Shedding On Thyroid?

[chompie]

T3/T4 will make you lose hair, it's a common side effect. And it's not guaranteed hair will grow back in the full density after stopping

Can you provide a bit more info here?

 

[iso1]

Up your minerals with liver and shellfish and see if if helps.

If you google thyroid replacement and hair loss, you could find billions of reports. it's very common reaction, but i dont know about mechanism, I remember reading T3 upregulating AR. so that can be one of mechanisms. Minerals and vitamins is just cope and not going to help here.
just 5 sec search for example this archived thread

thyroid (medication) and hair loss [Archive] - The Long Hair Community Discussion Boards

Hi all, I have a question. I am losing my hair!! I found out i am hypothyroid and start medication soon. I am reading a lot of horror stories about people losing their hair due to their thyroid medication? I wonder if there are any success stories on thyroid medication and hair regrowth...

forums.longhaircommunity.com

And study here.

Conversely, T3 increased androgen receptor levels up to twofold. Androgen as well as T3 stimulation of proliferation was abolished by high concentrations of the retinoid 9-cis-retinoic acid

Triiodothyronine modulates growth, secretory function and androgen receptor concentration in the prostatic carcinoma cell line LNCaP - PubMed

There is increasing evidence that the course of prostatic carcinoma is determined by a complex interplay between genetic events, paracrine interactions, and hormonal and dietary factors. These latter factors include several ligands of the nuclear receptor family such as androgens, vitamin D3 and...

pubmed.ncbi.nlm.nih.gov

 

[Kayaker]

If you google thyroid replacement and hair loss, you could find billions of reports. it's very common reaction, but i dont know about mechanism, I remember reading T3 upregulating AR. so that can be one of mechanisms. Minerals and vitamins is just cope and not going to help here.
just 5 sec search for example this archived thread

thyroid (medication) and hair loss [Archive] - The Long Hair Community Discussion Boards

Hi all, I have a question. I am losing my hair!! I found out i am hypothyroid and start medication soon. I am reading a lot of horror stories about people losing their hair due to their thyroid medication? I wonder if there are any success stories on thyroid medication and hair regrowth...

forums.longhaircommunity.com

And study here.

Triiodothyronine modulates growth, secretory function and androgen receptor concentration in the prostatic carcinoma cell line LNCaP - PubMed

There is increasing evidence that the course of prostatic carcinoma is determined by a complex interplay between genetic events, paracrine interactions, and hormonal and dietary factors. These latter factors include several ligands of the nuclear receptor family such as androgens, vitamin D3 and...

pubmed.ncbi.nlm.nih.gov

Thyroid damage or inhibition has underlying causes. If the cause of hypothyroidism isn't addressed, then thyroid is going to cause hair loss and other problems, even when it's within normal. Do healthy people have hair loss? No. It's hypothyroid people who start taking thyroid. It has nothing to do with androgen receptors.

 

[iso1]

Thyroid damage or inhibition has underlying causes. If the cause of hypothyroidism isn't addressed, then thyroid is going to cause hair loss and other problems, even when it's within normal. Do healthy people have hair loss? No. It's hypothyroid people who start taking thyroid. It has nothing to do with androgen receptors.

Thyroid supplementation will cause hair loss regardless of your t3/t4 status. And it's strange to me you trying to ignore such a huge factor such as AR upregulation, which is one of the roots of hair loss. The reality is thyroid replacemnet causing hair loss, and many people don't regrow them completely even after fixing thyroid issue.

 

[Kayaker]

Thyroid supplementation will cause hair loss regardless of your t3/t4 status. And it's strange to me you trying to ignore such a huge factor such as AR upregulation, which is one of the roots of hair loss. The reality is thyroid replacemnet causing hair loss, and many people don't regrow them even after fixing thyroid issue.

Exactly. People with good thyroid status have enough thyroid hormone, so they lose hair from more, and people with bad thyroid status often can't tolerate more, so they lose hair.

I ignore it because some people here believe DHT is good for hair follicles. I believe cortisol, which increases from deficiencies and insufficiencies, such as those that thyroid supplementation can cause, plays a bigger role.

 

[TheCalciumCad]

Exactly. People with good thyroid status have enough thyroid hormone, so they lose hair from more, and people with bad thyroid status often can't tolerate more, so they lose hair.

I ignore it because some people here believe DHT is good for hair follicles. I believe cortisol, which increases from deficiencies and insufficiencies, such as those that thyroid supplementation can cause, plays a bigger role.

So, low thyroid causes chronic loss of vitamins/minerals and taking thyroid ramps up demands significantly and inability to replenish (if you don't meet your new higher needs) is what keeps you losing hair even if you now have good metabolism? Maybe also people who do no lifestyle changes to lower their stress levels (causes of low thyroid to begin with) while taking thyroid will now have new found energy but still triggering stress on top.

 

[Kayaker]

So, low thyroid causes chronic loss of vitamins/minerals and taking thyroid ramps up demands significantly and inability to replenish (if you don't meet your new higher needs) is what keeps you losing hair even if you now have good metabolism? Maybe also people who do no lifestyle changes to lower their stress levels (causes of low thyroid to begin with) while taking thyroid will now have new found energy but still triggering stress on top.

