Reactive oxygen species and intrinsic apoptotic markers in thyroid dysfunction: Insights from experimental animal...

Thyroid disorders are associated with elevated reactive oxygen species (ROS) levels that trigger apoptosis. Nevertheless, the precise connection between ROS levels and apoptotic markers in thyroid dysfunction remains unclear.

To explore the relationship between ROS levels and intrinsic apoptotic (IA) markers in thyroid homogenates derived from hypothyroidism and hyperthyroidism mouse models.

Eighteen male Wistar rats, each weighing 240 ± 10 g, were allocated to three groups of six rats. Hypothyroidism and hyperthyroidism were induced over 8 weeks using 0.05% Propylthiouracil (PTU) and 0.0012% Levothyroxine (L-Thy), respectively. T3, T4, and thyroid-stimulating hormone levels were measured, and thyroid size and body weights were recorded. The levels of ROS markers [MDA, glutathione (GSH), SOD-1, CAT, and GPX) and IA markers (Bax, Bcl-2, and caspase-3) were assessed in tissue homogenates.

A gradual weight loss was observed in the hyperthyroidism group compared with the control group. The hypothyroid model showed elevated MDA levels and cleaved caspase-3, as well as a higher Bax/Bcl-2 ratio, whereas GSH, SOD-1, CAT, GPX, and Bcl-2 levels were lower than those in the control group (p < 0.05). In contrast, no changes were observed in the hyperthyroid models. Thyroid hormone levels are inversely correlated with ROS and positively correlated with antioxidant levels.

Hypothyroidism models exhibited increased oxidative stress and pro-apoptotic markers, suggesting the initiation of apoptosis and cellular damage. Conversely, the hyperthyroid models showed no such changes.