Diethyl Phthalate-Induced Oxidative Stress, Genotoxicity, and Thyroid Hormone Disruption in Female Wistar Rats

Abstract

Background: Diethyl phthalate (DEP), a common plasticizer in cosmetics and personal care products, is known to induce oxidative stress and endocrine disruption. Its widespread use raises concerns about thyroid toxicity. Objective: This study aimed to evaluate the genotoxic and endocrine effects of subacute DEP exposure on thyroid tissue in female Wistar albino rats using thyroid hormones, oxidative stress markers, DNA damage, and histopathology. Methods: Twenty-eight female Wistar albino rats were divided into four groups (n = 7): control, 100 mg/kg, 300 mg/kg, and 600 mg/kg DEP. DEP was administered orally for 21 days. DNA damage was assessed by Comet Assay, oxidative stress markers (TAS, TOS, OSI) were measured, and serum TSH, T3, and T4 levels were determined by ELISA. Body weights were monitored, and thyroid tissues were examined histologically. Results: Compared to the control group, T3 and T4 levels decreased (P < 0.05), TSH levels increased (p < 0.05), TAS levels decreased (p < 0.05), and TOS and OSI levels increased (p < 0.05). Comet Assay showed dose-dependent DNA damage (tail DNA%, p < 0.05). With higher DEP doses, thyroid tissue histopathology changed significantly. Conclusion: Subacute DEP exposure causes dose-dependent genotoxicity, oxidative stress, and endocrine disruption in thyroid tissue. These findings emphasize the need to limit environmental and human DEP exposure.