I meant more like, physiological stress, which can be generalized chronic stress (lack of sleep, malnutrition, etc) causes damage to the thyroid gland, and then symptoms are blamed on hypothyroidism. But taking thyroid hormone without addressing the cause only fixes the hypothyroidism, and not the cause behind the deterioration.

This "newfound energy", using hypothyroidism as a scapegoat, and having low TSH from supplementation convinces people they are well, when in reality they need to either take the time to heal, or there's a specific problem that doesn't respond to healing. Instead, they push themselves as if they are healthy, and are surprised they are losing hair.

 

[chompie]

I meant more like, physiological stress, which can be generalized chronic stress (lack of sleep, malnutrition, etc) causes damage to the thyroid gland, and then symptoms are blamed on hypothyroidism. But taking thyroid hormone without addressing the cause only fixes the hypothyroidism, and not the cause behind the deterioration.

This "newfound energy", using hypothyroidism as a scapegoat, and having low TSH from supplementation convinces people they are well, when in reality they need to either take the time to heal, or there's a specific problem that doesn't respond to healing. Instead, they push themselves as if they are healthy, and are surprised they are losing hair.

In theory, "root cause" sounds like a great idea but in practice it's incredibly vague and even more difficult. Most of us who have come this far came here because we exhausted the allopathic medicine route, the integrative route, and various other routes.

Not a single one of us would be on this forum if everything worked as it should. All of us that have problems and we would love to know exactly what the root cause is. Likely, nearly everyone with hypothyroidism wouldn't be if there was some root problem that could be found out. Most of us came here because we thought and might believe that having a higher metabolism could help fix that mysterious root problem if we surround the supplementation with plenty of nutrients, sunlight, joy, etc.

Unfortunately, reality is much more nuanced. Don't be stressed and sleep better is a good platitude but isn't helpful.

I'm very grateful for those who have chimed in here, fwiw

 

[BearWithMe]

I meant more like, physiological stress, which can be generalized chronic stress (lack of sleep, malnutrition, etc) causes damage to the thyroid gland, and then symptoms are blamed on hypothyroidism. But taking thyroid hormone without addressing the cause only fixes the hypothyroidism, and not the cause behind the deterioration.

This "newfound energy", using hypothyroidism as a scapegoat, and having low TSH from supplementation convinces people they are well, when in reality they need to either take the time to heal, or there's a specific problem that doesn't respond to healing. Instead, they push themselves as if they are healthy, and are surprised they are losing hair.

What are some other typical causes of damage to thyroid gland?

 

[Kayaker]

What are some other typical causes of damage to thyroid gland?

Early in life, dental x-rays would be the most common cause of damage. Fluoride, lithium, and excess or deficient iodine also cause specific damage or suppression.

RP: "Very large doses of potassium iodide used to be used for certain inflammations or infections, but its effects haven’t been understood. The small amount of iodide added to salt has been reported in more than 70 studies to damage the thyroid gland, even increasing thyroid cancer."

Spoiler: STUDIES HE SHARED

1. Food Chem Toxicol. 2000 Sep;38(9):773-81.
Studies on the carcinogenicity of potassium iodide in F344 rats.
Takegawa K(1), Mitsumori K, Onodera H, Shimo T, Kitaura K, Yasuhara K, Hirose M,
Takahashi M.
(1)Division of Pathology, National Institute of Health Sciences, 1-18-1 Kamiyoga,
Setagaya-ku, 158-8501, Tokyo, Japan.
A chronic toxicity and carcinogenicity study, in which male and female F344/DuCrj
rats were given potassium iodide (KI) in the drinking water at concentrations of
0, 10, 100 or 1000 ppm for 104 weeks, and a two-stage carcinogenicity study of
application at 0 or 1000 ppm for 83 weeks following a single injection of
N-bis(2-hydroxypropyl)nitrosamine (DHPN), were conducted. In the former, squamous
cell carcinomas were induced in the salivary glands of the 1000 ppm group, but no
tumors were observed in the thyroid. In the two-stage carcinogenicity study,
thyroidal weights and the incidence of thyroid tumors derived from the follicular
epithelium were significantly increased in the DHPN+KI as compared with the DHPN
alone group. The results of our studies suggest that excess KI has a thyroid
tumor-promoting effect, but KI per se does not induce thyroid tumors in rats. In
the salivary gland, KI was suggested to have carcinogenic potential via an
epigenetic mechanism, only active at a high dose.

3. Jpn J Cancer Res. 1998 Feb;89(2):105-9.
Induction of squamous cell carcinomas in the salivary glands of rats by potassium
iodide.
Takegawa K(1), Mitsumori K, Onodera H, Yasuhara K, Kitaura K, Shimo T, Takahashi
M.
(1)Division of Pathology, National Institute of Health Sciences, Tokyo.
In a 2-year carcinogenicity study of potassium iodide (KI) in F344/DuCrj rats,
squamous cell carcinomas (SCCs) were observed in the salivary glands of 4/40
males and 3/40 females receiving 1000 ppm KI in the drinking water. Ductular
proliferation with lobular atrophy was observed at high incidence in the
submandibular glands of the high-dose animals, and squamous metaplasia was
frequently evident within the proliferative ductules and the larger interlobular
ducts. A transition from metaplasia to SCC was apparent. The results suggest that
squamous metaplasia in proliferative ductules, occurring secondarily to lobular
impairment induced by KI, may develop into SCCs via a non-genotoxic,
proliferation-dependent mechanism.

