Total oxidant/antioxidant status in sera of patients with thyroid cancers

Department of Oncology, Mianyang Central Hospital, Mianyang, Sichuan Province, China.
Endocrine Related Cancer (Impact Factor: 4.81). 12/2011; 18(6):773-82. DOI: 10.1530/ERC-11-0230
Source: PubMed


Oxidative stress is considered to be involved in the pathophysiology of all cancers. In order to evaluate the total oxidant/antioxidant status in patients with thyroid cancer and to investigate the relationship between oxidative stress parameters and serum thyroid profiles among thyroid cancer patients and various controls, we determined oxidative status including total antioxidant status (TAS) and total oxidant status (TOS) and calculation of oxidative stress index (OSI) in sera in 82 thyroid cancer patients, 56 benign thyroid disease patients, and 50 healthy controls. It was found that serum TAS levels were significantly lower in patients with thyroid cancer than in controls (P<0.001), while serum TOS levels and OSI values were significantly higher (both P<0.001) in the cancer patients. No significant correlations were observed between various oxidative stress markers and thyroid profiles in either the thyroid cancer patients or the controls. Receiver operating characteristic curve analysis demonstrated that OSI was the best indicator for distinguishing cancer patients from benign thyroid diseased or healthy controls, followed by TOS and TAS. Risk estimate statistics also indicated that TOS and/or OSI were good risk factors to discriminate patients with thyroid cancer from two controls. These findings suggested that oxidants are increased and antioxidants are decreased in patients with thyroid cancer. OSI may be a more useful oxidative stress biomarker than TAS and TOS for monitoring the clinical status of thyroid cancer patients.

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    • "Recently, attention has been focused on the role of oxidative stress and reactive oxygen species (ROS) production in neoplastic transformation and progression (Duracková 2010). Strong evidence suggests a close relationship even between oxidative stress and thyroid cancer (Wang et al. 2011, Xing 2012), encouraging testing of antioxidant molecules as potential novel targeted therapeutics. Many reports have stated the ability of oleuropein (OLE) and its derivatives, seco-phenolic compounds present in considerable amounts in olive leaves, drupes, and virgin olive oils, to scavenge ROS (Visioli et al. 2002, El & Karakaya 2009, Cicerale et al. 2010) and inhibit the proliferation of several tumor cell lines (Hamdi & Castellon 2005, El & Karakaya 2009, Goulas et al. 2009, Cicerale et al. 2010, Bulotta et al. 2011). "
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    ABSTRACT: The olive tree phenolic components oleuropein and its derivatives have shown many biological properties, so representing promising novel therapeutics for the treatment of several diseases, including neoplasia. In this study we evaluated the activities of oleuropein (OLE) and its peracetylated derivative (peracetylated oleuropein, Ac-OLE), against two thyroid tumour cell lines which host genotypic alterations detected in human papillary thyroid cancer. TPC-1 and BCPAP cells were treated with OLE and Ac-OLE, and the effects on viability evaluated by MTT, cell counting and Trypan blue exclusion assays. Antioxidant effects were analyzed by measuring the radical oxygen species (ROS) in basal conditions and after treatment with hydrogen peroxide (H2O2). Activity of MAP kinase and PI3k-Akt signalling pathways were evaluated by examining the levels of phosphorylated ERK and Akt by western blot. We found that OLE inhibited significantly the proliferation of both cell lines. This effect was paralleled by a reduction of basal phospho-Akt and phospho-ERK levels and H2O2-induced ROS levels. A stronger effect was elicited by Ac-OLE either in inhibiting cell growth or as antioxidant, in particular on BCPAP cells. Our results demonstrate that OLE and especially Ac-OLE inhibit in vitro thyroid cancer cell proliferation acting on growth promoting signal pathways, as well as exerting antioxidant effects. Further studies will reveal the potential application as novel targeted therapeutics in thyroid cancer.
    Journal of Molecular Endocrinology 05/2013; 51(1). DOI:10.1530/JME-12-0241 · 3.08 Impact Factor
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    • "The results, obtained in humans and in animal models, suggest that oxidative damage in the thyroid, especially this associated with thyroid cancer, is accompanied by increased activities of antioxidative enzymes or increased production of antioxidants, what – probably – represents the defence mechanism [27]. "
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    ABSTRACT: Whereas oxidative reactions occur in all tissues and organs, the thyroid gland constitutes such an organ, in which oxidative processes are indispensable for thyroid hormone synthesis. It is estimated that huge amount of reactive oxygen species, especially of hydrogen peroxide (H2O2), are produced in the thyroid under physiological conditions, justifying the statement that the thyroid gland is an organ of "oxidative nature". Apart from H2O2, also other free radicals or reactive species, formed from iodine or tyrosine residues, participate in thyroid hormone synthesis. Under physiological conditions, there is a balance between generation and detoxification of free radicals. Effective protective mechanisms, comprising antioxidative molecules and the process of compartmentalization of potentially toxic molecules, must have been developed in the thyroid to maintain this balance. However, with additional oxidative abuse caused by exogenous or endogenous prooxidants (ionizing radiation being the most spectacular), increased damage to macromolecules occurs, potentially leading to different thyroid diseases, cancer included.
    Thyroid Research 12/2012; 5(1):25. DOI:10.1186/1756-6614-5-25
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    • "There is, nevertheless, a very recent report of a case of Hürthle cell carcinoma of the thyroid in a patient with Cowden syndrome carrying both a 10q23 and a mitochondrial DNA (mtDNA) germline mutation (Pradella et al. 2011). The high prevalence of Hürthle cell transformation in thyroid lesions may reflect the high oxidative stress and reactive oxygen species (ROS) production in thyroid cells, during normal iodine and thyroid hormone metabolism (Wang et al. 2011, Xing 2012). This high ROS levels can result in mutagenic genetic events, namely in mtDNA, leading to mitochondrial dysfunction (Wallace 1999). "
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    ABSTRACT: The biology and the genetics of Hürthle cell tumors are reviewed starting from the characterization and differential diagnosis of the numerous benign and malignant, neoplastic and nonneoplastic lesions of the thyroid in which Hürthle cell transformation is frequently observed. The clinicopathologic and molecular evidence obtained from the comparative study of the aforementioned conditions indicate that Hürthle cell appearance represents a phenotype that is superimposed on the genotypic and conventional histopathologic features of the tumors. Hürthle cell tumors differ from their non-Hürthle counterparts regarding the prevalence of large deletions of mitochondrial DNA (mtDNA), mutations of mtDNA genes coding for oxidative phosphorylation (OXPHOS) proteins (namely mutations of complex I subunit genes) and mutations of nuclear genes coding also for mitochondrial OXPHOS proteins. Such mitochondrial alterations lead to energy production defects in Hürthle cell tumors; the increased proliferation of mitochondria may reflect a compensatory mechanism for such defects and is associated with the overexpression of factors involved in mitochondrial biogenesis. The mitochondrial abnormalities are also thought to play a major role in the predisposition for necrosis instead of apoptosis which seems to be blocked in most Hürthle cell tumors. Finally, the results obtained in experimental models using cybrid cell lines and the data obtained from histopathologic and molecular studies of familial Hürthle cell tumors are used, together with the aforementioned genetic and epigenetic alterations, to progress in the understanding of the mechanisms through which mitochondrial abnormalities may be involved in the different steps of thyroid carcinogenesis, from tumor initiation to metastization.
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