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17β-estradiol plays a crucial role in regulating cellular processes in both reproductive and non-reproductive tissues, including the thyroid gland. It modulates oxidative stress and contributes to sexual dimorphism in thyroid diseases, with ROS production, particularly H2O2, generated by NOX/DUOX enzymes. This study aimed to investigate the effects of 17β-estradiol (10 nM or 100 nM) on the expression of NOX/DUOX, thyroid-specific genes, and endoplasmic reticulum (ER) stress-related genes in male and female porcine thyroid follicular cells. Expression of the studied genes was evaluated by RT-PCR before and after treatment with 17β-estradiol alone or with the addition of NOX4 inhibitor (GKT-136901). Additionally, the level of ROS was measured by flow cytometry analysis. Our results show that 17β-estradiol significantly upregulates thyroid-specific genes, particularly TPO, and stimulates NOX/DUOX expression, affecting the redox state of thyroid cells. It also stimulates ER stress-related genes such as CHOP. In conclusion, estrogen excess may contribute to thyroid disease development via such possible mechanisms as the upregulation of key thyroid-specific genes, particularly TPO, and of genes involved in the cellular response to ER stress, especially CHOP, as well as by the stimulation of the NOX/DUOX system with consequent ROS overproduction. These mechanisms may play a certain role in the higher prevalence of thyroid diseases in women. [ABSTRACT FROM AUTHOR]

We present results on the potential protective antioxidant properties of indole-3-butyric acid. Indole-3-butyric acid is an indole derivative defined as an auxin and widely known as a plant growth regulator. It naturally occurs in Arabidopsis thaliana, which is applied as a model plant in genetic studies. Oxidative damage to membrane lipids (lipid peroxidation; LPO) in porcine thyroid homogenates was induced by Fenton reaction substrates (Fe2+ + H2O2). Iron (Fe2+) was used in very high concentrations of 1200, 600, 300, 150, 75, 37.5, 18.75, 9.375, 4.687, and 2.343 µM. Indole-3-butyric acid (10.0, 5.0, 2.5, 1.25, and 0.625 mM) was applied to check whether it prevents the above process. The LPO level, expressed as malondialdehyde + 4-hydroxyalkenals (MDA + 4-HDA) concentration, was measured spectrophotometrically. Expectedly, Fenton reaction substrates, in a Fe2+ concentration-dependent manner, increased LPO level, with the lowest effective concentration of iron being 9.375 µM. In the case of almost all concentrations of indole-3-butyric acid, this auxin has exhibited very promising antioxidant protection, with the most effective concentrations being 10.0 and 5.0 mM; however, as low concentrations of indole-3-butyric acid at 1.25 mM was still effective. Indole-3-butyric acid used alone did not change the basal level of LPO, which is a favourable effect. To summarise, indole-3-butyric acid has protective antioxidant properties against experimentally induced oxidative damage to membrane lipids in the thyroid, and this is for the first time documented in the literature. This compound can be considered a natural protective agent present in plants, which can serve as a dietary nutrient. [ABSTRACT FROM AUTHOR]

Simple Summary: Melatonin is a hormone primarily produced in the pineal gland in response to darkness. Apart from regulating our body's internal clock, it possesses strong antioxidant properties. Thanks to these characteristics, melatonin shows promise in preventing and treating various health issues, such as cancer. This review explores how melatonin can protect the thyroid gland from oxidative damage and, consequently, prevent the development of thyroid disease caused by documented or potential carcinogens. The article emphasizes the importance of melatonin in protecting the thyroid and how it can help to treat thyroid diseases, including cancer. Melatonin, primarily synthesized in the pineal gland, plays a crucial role in regulating circadian rhythms and possesses significant antioxidative properties. By neutralizing free radicals and reducing oxidative stress, melatonin emerges as a promising agent for the prevention and therapy of many different disorders, including cancer. This paper reviews the relationship between the thyroid gland and melatonin, presenting experimental evidence on the protective effects of this indoleamine against oxidative damage to macromolecules in thyroid tissue caused by documented carcinogens (as classified by the International Agency for Research on Cancer, IARC) or caused by potential carcinogens. Furthermore, the possible influence on cancer therapy in humans and the overall well-being of cancer patients are discussed. The article highlights melatonin's essential role in maintaining thyroid health and its contribution to management strategies in patients with thyroid cancer and other thyroid diseases. [ABSTRACT FROM AUTHOR]

