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Iodine Research

Resource Network of The Iodine Movement


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                              Iodine and the Body

Skin
A significant proportion of body iodine is found in the skin.  What it is doing there is not yet clear.

Iodine may be necessary for sweating.

Iodine deficiency appears to be related to dry, scaly skin.  Supplemental iodine improves skin
texture.

Iodine has long been used as an antiseptic for wound treatment.  It is useful in the treatment of
numerous skin diseases.

Iodine absorption can occur through the skin, but the mechanisms are not yet clear.


Sterling reviews the pharmacology, mechanism of action, indications, contraindications, and
adverse effects of potassium iodine as a therapeutic agent.

Flechas states that 20% of the body iodine is in the skin, and that iodine is necessary to sweat.

Wright discusses a variety of uses for iodine including certain skin conditions like keloids,
sebaceous cysts, acne, and disinfecting cuts and scrapes.

Al-Kaisy discusses the antioxidant effect of Vitamins E and C and povidone-iodine in the treatment
of burns.

West reports that iodine supplementation can improve skin texture.

Braught states that dry and scaly skin is a good indication of iodine deficiency.

Selvaggi, Burks, and Kramer discuss the role of iodine in antisepsis and wound management.

AL-KAISY
Role of the antioxidant effect of vitamin E with vitamin C and topical povidone-iodine ointment in the
treatment of burns
Al-Kaisy A.A., Salih Sahib A.
Annals of Burns and Fire Disasters - vol. XVIII - n. 1 - March 2005

Objective. Burns represent a major health problem worldwide, with high mortality and morbidity and
economic loss even with small burns. Changes in medical treatment protocols depending on a new
mechanism involved in the pathogenicity of burns, i.e. oxidative stress (such as the use of
povidone-iodine alone or in combination with vitamin E and vitamin C) may improve the outcome
and reduce the economic loss.

Patients and methods. Thirty-eight thermally injured patients of different age groups, sex, and
occupation with different burn size, admitted to the burn unit in Baquba General Hospital, Iraq, were
involved in this clinical trial. The patients were allocated to three groups: group A (8 patients),
treated according to hospital policy; group B (17 patients), treated with topical povidone-iodine
ointment; and group C (13 patients), treated with topical povidone-iodine ointment with systemic
once daily 400 mg vitamin E and 500 mg vitamin C in addition to the classical antibiotic used by our
hospital. In each group of oxidative stress parameters, the thyroid, liver, and kidney function test,
microbiological studies, the mortality rate and healing time measurements, and economic studies
were performed using standard methods.

Results. Treatment with topical povidone-iodine ointment or in combination with systemic vitamin E
and vitamin C was found to be of significant benefit in improving oxidative stress parameters, the
mortality rate, healing time, and cost, and was free of any adverse thyroid, hepatic, or renal effects.

Conclusion. Treatment of thermally injured patients with topical povidone-iodine ointment
significantly improved oxidative stress parameters, indicating its antioxidant effect. Further
investigation is needed to explain the exact mechanism by which povidone-iodine exerts this
antioxidant effect. Treatment with topical povidone-iodine ointment alone or in combination with
systemic vitamin E and vitamin C significantly improves the outcome of thermally injured patients in
a safe way, thanks to the newly emerged mechanism - oxidative stress - involved in burns
pathogenesis.


ATEMNKENG
Comparison of free iodine as a function of the dilution of two commercial povidone-iodine
formulations.
Atemnkeng MA, Plaizier-Vercammen JA.
J Pharm Belg. 2006;61(1):11-3.
[abstract only]

Binding studies by means of equilibrium dialysis on two different Povidone-lodine-solutions reveal
that the amount of available iodine and free iodine is very different as such and after dilution. The
free iodine concentration in the Braunol concentrate was found to be ca. 22 mg/L and in the
iso-Betadine concentrate only ca. 2.1 mg/L, despite the total amount of available iodine in
iso-Betadine being higher than that of Braunol. As the bactericidal level of free iodine is
characterised by concentrations >5 ppm, Braunol can be employed as a disinfectant as such,
iso-Betadine has to be diluted before use. In both concentrates more than 99% of available iodine
is present as reservoir for free iodine. Concerning the results as a function of dilution, it was
demonstrated that, for both solutions, free iodine reaches a maximum after a 50-fold dilution (ca. 31
mg/L and ca. 51 mg/L for iso-Betadine and Braunol respectively). After dilution, a more constant
level of free iodine was observed in the Braunol than in the iso-Betadine solution, and this is
attributed to the present molar ratio of I(2)/I- and the addition of iodate in the former. The pH for
both solutions approximates that of the skin, as such and after dilution. In summary, it can be stated
that Braunol is superior to iso-Betadine as to the release of free iodine in both the undiluted as well
as in the diluted form.


