Inhibition of goiter growth and of cyclic AMP formation in rat thyroid by 2-iodohexadecanal

Thomasz, Lisa; Oglio, Romina; Rivandeira, D. Toro; Dagrosa, María Alejandra; Jahn, Graciela A.; Piganataro, O.P.; Sartorio, G.; Pisarev, Mario A.; Juvenal, Guillermo

doi:10.1016/j.mce.2009.12.026

Cited by 17 publications

(12 citation statements)

References 36 publications

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“…4). In a manner similar to that observed here, 2-iodohexadeacanal (the major iodolipid in thyroid gland [41]) but not hexadecanal inhibited cell proliferation in a rat model of goiter [42]. Chlorinated lipids are potent signaling mediators: 2-ClHDA activates COX-2 [43] and is an inhibitor of eNOS biosynthesis [18].…”

Section: Discussionsupporting

confidence: 79%

Phloretin ameliorates 2-chlorohexadecanal-mediated brain microvascular endothelial cell dysfunction in vitro

Üllen

Fauler

Bernhart

et al. 2012

Free Radical Biology and Medicine

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2-Chlorohexadecanal (2-ClHDA), a chlorinated fatty aldehyde, is formed via attack on ether-phospholipids by hypochlorous acid (HOCl) that is generated by the myeloperoxidase–hydrogen peroxide–chloride system of activated leukocytes. 2-ClHDA levels are elevated in atherosclerotic lesions, myocardial infarction, and neuroinflammation. Neuroinflammatory conditions are accompanied by accumulation of neutrophils (an ample source of myeloperoxidase) in the brain. Microvessel damage by inflammatory mediators and/or reactive oxidants can induce blood–brain barrier (BBB) dysfunction, a pathological condition leading to cerebral edema, brain hemorrhage, and neuronal death. In this in vitro study we investigated the impact of 2-ClHDA on brain microvascular endothelial cells (BMVEC), which constitute the morphological basis of the BBB. We show that exogenously added 2-ClHDA is subject to rapid uptake and metabolism by BMVEC. Using C16 structural analogues of 2-ClHDA we found that the cytotoxic potential decreases in the following order: 2-ClHDA>hexadecanal>palmitic acid>2-ClHDA-dimethylacetal. 2-ClHDA induces loss of barrier function, mitochondrial dysfunction, apoptosis via activation of caspase 3, and altered intracellular redox balance. Finally we investigated potential protective effects of several natural polyphenols on in vitro BBB function. Of the compounds tested, phloretin almost completely abrogated 2-ClHDA-induced BMVEC barrier dysfunction and cell death. These data suggest that 2-ClHDA has the potential to induce BBB breakdown under inflammatory conditions and that phloretin confers protection in this experimental setting.

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Section: Discussionsupporting

confidence: 79%

Phloretin ameliorates 2-chlorohexadecanal-mediated brain microvascular endothelial cell dysfunction in vitro

Üllen

Fauler

Bernhart

et al. 2012

Free Radical Biology and Medicine

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“…Moreover it was shown that in the mammary gland, which organifies iodide (Arroyo-Helguera et al, 2006), the synthesis of IL-δ takes place (Aceves et al, 2009). On the contrary we have observed that 2-IHDA reproduces the effects of iodide on thyroid specific gene transcription (to be published elsewhere) while IL-δ had a moderate effect (Thomasz et al, 2010b). These results would indicate that 2-IHDA is the main compound in thyroid autoregulation while IL-δ has a broader effect and not restricted to the thyroid but this hypothesis remains to be elucidated.…”

Section: Discussionmentioning

confidence: 51%

“…It is important to remark that excess iodide does not alter TSH binding with its receptor (Uchimura et al, 1979) and that the growth inhibition by iodide occurs, at least, in part, at the level of the cAMP pathway (Pisarev and Itoiz, 1972). Moreover, previous in vitro (Panneels et al, 1994b) and in vivo (Thomasz et al, 2010b) studies showed that 2-IHDA inhibits cAMP formation.…”

Section: Discussionmentioning

confidence: 92%

Inhibitory effects of 2-iodohexadecanal on FRTL-5 thyroid cells proliferation

Thomasz

Coulonval

Salvarredi

et al. 2015

Molecular and Cellular Endocrinology

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“…As a therapeutic application of hexadecanal, it has been reported that injection of this chemical can prevent growth of goiter in rat. [14] After increasing the intracellular level of hexadecanal, fatty acyl-CoA reductase oxidizes this chemical to hexadecanoyl-CoA. This product can follow fatty acids oxidation pathway in cell and detoxifies in this pathway.…”

Section: Discussionmentioning

confidence: 99%

Comparative modeling of CCRL1, a key protein in masked immune diseases and virtual screening for finding inhibitor of this protein

Behjati¹,

Torktaz²,

Mohammadpour³

et al. 2012

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Human CCRL1 belongs to the family of silent chemokine receptors. This transmembrane protein plays a role in blunting function of chemokines through binding to them. This will attenuate immune responses. Interaction between CCRL1 and CCL21 determines this immune extinction. Thus inhibiting the action of this atypical chemokine seems to stimulate immune responses especially in the case of suppressed and immune deficient conditions. In this study we predicted 3D structure of CCRL1 using comparative modeling and Hiddebn Markov Model algorithm. Final predicted model optimized by Modeller v9.8 and minimized regarding energy level using UCSF chimera candidate version1.5.3. ClasPro webserver was used to find interacting residues between CCRL1 and CCL21. Interacting residues were used as target for chemical inhibitors by simulated docking study. For finding potential inhibitors, library of KEGG compounds screened and 97 obtained chemicals docked against interacting residues between CCRL1- CCL21 and MolDock was used as docking scoring function. Results indicated that Hexadecanal is a potential inhibitor of CCRL1- CCL21 interaction. Inhibition of this interaction will increase intercellular level of CCl21 and interaction between CCL21 and CCR7 causes immune potentiaiton.

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Inhibition of goiter growth and of cyclic AMP formation in rat thyroid by 2-iodohexadecanal

Cited by 17 publications

References 36 publications

Phloretin ameliorates 2-chlorohexadecanal-mediated brain microvascular endothelial cell dysfunction in vitro

Phloretin ameliorates 2-chlorohexadecanal-mediated brain microvascular endothelial cell dysfunction in vitro

Inhibitory effects of 2-iodohexadecanal on FRTL-5 thyroid cells proliferation

Comparative modeling of CCRL1, a key protein in masked immune diseases and virtual screening for finding inhibitor of this protein

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