2. Endocrinology. 2000 Feb;141(2):598-605.
Iodide excess induces apoptosis in thyroid cells through a p53-independent
mechanism involving oxidative stress.
Vitale M(1), Di Matola T, D'Ascoli F, Salzano S, Bogazzi F, Fenzi G, Martino E,
Rossi G.
(1)Dipartimento di Biologia e Patologia Cellulare e Molecolare, Università
Federico II, Naples, Italy. [email protected]
Thyroid toxicity of iodide excess has been demonstrated in animals fed with an
iodide-rich diet; in vitro iodide is cytotoxic, inhibits cell growth, and induces
morphological changes in thyroid cells of some species. In this study, we
investigated the effect of iodide excess in an immortalized thyroid cell line
(TAD-2) in primary cultures of human thyroid cells and in cells of nonthyroid
origin. Iodide displayed a dose-dependent cytotoxicity in both TAD-2 and primary
thyroid cells, although at different concentrations, whereas it had no effect on
cells of nonthyroid origin. Thyroid cells treated with iodide excess underwent
apoptosis, as evidenced by morphological changes, plasma membrane
phosphatidylserine exposure, and DNA fragmentation. Apoptosis was unaffected by
protein synthesis inhibition, whereas inhibition of peroxidase enzymatic activity
by propylthiouracil completely blocked iodide cytotoxicity. During KI treatment,
reactive oxygen species were produced, and lipid peroxide levels increased
markedly. Inhibition of endogenous p53 activity did not affect the sensitivity of
TAD-2 cells to iodide, and Western blot analysis demonstrated that p53, Bcl-2,
Bcl-XL, and Bax protein expression did not change when cells were treated with
iodide. These data indicate that excess molecular iodide, generated by oxidation
of ionic iodine by endogenous peroxidases, induces apoptosis in thyroid cells
through a mechanism involving generation of free radicals. This type of apoptosis
is p53 independent, does not require protein synthesis, and is not induced by
modulation of Bcl-2, Bcl-XL, or Bax protein expression.


4. Toxicol Pathol. 1994 Jan-Feb;22(1):23-8.
Effects of a six-week exposure to excess iodide on thyroid glands of growing and
nongrowing male Fischer-344 rats.
Kanno J(1), Nemoto T, Kasuga T, Hayashi Y.
(1)Department of Pathology, Faculty of Medicine, Tokyo Medical and Dental
University, Japan.
A 6-wk exposure to excess iodide intake (EII) via drinking water (260 mg
potassium iodide/L) demonstrated different effects on growing (4-wk old) and
nongrowing (45-wk old) male Fischer-344 rats. In growing rats, EII induced a
significant increase in thyroid weight, pituitary weight, serum
thyroid-stimulating hormone (TSH), and thyroxine (T4). The labeling index (LI) of
thyroid follicular cells was slightly increased, although not statistically
significant. Histologically, an increase in follicular cell height, an increase
in colloid accumulation, and evidence of colloid absorption were noted. The
effect of bovine TSH (bTSH) and protirelin tartrate (TRH-t) on LI was
significantly augmented by EII. In nongrowing rats, EII induced a significant
increase in thyroid weight and serum T4 but no increase in pituitary weight,
serum TSH, and the LI of follicular cells. Histologically, an increase in colloid
accumulation was found in small follicles. EII did not augment the effect of bTSH
and TRH-t on the LI of follicular cells. This study suggests that growing rats
are still susceptible to acute hypothyroidism even after 6 wk of continuous
exposure to excess iodide, whereas nongrowing rats are refractory within an
equivalent treatment period.


5. Food Chem Toxicol. 1984 Dec;22(12):963-70.
Developmental toxicity and psychotoxicity of potassium iodide in rats: a case for
the inclusion of behaviour in toxicological assessment.
Vorhees CV, Butcher RE, Brunner RL.
Potassium iodide (KI) was fed to male and female rats before and during breeding,
to females only during gestation and lactation, and to their offspring after
weaning (day 21 after birth) through to day 90, at levels of 0, 0.025, 0.05 or
0.1% (w/w) of the diet. Dams in a fifth group (positive controls) were given 4
mg/kg ip of the anti-mitotic/cytotoxic drug 5-azacytidine on day 17 of gestation.
All offspring were reared by their natural dams and were evaluated blind with
respect to treatment in a battery of standardized behavioural tests between 3 and
90 days of age. KI produced no significant reductions in parental body weight or
food consumption, though it significantly reduced litter size and increased
offspring mortality at the highest dose, and decreased weight gain at the two
highest doses throughout the first 90 days after birth. Functionally, KI delayed
auditory startle at the two highest doses, delayed olfactory orientation to the
home-cage scent at the middle dose and decreased female running-wheel activity at
all dose levels. In rats killed on day 90 after birth KI reduced brain and body
weight at a dose of 0.1% of the diet, and reduced body but not brain weight at a
dose of 0.05% of the diet. No significant effect was found on absolute or
relative thyroid weight at 90 days of age. Several additional behavioural effects
were observed in the low-dose KI group, but because these effects were not
dose-dependent, they were not regarded as reliable. 5-Azacytidine produced
evidence of substantially greater developmental toxicity than KI. It was
concluded that KI produced evidence of developmental toxicity consistent with a
picture of impaired thyroid function. The inclusion of tests of functional
development added useful evidence to the overall picture of KI developmental
toxicity.