Comparison of free and bound iodine and iodide species as a function of the dilution of three
commercial povidone-iodine formulations and their microbicidal activity.
Atemnkeng MA, Plaizier-Vercammen J, Schuermans A.
Int J Pharm. 2006 Jul 24;317(2):161-6. Epub 2006 Mar 22.
[abstract only]

Equilibrium dialysis on povidone-iodine-solutions (Braunol, standardized Betadine and
non-standardized iso-Betadine reveal that the amount of available iodine, free iodine, iodide and
triiodide varies significantly both in the undiluted and diluted forms. These differences are reflected
in the different bactericidal activity against Staphyloccus aureus as determined by the standard
quantitative in vitro suspension test. The amount of available iodine is not an appropriate measure
for an assessment of the microbicidal activity. For this, the free iodine has to be determined by
means of equilibrium dialysis. The free iodine concentration in the Braunol concentrate was found
to be 22 mg/L, in the standardized Betadine 9.7 mg/L and in the non-standardized Betadine
concentrate only 2.1mg/L. Because of the atypical behaviour of iodophores and the increase of free
iodine at dilution and because of a bactericidal level of free iodine of 5mg/L, Braunol and
standardized Betadine can be employed as disinfectant as such, iso-Betadine has to be diluted
before use. Summarizing all results, it can be stated that Braunol is superior to standardized
Betadine and unstandardized iso-Betadine both as to the release of free iodine in the undiluted and
in the diluted forms as in the killing rate of S. aureus.


BRAUGHT

Iodine
Braught, L

Iodine, through the thyroid gland, also helps control a lot of the digestion that goes on, as well as
heart rate, body temperature, nervous system, reproductive system, and body weight.  Iodine is
also known to destroy harmful toxins in the brain and helps neutralize toxins in the rest of the body.  
Iodine aids in the assimilation of calcium and silicone. Dry and scaly skin is a good indication of
iodine deficiency.

Symptoms of iodine deficiency may include: acne, depression, frustration, goiter, hormonal
imbalance, hyper and hypothyroidism, lethargy, miscarriages, scaly or dry skin, sterility or infertility.


BRODSKY, WORMSER

Protection from toxicants.
Brodsky B, Wormser U.
Curr Probl Dermatol. 2007;34:76-86.

Exposures to skin irritants frequently occur in daily life at the workplace, in laboratories and during
housekeeping. Apart from the physical protective countermeasures, there is a need for
pharmacological preparations for the topical treatment of the exposed skin to prevent the
development of burns. Exposure of the skin to a chemical irritant initiates an inflammatory response
which progressively intensifies, leading to epidermal and dermal lesions. Topical treatment with
povidone-iodine (PI) or iodine ointment significantly reduced skin damage induced by mustard gas
(sulfur mustard), hydrofluoric acid and other chemical irritants. Human studies showed the efficacy
of PI and iodine against thermal burns. The combination of anti-inflammatory agents and iodine
increased the counterirritating activity. Both human and experimental animal studies demonstrated
that the ointment should be immediately applied after occurrence: the earlier the treatment, the
better the therapeutic effect. In addition, the ointment should be left on the skin long enough for
achieving the therapeutic effect. This simple topical treatment can prevent suffering, skin
transplantation and complications associated with skin burns.


