Increased Lipid Peroxidation in Hyperthyroid Patients: Suppression by Propylthiouracil Treatment

Videla, Luis A.; Sir, Teresa; Wolff, Carlos

doi:10.3109/10715768809068553

Cited by 64 publications

(40 citation statements)

References 26 publications

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“…Accordingly, PTU has been shown to act as a highly efficient scavenger of OH radicals, to be a potent inhibitor of lipid peroxidation in model membranes (Hicks et al 1992) and to inhibit H 2 O 2 production in neutrophils (Imamura et al 1986) or Graves' retro-ocular fibroblasts (Heufelder et al 1992). It has also been observed that hyperthyroid patients treated with PTU have decreased serum MDA levels, suggesting that PTU may scavenge ROMs or may directly protect lipids from peroxidative attack (Videla et al 1988). In accordance with these results, in the present study tissue MDA was increased in the lung, liver, kidney and ileum of whole-body irradiated rats, indicating the presence of radiation-induced oxidative damage.…”

Section: Discussionmentioning

confidence: 99%

Propylthiouracil-induced hypothyroidism protects ionizing radiation-induced multiple organ damage in rats

Şener¹,

Kabasakal²,

Atasoy³

et al. 2006

Journal of Endocrinology

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The objective of this study was to examine the potential radioprotective properties of propylthiouracil (PTU)-induced hypothyroidism against oxidative organ damage induced by irradiation. Sprague-Dawley rats were pretreated with saline or PTU (10 mg/kg i.p.) for 15 days, and were then exposed to whole-body irradiation (800 cGy). A group of rats were decapitated at 6 h after exposure to irradiation, while another group was followed for 72 h after irradiation, during which saline or PTU injections were repeated once daily. Lung, liver, kidney and ileum samples were obtained for the determination of malondialdehyde (MDA; an index of lipid peroxidation) and glutathione (GSH, an antioxidant) levels, myeloperoxidase activity (MPO; an index of tissue neutrophil accumulation) and collagen contents, while oxidantinduced DNA fragmentation was evaluated in the ileal tissues. All tissues were also examined microscopically and assayed for the production of reactive oxidants using chemiluminescence (CL). Lactate dehydrogenase (LDH), an indicator of tissue damage, and tumour necrosis factor-(TNF ) were assayed in serum samples. Irradiation caused a significant decrease in GSH level, which was accompanied by significant increases in MDA levels, MPO activity, CL levels and collagen content of the tissues studied (P<0·05-0·001). Similarly, serum TNF and LDH were elevated in the irradiated rats as compared with the control group. On the other hand, PTU treatment reversed all these biochemical indices, as well as histopathological alterations induced by irradiation. Our results suggested that PTU-induced hypothyroidism reduces oxidative damage in the lung, hepatic, renal and ileal tissues probably due to hypometabolism, which is associated with decreased production of reactive oxygen metabolites and enhancement of antioxidant mechanisms.

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Section: Discussionmentioning

confidence: 99%

Propylthiouracil-induced hypothyroidism protects ionizing radiation-induced multiple organ damage in rats

Şener¹,

Kabasakal²,

Atasoy³

et al. 2006

Journal of Endocrinology

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“…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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“…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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Increased Lipid Peroxidation in Hyperthyroid Patients: Suppression by Propylthiouracil Treatment

Cited by 64 publications

References 26 publications

Propylthiouracil-induced hypothyroidism protects ionizing radiation-induced multiple organ damage in rats

Propylthiouracil-induced hypothyroidism protects ionizing radiation-induced multiple organ damage in rats

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

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

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