Rodrigo Valenzuela1, Miguel Ángel Rincón-Cervera2, Francisca Echeverría3, Cynthia Barrera3, Alejandra Espinosa4, María Catalina Hernández-Rodas3, Macarena Ortiz5, Alfonso Valenzuela2, Luis A Videla6. 1. Nutrition Department, Faculty of Medicine, University of Chile, Santiago, Chile; Lipid Center, Institute of Nutrition and Food Technology (INTA), University of Chile, Santiago, Chile. Electronic address: rvalenzuelab@med.uchile.cl. 2. Lipid Center, Institute of Nutrition and Food Technology (INTA), University of Chile, Santiago, Chile. 3. Nutrition Department, Faculty of Medicine, University of Chile, Santiago, Chile. 4. Medical Technology Department, Faculty of Medicine, University of Chile, Santiago, Chile. 5. Nutrition and Dietetics School, Faculty of Health Sciences, Catholic University of Maule, Curicó, Chile. 6. Molecular and Clinical Pharmacology Program, Institute of Biomedical Science, Faculty of Medicine, University of Chile, Santiago, Chile.
Abstract
OBJECTIVES: Iron is involved in processes involving oxygen transfer and utilization. Excess iron is linked to cardiovascular diseases and some types of cancer. Iron overload is associated with oxidative stress development, and may have important interactions with lipid metabolism in the liver favoring the development and progression of non-alcoholic fatty liver disease. The aim of the study described here was to assess the effect of high intake of iron on oxidative stress-related parameters, lipid metabolism, and levels of long-chain polyunsaturated fatty acids (LCPUFAs) in liver and other tissues of the rat. METHODS: Male Wistar rats (21 d old) were fed an iron-rich diet (200 mg iron/kg diet, IRD) versus a control diet (50 mg iron/kg diet; CD) for 21 d. Samples of erythrocytes, liver, adipose tissue, brain, heart, and testicles were evaluated for fatty acid composition and hepatic biochemical and oxidative stress parameters, Δ-6 and Δ-5 desaturase activities, SREBP-1c and PPAR-α mRNA expression and DNA-binding capacity, and lipolytic, lipogenic, and antioxidant enzymatic activities. RESULTS: The IRD caused liver steatosis and increased activity of plasma transaminases, with higher oxidative stress status in plasma and liver. Liver Δ-6 and Δ-5 desaturase exhibited decreased activity, but enhanced expression in response to the IRD compared with the CD, with lower levels of ω-3 and ω-6 LCPUFAs and higher expression and DNA binding of SREBP-1c, whereas expression and DNA-binding activity of PPAR-α were diminished. CONCLUSIONS: IRD induced oxidative stress and a reduction in the desaturation capacity of the liver, with LCPUFA depletion in the different tissues studied, thus promoting a pro-steatotic condition in the liver.
OBJECTIVES:Iron is involved in processes involving oxygen transfer and utilization. Excess iron is linked to cardiovascular diseases and some types of cancer. Iron overload is associated with oxidative stress development, and may have important interactions with lipid metabolism in the liver favoring the development and progression of non-alcoholic fatty liver disease. The aim of the study described here was to assess the effect of high intake of iron on oxidative stress-related parameters, lipid metabolism, and levels of long-chain polyunsaturated fatty acids (LCPUFAs) in liver and other tissues of the rat. METHODS: Male Wistar rats (21 d old) were fed an iron-rich diet (200 mg iron/kg diet, IRD) versus a control diet (50 mg iron/kg diet; CD) for 21 d. Samples of erythrocytes, liver, adipose tissue, brain, heart, and testicles were evaluated for fatty acid composition and hepatic biochemical and oxidative stress parameters, Δ-6 and Δ-5 desaturase activities, SREBP-1c and PPAR-α mRNA expression and DNA-binding capacity, and lipolytic, lipogenic, and antioxidant enzymatic activities. RESULTS: The IRD caused liver steatosis and increased activity of plasma transaminases, with higher oxidative stress status in plasma and liver. Liver Δ-6 and Δ-5 desaturase exhibited decreased activity, but enhanced expression in response to the IRD compared with the CD, with lower levels of ω-3 and ω-6 LCPUFAs and higher expression and DNA binding of SREBP-1c, whereas expression and DNA-binding activity of PPAR-α were diminished. CONCLUSIONS: IRD induced oxidative stress and a reduction in the desaturation capacity of the liver, with LCPUFA depletion in the different tissues studied, thus promoting a pro-steatotic condition in the liver.
Authors: Ethan Baratz; Shyamalagauri Jadhav; Olga Protchenko; Fengmin Li; Minoo Shakoury-Elizeh; Oksana Gavrilova; Manik C Ghosh; James E Cox; J Alan Maschek; Vladimir A Tyurin; Yulia Y Tyurina; Hülya Bayir; Allegra T Aron; Christopher J Chang; Valerian E Kagan; Caroline C Philpott Journal: Hepatology Date: 2020-11-03 Impact factor: 17.298
Authors: Rodrigo Chamorro; Karla A Bascuñán; Cynthia Barrera; Jorge Sandoval; Claudia Puigrredon; Rodrigo Valenzuela Journal: Int J Environ Res Public Health Date: 2022-02-09 Impact factor: 3.390