Effect of different iodine formulations on the expression and activity of Streptococcus mutans
glucosyltransferase and fructosyltransferase in biofilm and planktonic environments.
Tam A, Shemesh M, Wormser U, Sintov A, Steinberg D.
J Antimicrob Chemother. 2006 May;57(5):865-71. Epub 2006 Mar 20.
[abstract only]

OBJECTIVES: The glucosyltransferase (GTF) and fructosyltransferase (FTF) enzymes play a
pivotal role in dental biofilm formation as they synthesize polysaccharides that act as the
extracellular matrix of the biofilm. Iodine is a unique antibacterial agent that has distinct properties
from other conventional antibacterial agents. In this study we have examined the effect of iodine
and povidone iodine (PI) on gtf and ftf expression in biofilm and planktonic environments and on
immobilized and unbound GTF and FTF activity.

METHODS: Real-time reverse transcription-PCR was used to investigate the effect of iodine and PI
on ftf, gtfB and gtfC expression. The effect of iodine and PI on GTF and FTF activity was tested
using radioactive assays.

RESULTS: Our results indicate that iodine and PI in a tetraglycol carrier cause enhancement of
expression of gtfB in Streptococcus mutans in biofilms but not in planktonic bacteria. PI in water
induced expression of gtfB and gtfC in planktonic bacteria. However, iodine and PI strongly inhibit
polysaccharide production by GTF and to a lesser extent by FTF activity. The inhibitory effect on
GTF activity was similar in solution compared to its activity in the immobilized environment. This
unique effect may be attributed to the distinct chemical properties of iodine compared with other
antibacterial agents.

CONCLUSIONS: This study indicates that iodine at sub-bactericidal concentrations demonstrates
molecular and enzymatic effects that are highly associated with biofilm formation.


Early effects of iodine on DNA synthesis in sulfur mustard-induced skin lesions.
Brodsky B, Trivedi S, Peddada S, Flagler N, Wormser U, Nyska A.
Arch Toxicol. 2006 Apr;80(4):212-6.
[abstract only]

Sulfur mustard (SM) is powerful alkylator and highly cytotoxic blisterogen in both humans and
animals. This study in male guinea pigs shows that, at an early stage (5 h) after SM exposure, a
marked increase occurred in epithelial nuclear vacuolation, epidermal thickening, and dermal acute
inflammation. Topical iodine treatment reduced the severity of these parameters. The rate of DNA
synthesis expressed by incorporation of bromodeoxyuridine was reduced upon topical treatment
with iodine only or SM only by 46 and 72%, respectively. Iodine treatment following SM exposure
exerted an effect similar to that of SM only, indicating that DNA synthesis is not directly involved in
the mechanism of action of iodine-induced protection.


Involvement of tumor necrosis factor-alpha in sulfur mustard-induced skin lesion; effect of topical
iodine.
Wormser U, Brodsky B, Proscura E, Foley JF, Jones T, Nyska A.
Arch Toxicol. 2005 Nov;79(11):660-70. Epub 2005 Jul 7.
[abstract only]

Sulfur mustard (SM), also termed mustard gas, is a potent vesicant that elicits an inflammatory
response upon exposure of the skin. Evaluation of mouse ear 3 h after SM exposure revealed acute
inflammatory-cell aggregates in the vascular beds accompanied by strongly TNF-alpha-positive
neutrophils. Eight hours after SM exposure, this phenomenon became intensified and associated
with infiltration into the adjacent dermis. In ear skin topically treated with iodine, however, no
inflammatory cells were observed 3 h after SM exposure; 8 h postexposure, blood vessels
contained very few TNF-alpha-positive inflammatory cells. Since TNF-alpha induction was shown to
be associated with reactive oxygen species production, we studied the effect of iodine on activated
peritoneal mouse neutrophils. Iodine elicited a concentration-dependent reduction in the oxidative
burst of activated neutrophils. Iodine also scavenged hydroxyl radicals generated by glucose
oxidase in a concentration-dependent manner. The involvement of TNF-alpha in SM-induced skin
toxicity was confirmed by reduction of 49 and 30% in ear edema following administration of 1 and 2
mug anti-TNF-alpha antibodies, respectively. These findings were corroborated by quantitative
analysis of the histological findings showing 46% reduction in acute inflammation and no signs of
subacute inflammation in the treated group, in contrast to the control group treated with SM only.
Other epidermal (microblister formation, ulceration, and necrosis) and dermal (neutrophilia,
hemorrhage, and necrosis) parameters also showed marked reductions in the antibodies-treated
group in comparison to controls. The combination of iodine and antiTNF-alpha antibodies might
constitute a new approach for treatment of SM-exposed individuals.


