Abstract
Cellular and mitochondrial damage can be caused by labile iron pool (LIP) and mediated by reactive oxygen species (ROS). Livers of the thalassemias have highly increased levels of LIP and ROS. Green tea extract (GTE) and epigallocatechin 3-gallatte (EGCG) can potentially protect liver inflammation, fibrosis and cancer due to their anti-oxidative and iron-chelating activities. We studied the effects of GTE and EGCG on intracellular LIP and ROS, and mitochondrial membrane potential (ΔΨm) in mouse hepatocyte and HepG2 cell cultures using specific fluorescent techniques. Treatment with GTE (12.5 - 25 mg/dl) and EGCG (25 - 50 μM) significantly lowered levels of ΔΨm in the mouse hepatocytes; however, combined treatment of 25 μM DFP with GTE and EGCG did not enhance the decrease of hepatic ΔΨm. The results showed that GTE and EGCG effectively removed the intracellular LIP and ROS, and relieved the mitochondria membrane collapse of the liver cells, suggesting a hepatoprotective effect of green tea extract and EGCG in the hepatocytes with iron overload. Their actions might be related to iron-chelating and free radical-scavenging capacities. Whether the effects can improve iron overload and oxidative stress in thalassemia patients remains to be seen upon further examination.
Highlights
Excess iron catalyzes production of reactive oxygen spe*Corresponding author.OPEN ACCESS cies (ROS) via Fenton/Haber-Weiss reaction [1], which in turn induces the oxidation of proteins, lipids and lipoproteins, nucleic acids, carbohydrates [2,3]
The results showed that Green tea extract (GTE) and epigallocatechin 3-gallatte (EGCG) effectively removed the intracellular labile iron pool (LIP) and reactive oxygen species (ROS), and relieved the mitochondria membrane collapse of the liver cells, suggesting a hepatoprotective effect of green tea extract and EGCG in the hepatocytes with iron overload
The deleterious effects result in cell and organelle damage, cell death, tissue necrosis, and organ dysfunction. bThalassemia patients suffer from secondary iron overload and require effective iron chelation with desferrioxamine (DFO), deferiprone (DFP) and deferasirox (DFX)
Summary
Excess iron catalyzes production of reactive oxygen spe*Corresponding author.OPEN ACCESS cies (ROS) via Fenton/Haber-Weiss reaction [1], which in turn induces the oxidation of proteins, lipids and lipoproteins, nucleic acids, carbohydrates [2,3]. The deleterious effects result in cell and organelle damage, cell death, tissue necrosis, and organ dysfunction. A wide range of LIP concentrations have been reported in erythroid and myeloid cells [5], peripheral blood lymphocytes [6], mouse lymphoma cells [7] and rat hepatocytes, as well as subcellular organelles [8]. In the liver with iron overload and oxidative stress, free radicals and their lipid-peroxidation products can trigger organelle dysfunctions, inflammation, fibrosis and eventually cell death [9]. Reduction of the LIP with iron chelators or/and antioxidants prevents nuclear and mitochondrial DNA breaks of the liver cells. An association of CYP2E1-dependent oxidative stress, mitochondrial membrane-potential ( m) collapse and GSH depletion possibly contributes toward the developing toxicity of iron to the liver [10]
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