6. J Allergy Clin Immunol. 1980 Sep;66(3):177-8.
A time to abandon the use of iodides in the management of pulmonary diseases.
Hendeles L, Weinberger M.


7. Endocrinol Jpn. 1975 Oct;22(5):389-97.
The effect of iodide administration on hog thyroid gland and the composition of
thyroglobulin and 27-S iodoprotein.
Tarutani O, Kondo T, Horiguchi-Sho K.
The effect of excess iodide on hog thyroid gland has been examined with regard to
the change in the chemical composition of thyroglobulin and in the accumulation
of 27-S iodoprotein by the in vivo treatment of hogs with iodide for various
lengths of time. The iodine content of thyroglobulin was either unchanged by
short term administration of excess iodide, or somewhat lowered. However, the
iodine content as well as the total amount of thyroglobulin increased in the
glands enlarged by prolonged treatment with iodide. The iodine highest reached
1.17% of the protein on an average. On the other hand, 27-S iodoprotein decreased
and finally disappeared after the chronic treatment. Monoiodotyrosine and
diiodotyrosine increased in parallel with the increase in the iodine content
(0.15 to 1.17%) caused by the iodide treatment, while thyroxine increased but
reached a plateau at the level of three residues per mole of thyroglobulin, and
no change was observed even in the proteins with the higher iodine content than
0.75%. Proteolytic activity measured by amino acid release from the thyroid
protein was depressed by the chronic treatment. On the other hand, the amount of
iodocompound released by the autoproteolysis, which may reflect hormone
secretion, increased, possibly because of the marked increase in the iodine
content of thyroglobulin.


8. Am J Vet Res. 1973 Jan;34(1):65-70.
Experimentally induced iodide toxicosis in lambs.
McCauley EH, Linn JG, Goodrich RD.



9. Toxicol Appl Pharmacol. 1966 Mar;8(2):185-92.
The toxicology of potassium and sodium iodates. 3. Acute and subacute oral
toxicity of potassium iodate in dogs.
Webster SH, Stohlman EF, Highman B.



10. Clin Toxicol (Phila). 2013 Jul;51(6):521. doi: 10.3109/15563650.2013.804549. Epub
2013 May 23.
Regional centers: added value to poison center surveillance.
Durigon M, Kosatsky T.
Comment on
Clin Toxicol (Phila). 2013 Jan;51(1):41-6.



11. Environ Toxicol Pharmacol. 2014 Jul;38(1):332-40. doi:
10.1016/j.etap.2014.06.008. Epub 2014 Jun 27.
The effects and underlying mechanism of excessive iodide on excessive
fluoride-induced thyroid cytotoxicity.
Liu H(1), Zeng Q(2), Cui Y(2), Yu L(3), Zhao L(2), Hou C(2), Zhang S(4), Zhang
L(2), Fu G(2), Liu Y(3), Jiang C(4), Chen X(4), Wang A(5).
(1)Tianjin Centers for Disease Control and Prevention, 6 Huayue Road, Hedong
District, Tianjin 300011, PR China; School of Public Health, Tianjin Medical
University, 22 Qi Xiang Tai Road, Heping District, Tianjin 300070, PR China.
Electronic address: [email protected].
(2)Tianjin Centers for Disease Control and Prevention, 6 Huayue Road, Hedong
District, Tianjin 300011, PR China.
(3)School of Public Health, Tianjin Medical University, 22 Qi Xiang Tai Road,
Heping District, Tianjin 300070, PR China.
(4)Department of Environmental Health and MOE Key Lab of Environment and Health,
School of Public Health, Tongji Medical College, Huazhong University of Science
and Technology, 13 Hangkong Road, Hubei, Wuhan 430030, PR China.
(5)Department of Environmental Health and MOE Key Lab of Environment and Health,
School of Public Health, Tongji Medical College, Huazhong University of Science
and Technology, 13 Hangkong Road, Hubei, Wuhan 430030, PR China. Electronic
address: [email protected].
In many regions, excessive fluoride and excessive iodide coexist in groundwater,
which may lead to biphasic hazards to human thyroid. To explore fluoride-induced
thyroid cytotoxicity and the mechanism underlying the effects of excessive iodide
on fluoride-induced cytotoxicity, a thyroid cell line (Nthy-ori 3-1) was exposed
to excessive fluoride and/or excessive iodide. Cell viability, lactate
dehydrogenase (LDH) leakage, reactive oxygen species (ROS) formation, apoptosis,
and the expression levels of inositol-requiring enzyme 1 (IRE1) pathway-related
molecules were detected. Fluoride and/or iodide decreased cell viability and
increased LDH leakage and apoptosis. ROS, the expression levels of
glucose-regulated protein 78 (GRP78), IRE1, C/EBP homologous protein (CHOP), and
spliced X-box-binding protein-1 (sXBP-1) were enhanced by fluoride or the
combination of the two elements. Collectively, excessive fluoride and excessive
iodide have detrimental influences on human thyroid cells. Furthermore, an
antagonistic interaction between fluoride and excessive iodide exists, and
cytotoxicity may be related to IRE1 pathway-induced apoptosis.
Copyright © 2014. Published by Elsevier B.V.



