Article

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: 4.91). 12/2011; 18(6):773-82. DOI: 10.1530/ERC-11-0230
Source: PubMed

ABSTRACT 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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Available from: Jiafu Feng, Aug 22, 2015
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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.
    Endocrine Related Cancer 04/2012; 19(4):R131-47. DOI:10.1530/ERC-11-0354 · 4.91 Impact Factor
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    • "Although most of the mechanistic aspects or hypotheses discussed above regarding the role of OS in thyroid cancer remain to be directly tested, it seems to be convincing that high OS represents a new risk factor for thyroid cancer. It is thus tempting to propose that testing of OS, particularly in the form of total oxidant status and OS index as proposed by Wang et al. (2011), may be clinically useful in the risk assessment of thyroid nodules. "
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    ABSTRACT: Oxidative stress (OS) is a state of excessive free radicals and reactive metabolites among which the most important class is reactive oxygen species (ROS) - radicals derived from oxygen - as represented by the superoxide anion radical (O2(·-)) and its reactive metabolites, hydroxyl radical (·OH) and hydrogen peroxide (H(2)O(2)). In essence, OS represents an imbalance between the production of oxidants - ROS - and their elimination by antioxidative systems in the body. Many studies have linked OS to thyroid cancer by showing its association with abnormally regulated oxidative or antioxidative molecules. The study by Wang et al. in the December 2011 issue of Endocrine-Related Cancer (18, 773-782) further supports this relationship by demonstrating a high total oxidant status and OS index in thyroid cancer patients. The origin of ROS in thyroid cancer patients has not been defined, but thyroid cancer itself can be one since inflammation, a major event in it, is a classical source of ROS. ROS may in turn enhance the mitogen-activated protein (MAP) kinase and phosphatidylinositol-3-kinase (PI3K) pathways, forming a vicious cycle propelling thyroid tumorigenesis. Regardless of the mechanism, the clinical implication of the association of OS with thyroid cancer is severalfold: one, OS is a new risk factor for thyroid cancer; two, OS confers thyroid cancer patients an increased risk for cardiovascular diseases, degenerative neurological disorders, and other cancers that are classically associated with OS; and three, interference with OS may reduce this risk and be therapeutically beneficial to thyroid cancer itself in thyroid cancer patients. These interesting possibilities deserve further studies.
    Endocrine Related Cancer 12/2011; 19(1):C7-11. DOI:10.1530/ERC-11-0360 · 4.91 Impact Factor
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