Department of Clinical and Experimental Medicine, University of Pisa, I‑56126 Pisa, Italy.
Department of Translational Research of New Technologies in Medicine and Surgery, University of Pisa, I‑56126 Pisa, Italy.
Mol Med Rep. 2018 May;17(5):7415-7420. doi: 10.3892/mmr.2018.8764. Epub 2018 Mar 16.
Recently it has been hypothesized that vanadium serves a carcinogenic role in the thyroid. However, to date, no in vivo or in vitro studies have evaluated thyroid disruption in humans and/or animals following exposure to vanadium. The present study evaluated the effect of vanadium pentoxide (V2O5) on cell viability and proliferation, and chemokine (C‑X‑C motif) ligand (CXCL)8 and CXCL11 secretion in normal thyrocytes. The results demonstrated that V2O5 had no effect on thyroid follicular cell viability and proliferation. However, V2O5 was able to induce the secretion of CXCL8 and CXCL11 chemokines from thyrocytes. Notably, V2O5 synergistically increased the effect of the interferon (IFN)‑γ on CXCL11 secretion. In addition, V2O5 synergistically increased the effect of tumor necrosis factor‑α on CXCL8 secretion, and abolished the inhibitory effect of IFN‑γ. Overall this induction of CXCL8 and CXCL11 secretion may lead to the induction and perpetuation of an inflammatory reaction in the thyroid. Further studies are now required to evaluate thyroid function and nodule development in subjects who are occupationally exposed, or living in polluted areas.
最近有人假设，钒在甲状腺中具有致癌作用。然而，迄今为止，尚无研究评估过人类和/或动物在接触钒后甲状腺功能紊乱的情况。本研究评估了五氧化二钒（V2O5）对正常甲状腺细胞活力和增殖的影响，以及趋化因子（C-X-C 基序）配体（CXCL）8 和 CXCL11 的分泌。结果表明，V2O5 对甲状腺滤泡细胞活力和增殖没有影响。然而，V2O5 能够诱导甲状腺细胞分泌 CXCL8 和 CXCL11 趋化因子。值得注意的是，V2O5 可协同增强干扰素（IFN）-γ对 CXCL11 分泌的作用。此外，V2O5 协同增强肿瘤坏死因子-α对 CXCL8 分泌的作用，并消除了 IFN-γ的抑制作用。总的来说，这种 CXCL8 和 CXCL11 分泌的诱导可能导致甲状腺中炎症反应的诱导和持续。现在需要进一步研究评估职业暴露或生活在污染地区的人群的甲状腺功能和结节形成。