12. Chemosphere. 2015 Feb;120:299-304. doi: 10.1016/j.chemosphere.2014.07.011. Epub
2014 Aug 24.
Toxicity of tetramethylammonium hydroxide to aquatic organisms and its
synergistic action with potassium iodide.
Mori IC(1), Arias-Barreiro CR(2), Koutsaftis A(2), Ogo A(2), Kawano T(3),
Yoshizuka K(3), Inayat-Hussain SH(4), Aoyama I(2).
(1)Institute of Plant Science and Resources, Okayama University, Kurashiki
710-0046, Japan. Electronic address: [email protected].
(2)Institute of Plant Science and Resources, Okayama University, Kurashiki
710-0046, Japan.
(3)School of International Environmental Science, The University of Kitakyushu,
Kitakyushu 808-0135, Japan.
(4)Faculty of Health Sciences, Univerisiti Kebangsaan Malaysia, Kuala Lumpur,
Malaysia.
The aquatic ecotoxicity of chemicals involved in the manufacturing process of
thin film transistor liquid crystal displays was assessed with a battery of four
selected acute toxicity bioassays. We focused on tetramethylammonium hydroxide
(TMAH, CAS No. 75-59-2), a widely utilized etchant. The toxicity of TMAH was low
when tested in the 72 h-algal growth inhibition test (Pseudokirchneriellia
subcapitata, EC50=360 mg L(-1)) and the Microtox® test (Vibrio fischeri, IC50=6.4
g L(-1)). In contrast, the 24h-microcrustacean immobilization and the 96 h-fish
mortality tests showed relatively higher toxicity (Daphnia magna, EC50=32 mg
L(-1) and Oryzias latipes, LC50=154 mg L(-1)). Isobologram and mixture toxicity
index analyses revealed apparent synergism of the mixture of TMAH and potassium
iodide when examined with the D. magna immobilization test. The synergistic
action was unique to iodide over other halide salts i.e. fluoride, chloride and
bromide. Quaternary ammonium ions with longer alkyl chains such as
tetraethylammonium and tetrabutylammonium were more toxic than TMAH in the D.
magna immobilization test.
Copyright © 2014 Elsevier Ltd. All rights reserved.


13. J Invest Dermatol. 1981 May;76(5):381-3.
Sterile cutaneous pustules: a manifestation of primary irritancy? Identification
of contact pustulogens.
Wahlberg JE, Maibach HI.
An animal model (the rabbit) was used to define which of 8 chemicals caused
pustule formation on topical application. Large occlusive chambers (diameter 12
mm), petrolatum as the vehicle and wrapping contributed to efficient occlusion
and pustulation. Sodium lauryl sulfate and mecuric chloride gave reproducible
results and clear dose-responses indicating that this pustulation is an
expression of primary irritancy. Ammonium fluoride pustulation was not
reproducible; croton oil pustules were more difficult to evaluate due to
simultaneous erythema and edema. Sodium arsentate, nickel sulfate and potassium
iodide pustules developed at sites where the skin barriers had been damaged by a
stab injury. Benzalkonium chloride caused yellow staining and edema but not
pustules. Because of lack of epidemiologic data, we do not know how frequently
similar findings occur in man.

 

[BearWithMe]

Early in life, dental x-rays would be the most common cause of damage. Fluoride, lithium, and excess or deficient iodine also cause specific damage or suppression.

RP: "Very large doses of potassium iodide used to be used for certain inflammations or infections, but its effects haven’t been understood. The small amount of iodide added to salt has been reported in more than 70 studies to damage the thyroid gland, even increasing thyroid cancer."

Spoiler: STUDIES HE SHARED

1. Food Chem Toxicol. 2000 Sep;38(9):773-81.
Studies on the carcinogenicity of potassium iodide in F344 rats.
Takegawa K(1), Mitsumori K, Onodera H, Shimo T, Kitaura K, Yasuhara K, Hirose M,
Takahashi M.
(1)Division of Pathology, National Institute of Health Sciences, 1-18-1 Kamiyoga,
Setagaya-ku, 158-8501, Tokyo, Japan.
A chronic toxicity and carcinogenicity study, in which male and female F344/DuCrj
rats were given potassium iodide (KI) in the drinking water at concentrations of
0, 10, 100 or 1000 ppm for 104 weeks, and a two-stage carcinogenicity study of
application at 0 or 1000 ppm for 83 weeks following a single injection of
N-bis(2-hydroxypropyl)nitrosamine (DHPN), were conducted. In the former, squamous
cell carcinomas were induced in the salivary glands of the 1000 ppm group, but no
tumors were observed in the thyroid. In the two-stage carcinogenicity study,
thyroidal weights and the incidence of thyroid tumors derived from the follicular
epithelium were significantly increased in the DHPN+KI as compared with the DHPN
alone group. The results of our studies suggest that excess KI has a thyroid
tumor-promoting effect, but KI per se does not induce thyroid tumors in rats. In
the salivary gland, KI was suggested to have carcinogenic potential via an
epigenetic mechanism, only active at a high dose.

