Protective Role of Vitamin D in Attenuating RAI-Induced Liver Injury in Rats

Objective: Radioiodine (RAI) therapy is widely used for thyroid ablation, but I-131 accumulation in non-thyroid tissues may cause adverse effects. Vitamin D, known for its anti-apoptotic and immunomodulatory roles, may help protect against such damage. This study investigates the potential protective effects of vitamin D on RAI-induced liver injury through biochemical, histopathological, and immunohistochemical evaluations. Methods: Thirty male Wistar albino rats were randomly assigned to three groups: Control (Group I, n=10), RAI-treated (Group II, 111 MBq/kg, n=10), and RAI+Vitamin D (Group III, 200 ng/kg/day, n=10). Liver function was evaluated through serum analysis. Liver tissues were examined histopathologically and immunohistochemically. Oxidative stress markers—malondialdehyde (MDA), fluorescent oxidation products (FOP), catalase (CAT), and total sulfhydryl (T-SH)—were measured in liver homogenates. Results: RAI increased apoptotic cell numbers and elevated MDA, FOP, AST, and ALT levels. In contrast, T-SH and CAT levels were highest in the control group. Histopathology showed marked liver damage in the RAI group, which was less severe in the vitamin D group (p<0.001). TUNEL and caspase-3 analyses confirmed increased apoptosis in the RAI group compared to the others (p<0.001). Conclusions: Vitamin D alleviated RAI-induced liver injury, likely through its antioxidant, anti-apoptotic, and anti-inflammatory effects.