Abstract
Hyperthyroidism causes many injuries in its target organs and the consequences are reflected systemically. As systemic alterations in hyperthyroidism at earlier stages have received partial attention, this study aimed to investigate systemic redox and inflammatory status at an early stage of T4-induced hyperthyroidism. Male Wistar rats were assigned to control and hyperthyroid groups (n = 7/group). The hyperthyroid group received L-thyroxine (12 mg/L) in their drinking water for 14 days whereas control group received only the vehicle. Body weight was measured on the 1st and 14th day of the protocol. On the 14th day, animals were anaesthetized. Blood was then collected from the retro-orbital venous plexus and then the animals were euthanised. The blood was separated into plasma and erythrocytes. Plasma was used to measure ROS levels, sulfhydryl compounds, IL-10, TNF-α and LDH levels; erythrocytes were used for the analysis of thioredoxin reductase activity, glutaredoxin content, and pentose cycle enzymes (total G6PD, G6PD and 6PGD). Hyperthyroid animals presented body weight gain and final body weight reduction, which was associated with increased ROS levels and decreased sulfhydryl content in plasma. Thioredoxin reductase activity, glutaredoxin content, and pentose cycle enzymes levels in erythrocytes, as well as IL-10, TNF-α and LDH plasma levels were unaltered. Taken together, our results suggest an impairment in corporal mass associated with systemic oxidative stress at this stage of hyperthyroidism. Meanwhile, the pentose cycle was not influenced and systemic inflammation and tissue damage seem to be absent at this stage of hyperthyroidism.
Highlights
Hyperthyroidism is characterised by reduced thyroidstimulating hormone (TSH) concentration associated with increased thyroid hormones levels, elevated heart rate, and cardiac hypertrophy [1,2]
The activity of thioredoxin reductase, glutaredoxin content, glucose-6-phosphate dehydrogenase (G6PD) total activity, isolated activity of G6PD, and 6-phosphogluconate dehydrogenase (6PGD) activity in erythrocytes was similar between groups (Table 1)
There was no significant difference between groups in terms of interleukin 10 (IL-10) (Figure 3A), TNF-α levels (Figure 3B), the IL-10/TNF-α ratio (Figure 3C) and lactate dehydrogenase (LDH) levels (Figure 3D)
Summary
Hyperthyroidism is characterised by reduced thyroidstimulating hormone (TSH) concentration associated with increased thyroid hormones (thyroxine – T4 and/or triiodothyronine – T3) levels, elevated heart rate, and cardiac hypertrophy [1,2]. Characterised the thyroid hormone-dependent cardiac hypertrophy at 15 days of hyperthyroidism induction [1]. Showed an association among cardiac hypertrophy and pro-apoptotic signalling in the heart [3]. The oxidative stress may provoke an antioxidant response in order to react to eustress state disruption [5]. In this sense, thioredoxin and glutaredoxin, important antioxidant proteins, appear increased in stressful situations, such as Grave’s disease and experimental hyperthyroidism [6,7].
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