3. Jpn J Cancer Res. 1998 Feb;89(2):105-9.
Induction of squamous cell carcinomas in the salivary glands of rats by potassium
iodide.
Takegawa K(1), Mitsumori K, Onodera H, Yasuhara K, Kitaura K, Shimo T, Takahashi
M.
(1)Division of Pathology, National Institute of Health Sciences, Tokyo.
In a 2-year carcinogenicity study of potassium iodide (KI) in F344/DuCrj rats,
squamous cell carcinomas (SCCs) were observed in the salivary glands of 4/40
males and 3/40 females receiving 1000 ppm KI in the drinking water. Ductular
proliferation with lobular atrophy was observed at high incidence in the
submandibular glands of the high-dose animals, and squamous metaplasia was
frequently evident within the proliferative ductules and the larger interlobular
ducts. A transition from metaplasia to SCC was apparent. The results suggest that
squamous metaplasia in proliferative ductules, occurring secondarily to lobular
impairment induced by KI, may develop into SCCs via a non-genotoxic,
proliferation-dependent mechanism.

2. Endocrinology. 2000 Feb;141(2):598-605.
Iodide excess induces apoptosis in thyroid cells through a p53-independent
mechanism involving oxidative stress.
Vitale M(1), Di Matola T, D'Ascoli F, Salzano S, Bogazzi F, Fenzi G, Martino E,
Rossi G.
(1)Dipartimento di Biologia e Patologia Cellulare e Molecolare, Università
Federico II, Naples, Italy. [email protected]
Thyroid toxicity of iodide excess has been demonstrated in animals fed with an
iodide-rich diet; in vitro iodide is cytotoxic, inhibits cell growth, and induces
morphological changes in thyroid cells of some species. In this study, we
investigated the effect of iodide excess in an immortalized thyroid cell line
(TAD-2) in primary cultures of human thyroid cells and in cells of nonthyroid
origin. Iodide displayed a dose-dependent cytotoxicity in both TAD-2 and primary
thyroid cells, although at different concentrations, whereas it had no effect on
cells of nonthyroid origin. Thyroid cells treated with iodide excess underwent
apoptosis, as evidenced by morphological changes, plasma membrane
phosphatidylserine exposure, and DNA fragmentation. Apoptosis was unaffected by
protein synthesis inhibition, whereas inhibition of peroxidase enzymatic activity
by propylthiouracil completely blocked iodide cytotoxicity. During KI treatment,
reactive oxygen species were produced, and lipid peroxide levels increased
markedly. Inhibition of endogenous p53 activity did not affect the sensitivity of
TAD-2 cells to iodide, and Western blot analysis demonstrated that p53, Bcl-2,
Bcl-XL, and Bax protein expression did not change when cells were treated with
iodide. These data indicate that excess molecular iodide, generated by oxidation
of ionic iodine by endogenous peroxidases, induces apoptosis in thyroid cells
through a mechanism involving generation of free radicals. This type of apoptosis
is p53 independent, does not require protein synthesis, and is not induced by
modulation of Bcl-2, Bcl-XL, or Bax protein expression.


4. Toxicol Pathol. 1994 Jan-Feb;22(1):23-8.
Effects of a six-week exposure to excess iodide on thyroid glands of growing and
nongrowing male Fischer-344 rats.
Kanno J(1), Nemoto T, Kasuga T, Hayashi Y.
(1)Department of Pathology, Faculty of Medicine, Tokyo Medical and Dental
University, Japan.
A 6-wk exposure to excess iodide intake (EII) via drinking water (260 mg
potassium iodide/L) demonstrated different effects on growing (4-wk old) and
nongrowing (45-wk old) male Fischer-344 rats. In growing rats, EII induced a
significant increase in thyroid weight, pituitary weight, serum
thyroid-stimulating hormone (TSH), and thyroxine (T4). The labeling index (LI) of
thyroid follicular cells was slightly increased, although not statistically
significant. Histologically, an increase in follicular cell height, an increase
in colloid accumulation, and evidence of colloid absorption were noted. The
effect of bovine TSH (bTSH) and protirelin tartrate (TRH-t) on LI was
significantly augmented by EII. In nongrowing rats, EII induced a significant
increase in thyroid weight and serum T4 but no increase in pituitary weight,
serum TSH, and the LI of follicular cells. Histologically, an increase in colloid
accumulation was found in small follicles. EII did not augment the effect of bTSH
and TRH-t on the LI of follicular cells. This study suggests that growing rats
are still susceptible to acute hypothyroidism even after 6 wk of continuous
exposure to excess iodide, whereas nongrowing rats are refractory within an
equivalent treatment period.


