Inhibition of H2O2 production by iodoaldehydes in cultured dog thyroid cells

Panneels, Valérie; Bergen, Hugues Van den; Jacoby, C.; Braekman, Jean Claude; Sande, Jacqueline Van; Dumont, Jacques Emile; Boeynaems, Jean Marie

doi:10.1016/0303-7207(94)90110-4

Cited by 45 publications

(35 citation statements)

References 36 publications

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“…02 radical interaction with cellular iodide in the thyroid gland led to the generation of activated iodide free radical [13,14], which may go waste if not channelled to peroxidase-dependent and TSH-tuned iodination of the tyrosyl moiety in thyroglobulin. Activated iodide free radical may also result in structural damage to thyroid peroxidase or other thyroid proteins [30] and lipids [31].…”

Section: Resultsmentioning

confidence: 99%

Starvation induced hypothyroidism involves perturbations in thyroid superoxide‐sod system in pigeons

Prakash¹,

Laloraya

Kumar

1998

IUBMB Life

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: This study investigated the influence of starvation over seven days on avian thyroidal superoxide radical levels and superoxide dismutase activity profiles in the Indian rock pigeon Columba fivia intermeida, in relation with iodine metabolism. The serum thyroid hormone profile was assayed to correlate the thyroidal redox status with the circulating thyroid hormone levels. The spin-trapping results suggest a role for thyroidal superoxide anion (O2-) in causing a hypothyroid state in pigeons during long term energy withdrawal. Pigeons starved for 1 day generated superoxide and iodide free radicals in their thyroids, with a significant decrease in SOD activity. Regain of SOD activity in 2nd-and 3rd-day starved birds is marked by complete scavenging of radicals in the thyroid, suggesting the significance of SOD in thyroid glands as a potential antioxidant sink against reactive oxygen species, O2-. Resurgence of 02 radicals with a parallel decrease in SOD activity in the thyroid gland on 5th-and 7th-day of starvation provides evidence of disruption of homeostasis between pro-oxidant and antioxidant states, leading to oxidative stress in avian thyroid during long-term calorie crisis. Following starvation both thyroid hormones thyroxine (T4) and triiodothyronine (T3) decreased, putting pigeons in a hypothyroid state. We argue that oxidative inactivation of thyroid peroxidase and other thyroid proteins by radical attack during starvation invoked oxidative stress, which could be one of the factors responsible for the hypothyroid state in pigeons.

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Section: Resultsmentioning

confidence: 99%

Starvation induced hypothyroidism involves perturbations in thyroid superoxide‐sod system in pigeons

Prakash¹,

Laloraya

Kumar

1998

IUBMB Life

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“…Specifically, we suggest that the down-regulation of the two dehalogenases contributes to the mechanisms involved in the escape from the Wolff-Chaikoff effect. In addition to the effect on TSH responsiveness, Wolff-Chaikoff effect involves the inhibition in the expression of NIS and TPO, as well as inhibition in H 2 O 2 generation, all of which result in a negative impact on TH hormonogenesis (Cochaux et al 1987, Corvilain et al 1988, Laurent et al 1989, Panneels et al 1994, Uyttersprot et al 1997, Eng et al 1999. Paradoxically, for this inhibition to occur, it is mandatory that iodide uptake and/or organification remain intact; i.e.…”

Section: Discussionmentioning

confidence: 99%

Inhibition of intrathyroidal dehalogenation by iodide

Solís-S

Villalobos

Orozco

et al. 2010

Journal of Endocrinology

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Iodide is a trace element and a key component of thyroid hormones (TH). The availability of this halogen is the ratelimiting step for TH synthesis; therefore, thyroidal iodide uptake and recycling during TH synthesis are of major importance in maintaining an adequate supply. In the rat, the thyroid gland co-expresses a distinctive pair of intrathyroidal deiodinating enzymes: the thyroid iodotyrosine dehalogenase (tDh) and the iodothyronine deiodinase type 1 (ID1). In the present work, we studied the activity of these two dehalogenases in conditions of hypo-and hyperthyroidism as well as during acute and chronic iodide administration in both intact and hypophysectomized (HPX) rats. In order to confirm our observations, we also measured the mRNA levels for both dehalogenases and for the sodium/iodide symporter, the protein responsible for thyroidal iodide uptake. Our results show that triiodothyronine differentially regulates tDh and ID1 enzymatic activities, and that both acute and chronic iodide administration significantly decreases rat tDh and ID1 activities and mRNA levels. Conversely, both enzymatic activities increase when intrathyroidal iodide is pharmacologically depleted in TSH-replaced HPX rats. These results show a regulatory effect by iodide on the intrathyroidal dehalogenating enzymes and suggest that they contribute to the iodide-induced autoregulatory processes involved in the Wolff-Chaikoff effect.

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“…These effects are at least in part mediated by 2-iodohexadecanal (IHDA), a compound which is produced in dog thyrocytes incubated with iodide (in culture, this generation requires an exogenous H 2 O 2 generating system; see above) (62) and mimics the inhibitory effects of iodide on adenylyl cyclase (63) and cell function (64).…”

Section: Factors Acting On Cultured Dog Thyrocytes and The Signaling mentioning

confidence: 99%

“…As explained above, the protein iodinating capacity is low in dog thyrocyte primary cultures compared with the levels reached in dog thyroid tissue slices or freshly isolated follicles (14). In the different experimental systems, it is stimulated by TSH through cAMP (18,29 (64). The oxidation of glucose is stimulated by TSH (cAMP), Cch or TPA (66) in parallel with H 2 O 2 generation as a consequence of NADPH 2 oxidation by the H 2 O 2 generating and reducing systems (32).…”

Section: Regulation Of Dog Thyrocyte Functionmentioning

confidence: 99%