Tumor Promoting Effect of Goitrogens on the Rat Thyroid

Kanno, Jun; Matsuoka, Chiaki; Furuta, Kyoko; Oda, Hiroshi; Miyajima, Hiroaki; Maekawa, Akihiko; Hayashi, Yuzo

doi:10.1177/019262339001800202

Cited by 56 publications

(33 citation statements)

References 28 publications

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“…As a quantitative index for diffuse morphologic changes induced in DHPN-untreated rat thyroids, the percentage of total thyroid area occupied by follicular epithelial cells designated as percentage of follicular tissue area (Yo FTA) was measured by a TAS-plus image analyzer (Leitz Wetzlar, West Germany). In general, a high percentage for FTA indicates depletion of colloid with follicular cellular hyperplasia, whereas a low percentage for FTA generally indicates colloid goiter (27).…”

Section: Histological and Histometrical Exaiiiiiiatioiimentioning

confidence: 98%

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Tumor-Promoting Effects of Both Iodine Deficiency and Iodine Excess in the Rat Thyroid

et al. 1992

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A B S T R A~Thyroid tumor-promoting effects of iodine deficiency and iodine excess were investigated in a rodent 2-stage model to estimate an optimal iodine intake range that would not effectively promote development of thyroid neoplasia. Six-week-old male F344 rats were given a single subcutaneous injection of 2,800 mg/ kg body weight N-bis(2-hydroxypropyI)-nitrosamine (DHPN) or saline vehicle, maintained on Remington's iodine-deficient diet (21 k 2 ng/g iodide), and supplemented with various amounts of potassium iodide up to 260 mg/liter in drinking water to generate conditions ranging from severe iodine deficiency to severe iodine excess. In DHPN-treated rats, both conditions significantly increased thyroid follicular tumorigenesis. In DHPN-untreated rats, iodine deficiency produced diffuse thyroid hyperplasia, characterized by small follicles with tall epithelium and reduced colloid, together with a decrease in thyroxine (T4) and an increase in thyroid-stimulating hormone (TSH). On the other hand, iodine excess produced colloid goiter, characterized by large follicles with flat epithelium and abundant colloid admixed with normal or small-sized follicles lined by cpithelium of normal height, together with normal serum T4 and slightly decreased TSH. These effects were directly proportional to the severity of iodine deficiency or extent of iodine excess and suggest that each condition has a different thyroid tumor promotion mechanism. Iodine intakes that showed the least tumor promotion were 2.6 and 9.7 pg/rat/day in this study. Promoting mechanisms and the problem of statistically estimating recommended daily iodine intake range are briefly discussed.

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Section: Histological and Histometrical Exaiiiiiiatioiimentioning

confidence: 98%

“…As previously reported (27), in order to keep correspondence with histological characteristics of human thyroid tumors (23), we classified rat thyroid > *. .…”

Section: Histological and Histometrical Exaiiiiiiatioiimentioning

confidence: 99%

Tumor-Promoting Effects of Both Iodine Deficiency and Iodine Excess in the Rat Thyroid

et al. 1992

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“…Although all of these compounds decrease serum T 4 concentrations, only PCN and PB are associated with increase in circulating concentrations of thyroid stimulating hormone (TSH) (Barter and Klaassen, 1994;Liu et al, 1995), which regulates thyroid hormone synthesis. Increased serum TSH concentrations are of concern because sustained increases in TSH have been associated with chemicals such as propylthiouracil and potassium percholorate that induce thyroid cancer in lab animals (Kanno et al, 1990;Hood et al, 1999). Thus, it would be of interest to determine which UGT isozyme(s) catalyze(s) the glucuronidation of thyroid hormones, and how xenobiotics induce UGT activities toward thyroid hormones.…”

Section: Chen Et Almentioning

confidence: 99%

NUCLEAR RECEPTOR, PREGNANE X RECEPTOR, IS REQUIRED FOR INDUCTION OF UDP-GLUCURONOSYLTRANSFERASES IN MOUSE LIVER BY PREGNENOLONE-16α-CARBONITRILE

