title: Vitamin E ameliorates iodine-induced cytotoxicity in thyroid.
abstract: Acute and excessive iodine supplementation leads to iodine-induced thyroid cytotoxicity. Excessive oxidative stress has been suggested to be one of the underlying mechanisms in the development of thyroid cytotoxicity. The aim of this study was to investigate whether vitamin E (VE), an important antioxidant, could ameliorate iodine-induced thyroid cytotoxicity. A goiter was induced in rats by feeding a low-iodine (LI) diet for 12 weeks. Involution of hyperplasia was obtained by administering a twofold physiological dose of iodine in feeding water with/without the supplementation of 25-, 50-, or 100-fold physiological dose of VE in the LI diet for 4 weeks. In iodine-supplemented rats, thyroid epithelial cell ultrastructure injuries remained and were more severe. Relative weights of iodine-induced involuting glands were significantly reduced compared with the goiter, but still higher than control. Immunohistochemistry indicated that the expression of 4-hydroxynonenal, 8-hydroxyguanine, peroxiredoxin 5, and CD68 in thyroid increased (P<0.01), whereas thioredoxin reductase 1 decreased (P<0.01). VE supplementation attenuated thyroid cytotoxicity induced by iodine. A 50-fold VE dose was optimal in attenuating twofold iodine-induced thyroid cytotoxicity. However, VE supplementation did not reduce the weight or relative weight of the iodine-induced involuting gland. These results show that excess iodine leads to thyroid damage and VE supplementation can partly ameliorate iodine-induced thyroid cytotoxicity.
authors.affiliation: The Endocrine Institute of China Medical University, Shenyang 110001, People’s Republic of China.
authors.forename: Jiashu
authors.initials: J
authors.lastname: Yu
authors.forename: Zhongyan
authors.initials: Z
authors.lastname: Shan
authors.forename: Wei
authors.initials: W
authors.lastname: Chong
authors.forename: Jinyuan
authors.initials: J
authors.lastname: Mao
authors.forename: Yuxiu
authors.initials: Y
authors.lastname: Geng
authors.forename: Caixia
authors.initials: C
authors.lastname: Zhang
authors.forename: Qian
authors.initials: Q
authors.lastname: Xing
authors.forename: Weiwei
authors.initials: W
authors.lastname: Wang
authors.forename: Ningna
authors.initials: N
authors.lastname: Li
authors.forename: Chenling
authors.initials: C
authors.lastname: Fan
authors.forename: Hong
authors.initials: H
authors.lastname: Wang
authors.forename: Hongmei
authors.initials: H
authors.lastname: Zhang
authors.forename: Weiping
authors.initials: W
authors.lastname: Teng
mesh_terms: D000818:Animals; D019587:Dietary Supplements; D007455:Iodine / Q000633:toxicity*; D009929:Organ Size; D018384:Oxidative Stress; D051381:Rats; D013959:Thyroid Diseases / Q000139:chemically induced* / Q000188:drug therapy; D013961:Thyroid Gland / Q000473:pathology; D016896:Treatment Outcome; D014810:Vitamin E / Q000627:therapeutic use*
chemical_list: D014810:Vitamin E; D007455:Iodine