Protective effect of topical iodine containing anti-inflammatory drugs against sulfur mustard-induced
skin lesions.
Wormser U, Sintov A, Brodsky B, Casillas RP, Nyska A.
Arch Toxicol. 2004 Mar;78(3):156-66. Epub 2003 Nov 15.
[abstract only]

Previous studies have shown the antidotal efficacy of topical iodine at 15 and 30 min post-exposure
to sulfur mustard (SM). Here we demonstrate efficacy at longer intervals (20, 30, 45, and 60 min,
respectively, for data) using an improved topical povidone-iodine preparation termed N66, which
contains steroidal and non-steroidal anti-inflammatory agents. In the mouse, N66 reduced severity
of ear edema by 43, 47, 44, and 36%; ear epidermal ulceration by 74, 58, 45, and 58%; and
epidermal necrosis by 54, 34, 26, and 31% at the respective time points. A similar effect was
observed with encrustation. The healing marker, grade of acanthotic area, showed dramatic
increases of 39.6-, 25.3-, 20.9-, and 22-fold. Severity of the dermal parameters, acute inflammation
and dermal necrosis, was reduced by 63, 34, 34, and 38% and 80, 54, 54, and 59%, respectively.
In guinea pig skin, topical treatment with N66 45 min post-exposure reduced the SM-induced
ulceration area by 75%. The histological parameters subepidermal microblister formation, epidermal
ulceration, epidermal necrosis, and encrustation were reduced by 63, 61, 41, and 41%,
respectively. The healing marker, grade of acanthotic area, was elevated by 73%. N66 induced a
statistically significant reduction in two dermal markers for tissue damage: acute inflammation (33%)
and dermal necrosis (48%). Reduced skin damage was also observed in areas adjacent the treated
sites. The pharmacologically active components of N66 showed additive effect. These findings
suggest that the povidone-iodine preparation combined with anti-inflammatory agents functions as a
potent antidote against skin lesions induced by SM at relatively long intervals between exposure
and treatment.


Protective effect of topical iodine preparations upon heat-induced and hydrofluoric acid-induced
skin lesions.
Wormser U, Sintov A, Brodsky B, Amitai Y, Nyska A.
Toxicol Pathol. 2002 Sep-Oct;30(5):552-8.
[abstract only]

In this study, the protective prophylactic and post-exposure effects of novel topical iodine
preparations were demonstrated upon heat- and hydrofluoric acid-induced skin lesions in the
haired guinea pig. Prophylactic treatment of thermal bums with a liquid iodine preparation resulted
in statistically significant reductions of 39% and 30%, respectively, in acute inflammation and
hemorrhage-microscopic dermal parameters indicative of acute tissue damage. A clear trend of
iodine-induced reduction in dermal necrosis occurred, and the epidermal healing markers,
acanthosis and hyperkeratosis, were increased. Postexposure treatment of thermal burns with an
iodine ointment preparation immediately after occurrence also conferred significant therapeutic
reduction in parameters of tissue damage such as epidermal ulceration (87%), acute inflammation
(58%), and hemorrhage (30%). Gross pathological evaluation showed that prophylactic and
postexposure treatments with the liquid iodine preparation significantly reduced the heat-induced
ulceration area by 97% and 65%, respectively. In addition, immediate treatment with an ointment
iodine formulation significantly decreased the ulceration area by 98%; its tetraglycol vehicle also
had a beneficial effect. Postexposure treatment with the iodine ointment proved efficacious upon
hydrofluoric acid-induced skin burns. We observed statistically significant reductions of 76% and
68% in ulceration areas at intervals of 5 and 10 minutes between exposure and treatment, whereas
a weaker effect was observed at a longer time interval of 15 minutes. Our findings suggest the
therapeutic usage of these newly developed iodine preparations for thermally induced and
hydrofluoric acid-induced skin burns.