Chen

Staudinger²,

Klaassen³

2003

Drug Metab Dispos

109

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This article is available online at http://dmd.aspetjournals.org ABSTRACT:The aim of this study was to determine the role of pregnane X receptor (PXR) in the induction of UDP-glucuronosyltransferases (UGTs) by pregnenolone-16␣-carbonitrile (PCN). Four-to sixmonth-old male wild-type and PXR-null mice received control or PCN-treated (1500 ppm) diet for 21 days. On day 22, livers were taken to prepare microsomes and total RNA to determine UGT activity and mRNA levels, respectively. In wild-type mice, PCN treatment significantly increased UGT activities toward bilirubin, 1-naphthol, chloramphenicol, thyroxine, and triiodothyronine. On control diet, the UGT activities toward the above substrates (except for 1-naphthol) in the PXR-null mice were significantly higher than those of wild-type mice. However, UGT activities in PXR-null mice were not increased by PCN. In agreement with the above findings, mRNA levels of mouse Ugt1a1 and Ugt1a9, which are involved in the glucuronidation of bilirubin and phenolic compounds, were increased about 100% in wild-type mice following PCN treatment, whereas the expression of Ugt1a2, 1a6, and 2b5 was not affected. In contrast, PCN treatment had no effect on the mRNA levels of these UGTs in PXR-null mice. Taken together, these results indicate that PCN treatment induces glucuronidation in mouse liver, and that PXR regulates constitutive and PCNinducible expression of some UGTs.

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“…According to epidemiological, clinical and experimental studies, both the dietary deficiency and excess of iodine have been associated with increased risk of thyroid carcinomas [5][6][7][8] . In this connection, the effect of salt water fish and shellfish consumption as a measure of iodine exposure has been discussed [9][10][11] .…”

Section: Introductionmentioning

confidence: 99%

Effect of long-term administration of arsenic (III) and bromine with and without selenium and iodine supplementation on the element level in the thyroid of rat

Kotyzová¹,

Eybl²,

Mihaljevič³

et al. 2005

Biomed Pap Med Fac Univ Palacky Olomouc Czech Repub

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The aim of this study was to evaluate the influence of arsenic and bromine exposure with or withour iodine and selenium supplementation on the element level in the thyroid of rats. Four major groups of Wistar female rats were fed with respective diets: group A -standard diet, group B -iodine rich diet (10 mg I/kg food), group C -selenium rich diet (1 mg Se/kg) and group D -iodine and selenium rich diet (as in group B and C). Each group was divided into four subgroups per 7 animals each receiving either NaAsO 2 ip (6.5 mg.kg -1 twice a week for two weeks and 3.25 mg.kg -1 for six weeks) or KBr in drinking water (58.8 mg.l -1 ) for 8 weeks or combined administration of both substances. Remaining subgroup served as controls. After 8 weeks thyroid glands were analyzed by ICP-MS for As, Br, Se, and I content. The exposition of rat to arsenic or bromine causes the accumulation of these elements in the thyroid gland (∼18 ppm of As, ∼90 ppm of Br) and significantly affects iodine and selenium concentration in the thyroid. In iodine and/or selenium supplemented rats the bromine intake into the thyroid was lowered to ∼50% of the level in unsupplemented animals. Also selenium thyroid level elevated due to KBr administration was lowered by iodine supplementation in the diet. The accumulation of arsenic in the thyroid was not influenced by selenium or iodine supplementation; however, As(III) administration increased iodine thyroid level and suppressed selenium thyroid level in selenium or iodine supplemented group of animals.

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Tumor Promoting Effect of Goitrogens on the Rat Thyroid

Cited by 56 publications

References 28 publications

Tumor-Promoting Effects of Both Iodine Deficiency and Iodine Excess in the Rat Thyroid

Tumor-Promoting Effects of Both Iodine Deficiency and Iodine Excess in the Rat Thyroid

NUCLEAR RECEPTOR, PREGNANE X RECEPTOR, IS REQUIRED FOR INDUCTION OF UDP-GLUCURONOSYLTRANSFERASES IN MOUSE LIVER BY PREGNENOLONE-16α-CARBONITRILE

Effect of long-term administration of arsenic (III) and bromine with and without selenium and iodine supplementation on the element level in the thyroid of rat

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