Abstract
Background:
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.

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

Methods:
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 (TSH) levels were measured, and thyroid size and body weights were recorded. The levels of ROS markers (MDA, GSH, SOD-1, CAT, and GPX) and IA markers (Bax, Bcl-2, and caspase-3) were assessed in tissue homogenates.

Results:
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.

Conclusion:
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.

Key words: Hypothyroidism; Hyperthyroidism; Intrinsic apoptotic markers; Rat models; ROS.