Topical treatment with povidone iodine reduces nitrogen mustard-induced skin collagenolytic activity.
Wormser U, Brodsky B, Reich R.
Arch Toxicol. 2002 Mar;76(2):119-21. Epub 2002 Jan 23.
[abstract only]

Recently we have shown that post-exposure treatment with povidone iodine (PI) protects against
nitrogen and sulfur mustard-induced skin lesions. Since proteolytic activity is involved in skin
damage caused by chemical irritants, we have studied the effect of iodine on mechlorethamine
(HN2)-induced skin collagenolytic activities in the haired guinea pig model. The matrix
metalloproteinase-9 (MMP-9) activity increased by 30, 46, 12 and 23% after 3, 24, 48 and 72 h of
HN2 exposure, respectively, whereas the MMP-2 was elevated by 8, 65, 8 and 30%, respectively.
Topical treatment with PI at 15 and 120 min after HN2 exposure decreased the MMP-9 activity by
67% and 60%, respectively, when skin was analyzed 3 h after exposure. The same trend was
observed in the MMP-2 and MMP-1 activities after PI treatment. A stronger effect of PI treatment 15
min following exposure was observed in skin analyzed 24 h after exposure, i.e. a decrease of 83%
and 88% in MMP-9 and MMP-2 activities, respectively. Similar findings were observed with an
interval of 120 min between HN2 exposure and PI treatment. A much weaker effect was observed on
MMP-1 activity. A similar trend of PI-induced reduction in the three types of collagenase activity was
found in skin analyzed 48 and 72 h after exposure. Reduced collagenolytic activity may serve as
one of the mechanisms by which iodine protects the skin against chemical insult.


Protective effect of povidone iodine ointment against skin lesions induced by chemical and thermal
stimuli.
Wormser U, Brodsky B, Green BS, Arad-Yellin R, Nyska A.
J Appl Toxicol. 2000 Dec;20 Suppl 1:S183-5.
[abstract only]

Mustard gas (sulfur mustard, HD) is a powerful vesicant employed as a chemical weapon. The
present study demonstrates the effect of povidone iodine (PI) ointment against skin toxicity caused
by HD. Gross and histopathological examinations showed that application of PI 20 min or less
following exposure to the vesicant resulted in marked skin protection. The shorter, interval between
exposure and treatment, the better was the protection achieved. Povidone iodine was also effective
against other mustards, such as carboxybutylchloroethyl sulfide (CBCS) and mechlorethamine. The
fact that PI protected the skin against agents that cannot be oxidized, such as iodoacetic acid,
divinylsulfone and cantharidine, indicated that the antidotal effect of PI was unrelated to oxidation of
the nitrogen and sulfur atoms of the mustards. Furthermore, NMR spectroscopy of CBCS treated
with iodine did not show oxidation of the sulfur atom. Clinical experience with patients after
accidential heat burns (mostly of grade I) has shown that topical application of PI ointment
immediately after the stimulus significantly reduced, and often prevented, skin lesions. Apart from
being a safe and widely used disinfectant, PI ointment is recommended as an efficient protective
agent against skin toxicity caused by hazardous chemicals and by heat stimuli.


Effects of iodine on inducible nitric oxide synthase and cyclooxygenase-2 expression in sulfur
mustard-induced skin.
Nyska A, Lomnitski L, Maronpot R, Moomaw C, Brodsky B, Sintov A, Wormser U.
Arch Toxicol. 2001 Feb;74(12):768-74.
[abstract only]

