Bingul, IlknurAydin, A. FatihKucukgergin, CananDogan-Ekici, IsinDogru-Abbasoglu, SemraUysal, Mujdat2023-02-212023-02-212021-01-0110.3906/sag-2007-289https://hdl.handle.net/11443/1563http://dx.doi.org/10.3906/sag-2007-289Background/aim: Oxidative stress and advanced glycation end products (AGEs) formation are proposed as effective mechanisms in the pathogenesis of nonalcoholic fatty liver disease (NAFLD) and alcoholic liver disease (ALD). 1,25(OH)(2)D-3 was proposed to have antioxidant, antiinflammatory and antiglycation properties. In this study, the effect of 1,25(OH)(2)D-3 treatment on oxidative stress parameters and AGEs levels together with hepatic histopathology was investigated in high fructose (HFr) or ethanol (EtOH)-treated rats. Materials and methods: Rats were treated with fructose (30\%) or ethanol (5-20\%) in drinking water with and without 1,25(OH)(2)D-3 treatment (5 mu g/kg two times a week) for 8 weeks. Insulin resistance (IR), oxidative stress parameters, AGEs, triglyceride (TG), and hydroxyproline (Hyp) levels together with histopathology were investigated in the liver. Results: 1,25(OH)(2)D-3 decreased hepatic reactive oxygen species, lipid and protein oxidation products together with histopathological improvements in HFr- and EtOH-treated rats. 1,25(OH)(2)D-3 treatment was observed to decrease significantly serum and hepatic AGEs in HFr group, and hepatic AGEs in EtOH group. Conclusion: Our results clearly show that 1,25(OH)(2)D-3 treatment may be useful in the alleviation of hepatic lesions by decreasing glycooxidant stress in both NAFLD and ALD models created by HFr- and EtOH-treated rats, respectively.Vitamin Dfructoseethanoloxidative stressglycation end productsArticleWOS:000668257500012