5. Food Chem Toxicol. 1984 Dec;22(12):963-70.
Developmental toxicity and psychotoxicity of potassium iodide in rats: a case for
the inclusion of behaviour in toxicological assessment.
Vorhees CV, Butcher RE, Brunner RL.
Potassium iodide (KI) was fed to male and female rats before and during breeding,
to females only during gestation and lactation, and to their offspring after
weaning (day 21 after birth) through to day 90, at levels of 0, 0.025, 0.05 or
0.1% (w/w) of the diet. Dams in a fifth group (positive controls) were given 4
mg/kg ip of the anti-mitotic/cytotoxic drug 5-azacytidine on day 17 of gestation.
All offspring were reared by their natural dams and were evaluated blind with
respect to treatment in a battery of standardized behavioural tests between 3 and
90 days of age. KI produced no significant reductions in parental body weight or
food consumption, though it significantly reduced litter size and increased
offspring mortality at the highest dose, and decreased weight gain at the two
highest doses throughout the first 90 days after birth. Functionally, KI delayed
auditory startle at the two highest doses, delayed olfactory orientation to the
home-cage scent at the middle dose and decreased female running-wheel activity at
all dose levels. In rats killed on day 90 after birth KI reduced brain and body
weight at a dose of 0.1% of the diet, and reduced body but not brain weight at a
dose of 0.05% of the diet. No significant effect was found on absolute or
relative thyroid weight at 90 days of age. Several additional behavioural effects
were observed in the low-dose KI group, but because these effects were not
dose-dependent, they were not regarded as reliable. 5-Azacytidine produced
evidence of substantially greater developmental toxicity than KI. It was
concluded that KI produced evidence of developmental toxicity consistent with a
picture of impaired thyroid function. The inclusion of tests of functional
development added useful evidence to the overall picture of KI developmental
toxicity.


6. J Allergy Clin Immunol. 1980 Sep;66(3):177-8.
A time to abandon the use of iodides in the management of pulmonary diseases.
Hendeles L, Weinberger M.


7. Endocrinol Jpn. 1975 Oct;22(5):389-97.
The effect of iodide administration on hog thyroid gland and the composition of
thyroglobulin and 27-S iodoprotein.
Tarutani O, Kondo T, Horiguchi-Sho K.
The effect of excess iodide on hog thyroid gland has been examined with regard to
the change in the chemical composition of thyroglobulin and in the accumulation
of 27-S iodoprotein by the in vivo treatment of hogs with iodide for various
lengths of time. The iodine content of thyroglobulin was either unchanged by
short term administration of excess iodide, or somewhat lowered. However, the
iodine content as well as the total amount of thyroglobulin increased in the
glands enlarged by prolonged treatment with iodide. The iodine highest reached
1.17% of the protein on an average. On the other hand, 27-S iodoprotein decreased
and finally disappeared after the chronic treatment. Monoiodotyrosine and
diiodotyrosine increased in parallel with the increase in the iodine content
(0.15 to 1.17%) caused by the iodide treatment, while thyroxine increased but
reached a plateau at the level of three residues per mole of thyroglobulin, and
no change was observed even in the proteins with the higher iodine content than
0.75%. Proteolytic activity measured by amino acid release from the thyroid
protein was depressed by the chronic treatment. On the other hand, the amount of
iodocompound released by the autoproteolysis, which may reflect hormone
secretion, increased, possibly because of the marked increase in the iodine
content of thyroglobulin.


8. Am J Vet Res. 1973 Jan;34(1):65-70.
Experimentally induced iodide toxicosis in lambs.
McCauley EH, Linn JG, Goodrich RD.



9. Toxicol Appl Pharmacol. 1966 Mar;8(2):185-92.
The toxicology of potassium and sodium iodates. 3. Acute and subacute oral
toxicity of potassium iodate in dogs.
Webster SH, Stohlman EF, Highman B.



10. Clin Toxicol (Phila). 2013 Jul;51(6):521. doi: 10.3109/15563650.2013.804549. Epub
2013 May 23.
Regional centers: added value to poison center surveillance.
Durigon M, Kosatsky T.
Comment on
Clin Toxicol (Phila). 2013 Jan;51(1):41-6.