In a previous study we demonstrated the protective effect of topical iodine as postexposure
treatment for sulfur mustard (SM) application. The iodine treatment results in significantly reduced
inflammation and necrosis and increased epidermal hyperplasia. The expression and localization of
inducible nitric oxide synthase (iNOS) and cyclooxygenase 2 (COX-2) in paraffin-embedded skin
samples from that study were evaluated in the present investigation. We compared the
immunoreactivity of iNOS and COX-2 using five samples from each of the following four test sites:
untreated control sites, SM-exposed sites, sites treated with iodine mixture 15 min after SM
exposure, and sites treated with iodine 30 min after SM exposure. All animals were killed 2 days
after irritant exposure. iNOS immunoreactivity was present only in skin sites exposed to SM without
iodine treatment. The ulcerated skin was covered with a relatively thick band of exudate composed
of iNOS-immunostained polymorphonuclear cells and macrophages. In untreated skin, COX-2
immunostaining was limited to the thin suprabasal epidermal layer. In SM-exposed skin, induction of
COX-2 was noted in inflammatory cells located close to the site of epidermal injury. In skin sites
treated with iodine 15 or 30 min after SM exposure, the regenerating hyperplastic epithelium
showed moderate cytoplasmic staining localized to the epithelium overlying the basal layer. This
pattern of staining was also present in the nearby dermal fibroblasts. Thus, in contrast to the skin
samples exposed to SM without iodine treatment, the epidermal layer expressing
immunohistochemical positivity for COX-2 was thicker and corresponded to the epidermal
hyperplasia noted in samples treated with iodine. It is well documented that prostaglandins (PGs)
promote epidermal proliferation, thereby contributing to the repair of injured skin. That the induction
of the COX-2 shown in our study may also play a role in the healing process is indicated by the
present evidence. The results suggest that nitric oxide radicals (NO*) are involved in mediating the
damage induced by the SM and that iodine-related reduction in acute epidermal inflammation is
associated with reduced iNOS expression.


Topical iodine preparation as therapy against sulfur mustard-induced skin lesions.
Wormser U, Sintov A, Brodsky B, Nyska A.
Toxicol Appl Pharmacol. 2000 Nov 15;169(1):33-9.
[abstract only]

Sulfur mustard (SM) is a powerful vesicant employed as an agent of chemical warfare. This study
demonstrates the therapeutic effect of a novel topical iodine preparation as a postexposure
treatment against SM-induced lesions in the fur-covered guinea-pig skin model. Iodine treatment 15
min after SM exposure resulted in statistically significant reductions of 48, 50, and 55% in dermal
acute inflammation, hemorrhage, and necrosis, respectively, whereas, the epidermal healing
markers, hyperkerathosis and acanthosis, were significantly elevated by 72 and 67%, respectively,
2 days after treatment. At the interval of 30 min between SM exposure and iodine treatment, there
was a significant degree of healing or recovery, albeit to a lesser extent than that observed in the
shorter interval. Although the epidermal healing markers were not elevated, the parameters
indicative of active tissue damage, such as subepidermal microblisters, epidermal ulceration, dermal
acute inflammation, hemorrhage, and necrosis, were significantly reduced by 35, 67, 43, 39, and
45%, respectively. At the 45-min interval between exposure and treatment, there was also a certain
degree of healing or recovery expressed as significant reductions in dermal subacute inflammation,
subepidermal microblister formation, and epidermal ulceration, whereas, acanthosis was statistically
elevated, indicating an increased healing potential. At the 60-min interval, iodine was less
efficacious; nevertheless, a significant reduction in the incidence of subepidermal microblisters and
an expansion of the acanthotic area were observed. Gross ulceration was significantly decreased at
intervals of 15 and 30 min between exposure and treatment. The local anesthetic, lidocaine, did not
alter the therapeutic effect of iodine. SM was not affected chemically by iodine as measured by gas
chromatography-mass spectrometry (GC-MS) analysis. These findings suggest that the iodine
preparation functions as an antidote against skin lesions induced by SM.


Protective effect of povidone-iodine ointment against skin lesions induced by sulphur and nitrogen
mustards and by non-mustard vesicants.
Wormser U, Brodsky B, Green BS, Arad-Yellin R, Nyska A.
Arch Toxicol. 1997;71(3):165-70.
[abstract only]

Mustard gas (sulphur mustard, SM) is a powerful vesicant employed as a chemical weapon. The
present study demonstrates the effect of povidone iodine (PI) ointment against skin toxicity caused
by SM. Gross and histopathological examinations showed that application of PI up to 20 min
following exposure to the vesicant resulted in marked skin protection. The shorter the interval
between exposure and treatment the better was the protection achieved. PI was also effective
against other mustards such as carboxybutyl chloroethyl sulphide (CBCS) and mechlorethamine.
The fact that PI protected the skin against agents which cannot be oxidized such as iodoacetic acid,
divinylsulphone and cantharidine showed that the antidotal effect of PI was unrelated to oxidation of
the nitrogen and sulphur atoms of the mustards. PI ointment is proposed as an efficient protective
agent against skin toxicity caused by mustards and other alkylators.
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