Oxidative Stress and Anti-Oxidant Metabolites in Patients with Hyperthyroidism: Effect of Treatement

Bianchi, G; Solaroli, Erica; Zaccheroni, V.; Grossi, G.; Bargossi, A.; Melchionda, N; Marchesini, G.

doi:10.1055/s-2007-978808

Cited by 102 publications

(82 citation statements)

References 11 publications

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“…2A), the resident macrophages of the liver (29,39). In man, hyperthyroidism is characterized by significant changes in circulating parameters related to oxidative stress, including (i) higher levels of lipid peroxidation indicators (40)(41)(42)(43)(44)(45)(46)(47)(48)(49); (ii) enhancement in hydrogen peroxide and lipid hydroperoxide levels (49); and (iii) diminished levels of antioxidants such as a-tocopherol (41), coenzyme Q (44), ascorbic acid (41), and reduced thiols (42,46,50). These changes correlated with the enhancement in urinary lipid peroxidation products (40) and chemiluminescence response (51) and are either significantly reduced or normalized by thyrostatic therapy or antioxidant supplementation (40-46, 49, 50).…”

Section: T 3 -Induced Enhancement Of Liver O 2 Consumption and Oxidatmentioning

confidence: 99%

Hormetic responses of thyroid hormone calorigenesis in the liver: Association with oxidative stress

Videla

2010

IUBMB Life

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SummaryThyroid hormone (L-3,3 0 ,5-triiodothyronine, T 3 ) exerts calorigenic effects by accelerating mitochondrial O 2 consumption through transcriptional activation of respiratory genes, with consequent increased reactive oxygen species (ROS) production. In the liver, ROS generation occurs at different sites of hepatocytes and in the respiratory burst of Kupffer cells, triggering the activation of the transcription factors nuclear factor-jB, signal transducer and activator of transcription 3, and activating protein 1. Under these conditions, the redox upregulation of Kupffer cell-dependent expression of cytokines [tumor necrosis factor-a, interleukin (IL)-1, and IL-6] is achieved, which upon interaction with specific receptors in hepatocytes trigger the expression of antioxidant enzymes (manganese superoxide dismutase, inducible nitric oxide synthase), antiapoptotic proteins (Bcl-2), and acute-phase proteins (haptoglobin, b-fibrinogen). These responses and the promotion of hepatocyte and Kupffer cell proliferation observed represent hormetic effects re-establishing redox homeostasis, promoting cell survival, and protecting the liver against ischemia-reperfusion (IR) injury. It is proposed that hormesis underlying T 3 action may constitute a novel preconditioning strategy for IR injury during liver surgery in man or in liver transplantation using reduced-size grafts from living donors, considering that (i) with the exception of the controversial ischemic preconditioning, all other studied strategies have failed to reach the clinical setting and (ii) T 3 is a well-tolerated therapeutic agent that either lacks major adverse effects or has minimal and controlled side effects. IUBMBIUBMB Life, 62(6): [460][461][462][463][464][465][466] 2010

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Section: T 3 -Induced Enhancement Of Liver O 2 Consumption and Oxidatmentioning

confidence: 99%

Hormetic responses of thyroid hormone calorigenesis in the liver: Association with oxidative stress

Videla

2010

IUBMB Life

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“…There is supporting evidence that lipid peroxidation may play a role in the potential anticarcinogenic effect of other breast cancer factors, including soy (28,(181)(182)(183)(184)(185)(186)(187), marine n-3 fatty acids (46), thyroid diseases (188)(189)(190)(191)(192)(193)(194)(195)(196)(197)(198)(199)(200)(201)(202), green tea (203)(204)(205)(206)(207), vitamin D (208), calcium (209)(210)(211)(212), folate (213), and isothiocyanates (214)(215)(216)(217).…”

Section: Other Suspected Protective/risk Factors For Breast Cancermentioning

confidence: 99%

Role of Lipid Peroxidation in the Epidemiology and Prevention of Breast Cancer

Gago‐Dominguez

Castelao

Pike

et al. 2005

Cancer Epidemiology, Biomarkers &Amp; Prevention

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We have recently proposed a common mechanistic pathway by which obesity and hypertension lead to increased renal cell cancer risk. Our hypothesis posits lipid peroxidation, which is a principal mechanism in rodent renal carcinogenesis, as an intermediate step that leads to a final common pathway shared by numerous observed risks (including obesity, hypertension, smoking, oophorectomy/hysterectomy, parity, preeclampsia, diabetes, and analgesics) or protective factors (including oral contraceptive use and alcohol) for renal cell cancer [Cancer Causes Control 2002;13:287 -93]. During this exercise, we have noticed how certain risk factors for renal cell carcinoma are protective for breast cancer and how certain protective factors for renal cell carcinoma increase risk for breast cancer. Parity and oophorectomy, for example, are positively associated with renal cell carcinoma but are negatively associated with breast cancer. Similarly, obesity and hypertension are positively associated with renal cell carcinoma, but obesity is negatively associated with breast cancer in premenopausal women and hypertension during pregnancy is negatively associated with breast cancer. Furthermore, alcohol intake, negatively associated with renal cell carcinoma, is also positively associated with breast cancer. We propose here the possibility that lipid peroxidation may represent a protective mechanism in breast cancer. Although this runs counter to the conventional view that lipid peroxidation is a process that is harmful and carcinogenic, we present here the chemical and biological rationale, based on epidemiologic and biochemical data, which may deserve further consideration and investigation. (Cancer Epidemiol Biomarkers Prev 2005;14(12):2829 -39)

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“…At a systemic level, also in humans, hyperthyroidism has been associated with reduced circulating levels of alpha-tocopherol (Ademoglu et al, 1998;Bianchi et al, 1990) and Coenzyme Q 10 (Bianchi et al, 1990;Mancini et al, 1991). Coenzyme Q 10 showed a trend to increase in hypothyroidism (Mancini et al, 1991); it appeared to be a sensitive index of tissue effect of thyroid hormones, in situations in which drug interference, such as amiodarone (Mancini et al, 1989) or systemic illness inducing a low-T3 conditions (Mancini et al, 2005) complicate the interpretation of thyroid hormone levels.…”

Section: Thyroid Hormones and Oxidative Stressmentioning

confidence: 99%