catalase and superoxide dismutase
(SOD) activity and on malondialdehyde (MDA) content. In addition, we determined serum
concentrations of glucose, cholesterol, triglycerides and thyroxine, and thyroid weight. To elucidate
the possible impact of exogenous iodine on impaired free radical tissue defense mechanisms STZ-
diabetic rats were exposed to iodine brine providing for a daily iodide uptake of about 300
micrograms/kg body weight. STZ-exposure caused a decline in thyroid weight (p less than 0.01) and
in total serum thyroxine (p less than 0.001), as well as a fall in hepatic catalase (CAT) activity (p less
than 0.01) versus control group. Impairment of catalase activity was related to serum glucose level
(r = -0.569, p less than 0.01), while hepatic MDA was positively related to serum glucose (r = + 0.5,
p less than 0.01). No protective effects of iodine brine were seen with regard to impairment by STZ
of antioxidant enzyme status. We conclude that impairment by STZ of antioxidant enzymes may
contribute to STZ-dependent experimental diabetes.