11. Environ Toxicol Pharmacol. 2014 Jul;38(1):332-40. doi:
10.1016/j.etap.2014.06.008. Epub 2014 Jun 27.
The effects and underlying mechanism of excessive iodide on excessive
fluoride-induced thyroid cytotoxicity.
Liu H(1), Zeng Q(2), Cui Y(2), Yu L(3), Zhao L(2), Hou C(2), Zhang S(4), Zhang
L(2), Fu G(2), Liu Y(3), Jiang C(4), Chen X(4), Wang A(5).
(1)Tianjin Centers for Disease Control and Prevention, 6 Huayue Road, Hedong
District, Tianjin 300011, PR China; School of Public Health, Tianjin Medical
University, 22 Qi Xiang Tai Road, Heping District, Tianjin 300070, PR China.
Electronic address: [email protected].
(2)Tianjin Centers for Disease Control and Prevention, 6 Huayue Road, Hedong
District, Tianjin 300011, PR China.
(3)School of Public Health, Tianjin Medical University, 22 Qi Xiang Tai Road,
Heping District, Tianjin 300070, PR China.
(4)Department of Environmental Health and MOE Key Lab of Environment and Health,
School of Public Health, Tongji Medical College, Huazhong University of Science
and Technology, 13 Hangkong Road, Hubei, Wuhan 430030, PR China.
(5)Department of Environmental Health and MOE Key Lab of Environment and Health,
School of Public Health, Tongji Medical College, Huazhong University of Science
and Technology, 13 Hangkong Road, Hubei, Wuhan 430030, PR China. Electronic
address: [email protected].
In many regions, excessive fluoride and excessive iodide coexist in groundwater,
which may lead to biphasic hazards to human thyroid. To explore fluoride-induced
thyroid cytotoxicity and the mechanism underlying the effects of excessive iodide
on fluoride-induced cytotoxicity, a thyroid cell line (Nthy-ori 3-1) was exposed
to excessive fluoride and/or excessive iodide. Cell viability, lactate
dehydrogenase (LDH) leakage, reactive oxygen species (ROS) formation, apoptosis,
and the expression levels of inositol-requiring enzyme 1 (IRE1) pathway-related
molecules were detected. Fluoride and/or iodide decreased cell viability and
increased LDH leakage and apoptosis. ROS, the expression levels of
glucose-regulated protein 78 (GRP78), IRE1, C/EBP homologous protein (CHOP), and
spliced X-box-binding protein-1 (sXBP-1) were enhanced by fluoride or the
combination of the two elements. Collectively, excessive fluoride and excessive
iodide have detrimental influences on human thyroid cells. Furthermore, an
antagonistic interaction between fluoride and excessive iodide exists, and
cytotoxicity may be related to IRE1 pathway-induced apoptosis.
Copyright © 2014. Published by Elsevier B.V.



12. Chemosphere. 2015 Feb;120:299-304. doi: 10.1016/j.chemosphere.2014.07.011. Epub
2014 Aug 24.
Toxicity of tetramethylammonium hydroxide to aquatic organisms and its
synergistic action with potassium iodide.
Mori IC(1), Arias-Barreiro CR(2), Koutsaftis A(2), Ogo A(2), Kawano T(3),
Yoshizuka K(3), Inayat-Hussain SH(4), Aoyama I(2).
(1)Institute of Plant Science and Resources, Okayama University, Kurashiki
710-0046, Japan. Electronic address: [email protected].
(2)Institute of Plant Science and Resources, Okayama University, Kurashiki
710-0046, Japan.
(3)School of International Environmental Science, The University of Kitakyushu,
Kitakyushu 808-0135, Japan.
(4)Faculty of Health Sciences, Univerisiti Kebangsaan Malaysia, Kuala Lumpur,
Malaysia.
The aquatic ecotoxicity of chemicals involved in the manufacturing process of
thin film transistor liquid crystal displays was assessed with a battery of four
selected acute toxicity bioassays. We focused on tetramethylammonium hydroxide
(TMAH, CAS No. 75-59-2), a widely utilized etchant. The toxicity of TMAH was low
when tested in the 72 h-algal growth inhibition test (Pseudokirchneriellia
subcapitata, EC50=360 mg L(-1)) and the Microtox® test (Vibrio fischeri, IC50=6.4
g L(-1)). In contrast, the 24h-microcrustacean immobilization and the 96 h-fish
mortality tests showed relatively higher toxicity (Daphnia magna, EC50=32 mg
L(-1) and Oryzias latipes, LC50=154 mg L(-1)). Isobologram and mixture toxicity
index analyses revealed apparent synergism of the mixture of TMAH and potassium
iodide when examined with the D. magna immobilization test. The synergistic
action was unique to iodide over other halide salts i.e. fluoride, chloride and
bromide. Quaternary ammonium ions with longer alkyl chains such as
tetraethylammonium and tetrabutylammonium were more toxic than TMAH in the D.
magna immobilization test.
Copyright © 2014 Elsevier Ltd. All rights reserved.


13. J Invest Dermatol. 1981 May;76(5):381-3.
Sterile cutaneous pustules: a manifestation of primary irritancy? Identification
of contact pustulogens.
Wahlberg JE, Maibach HI.
An animal model (the rabbit) was used to define which of 8 chemicals caused
pustule formation on topical application. Large occlusive chambers (diameter 12
mm), petrolatum as the vehicle and wrapping contributed to efficient occlusion
and pustulation. Sodium lauryl sulfate and mecuric chloride gave reproducible
results and clear dose-responses indicating that this pustulation is an
expression of primary irritancy. Ammonium fluoride pustulation was not
reproducible; croton oil pustules were more difficult to evaluate due to
simultaneous erythema and edema. Sodium arsentate, nickel sulfate and potassium
iodide pustules developed at sites where the skin barriers had been damaged by a
stab injury. Benzalkonium chloride caused yellow staining and edema but not
pustules. Because of lack of epidemiologic data, we do not know how frequently
similar findings occur in man.

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