Abstract Background The mitochondrial DNA (mtDNA) lies in close proximity to the free radical-producing electron transport chain, thus, it is highly prone to oxidative damage. Oxyphilic type of follicular thyroid carcinoma consists of cells filled – almost exclusively – with aberrant mitochondria. In turn, bivalent iron (Fe2+) and hydrogen peroxide (H2O2) are indispensable for thyroid hormone synthesis, therefore being available in physiological conditions presumably at high concentrations. They participate in Fenton reaction (Fe2++H2O2→Fe3++·OH + OH-), resulting in the formation of the most harmful free radical – hydroxyl radical (·OH). The same substrates may be used to experimentally induce oxidative damage to macromolecules. The aim of the study was to evaluate the background level of oxidative damage to mtDNA and the damaging effects of Fenton reaction substrates. Methods Thyroid mtDNA was incubated in the presence of either H2O2 [100, 10, 1.0, 0.5, 0.1, 0.001, 0.00001 mM] or FeSO4 (Fe2+) [300, 150, 30, 15, 3.0, 1.5 μM], or in the presence of those two factors used together, namely, in the presence of Fe2+ [30 μM] plus H2O2 [100, 10, 1.0, 0.5, 0.1, 0.001, 0.00001 mM], or in the presence of H2O2 [0.5 mM] plus Fe2+ [300, 150, 30, 15, 3.0, 1.5 μM]. 8-oxo-7,8-dihydro-2’-deoxyguanosine (8-oxodG) concentration, as the index of DNA damage, was measured by HPLC. Results Both Fenton reaction substrates, used separately, increased 8-oxodG level for the highest H2O2 concentration of 100 mM and in Fe2+ concentration-dependent manner [300, 150, and 30 μM]. When Fe2+ and H2O2 were applied together, Fe2+ enhanced H2O2 damaging effect to a higher degree than did H2O2 on Fe2+ effect. Conclusions The level of oxidized nucleosides in thyroid mtDNA is relatively high, when compared to nuclear DNA. Both substrates of Fenton reaction, i.e. ferrous ion and hydrogen peroxide, increase oxidative damage to mtDNA, with stronger damaging effect exerted by iron. High level of oxidative damage to mtDNA suggests its possible contribution to malignant transformation of thyroid oncocytic cells, which are known to be especially abundant in mitochondria, the latter characterized by molecular and enzymatic abnormalities.

Objectives: One of the most spectacular exogenous prooxidative agents is cigarette smoking, constituting a well documented risk factor for several diseases. In turn it is suggested that hormone replacement therapy (HRT) in postmenopausal women can contribute to oxidative status. The aim of the study was to evaluate the level of oxidative damage to membrane lipids in blood serum collected from never-smokers and former-smokers. The study was performed in postmenopausal women, who were or were not HRT users., Methods: Ninety (90) female volunteers, aged from 46 to 67 years, were enrolled. Two major groups were considered, i.e. never-smokers (n=44) and formersmokers (n=46), which were additionally subgrouped to HRT users (HRT+) and HRT non-users (HRT-). Anthropometric parameters related to obesity were also calculated. The main groups were well matched at baseline in terms of age. The level of malondialdehyde+4-hydroxyalkenals (MDA+4-HDA), as the index of LPO, was measured spectrophotometrically., Results: The level of LPO was higher in former-smokers than in never-smokers, regardless of HRT use. The level of LPO did constitute the only independent factor associated with past smoking in the entire examined group, as well as after stratification to HRT users and HRT non-users. LPO level was not associated with HRT treatment. No positive correlations were found between LPO level and anthropometric parameters., Conclusion: Past smoking is independently associated with the increased damage to membrane lipids regardless of the use of HRT in postmenopausal women. Smoking cessation is not always associated with complete reversion of excessive oxidative damage to all biological macromolecules.

Background: Obesity constitutes a common modifiable risk factor for certain non-communicable diseases (NCDs) associated with enhanced oxidative stress., Objectives and Methods: The aim of the study was to examine serum concentrations of malondialdehyde + 4-hydroxyalkenals (MDA+4-HDA), as an index of lipid peroxidation (LPO), and 8-oxo-7,8-dihydro-2'-deoxyguanosine (8-oxodG) concentration in peripheral blood lymphocytes, as an index of nuclear DNA damage, in overweight and obese adult patients. LPO and 8-oxodG, as well as clinical and laboratory parameters, which are frequently affected by obesity, were evaluated in 58 overweight and obese adult patients, and in 20 healthy volunteers., Results: Both LPO and 8-oxodG levels were increased in overweight and obese patients, with further increase observed with the increasing body mass index (BMI). LPO correlated positively with body mass, BMI, waist circumference, hip circumference, waist:hip ratio, systolic or diastolic blood pressure, glucose, C-reactive protein and ferritin concentrations. 8-oxodG correlated positively with body mass, BMI, hip circumference and triglyceride concentration, whereas it correlated negatively with iron concentration. Expectedly, positive correlation between LPO and 8-oxodG was also found., Conclusions: BMI constituted the only independent determinant (predictor) of LPO in overweight and obese patients. Consistently, LPO did constitute the only independent determinant of obesity. Overweight and obesity in adults are directly associated with increased oxidative damage to macromolecules.