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

Radioiodine (RAI) therapy is widely used for thyroid ablation; however, the accumulation of I-131 in non-thyroid tissues may lead to undesirable side 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. Thirty male Wistar albino rats were randomly divided into three groups: Control (Group I, n = 10), RAI-treated (Group II, 111 MBq/kg, n = 10), and RAI + Vitamin D–treated (Group III, 200 ng/kg/day, n = 10). Liver function was assessed through serum analysis. Liver tissues were evaluated histopathologically and immunohistochemically. Oxidative stress markers including malondialdehyde (MDA), fluorescent oxidation products (FOP), catalase (CAT), and total sulfhydryl (T-SH) levels were measured in liver homogenates. 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). Vitamin D alleviated RAI-induced liver injury, likely through its antioxidant, anti-apoptotic, and anti-inflammatory effects.