title: Taurine supplementation reduces oxidative stress and protects the liver in an iron-overload murine model.
abstract: We previously demonstrated that iron overload induces liver damage by causing the formation of reactive oxygen species (ROS). Taurine is a potent free radical scavenger that attenuates the damage caused by excessive oxygen free radicals. Therefore, the aim of the present study was to investigate whether taurine could reduce the hepatotoxicity of iron overload with regard to ROS production. Mice were intraperitoneally injected with iron 5 days/week for 13 weeks to achieve iron overload. It was found that iron overload resulted in liver dysfunction, increased apoptosis and elevated oxidative stress. Taurine supplementation increased liver taurine levels by 40% and led to improved liver function, as well as a reduction in apoptosis, ROS formation and mitochondrial swelling and an attenuation in the loss of the mitochondrial membrane potential. Treatment with taurine mediated a reduction in oxidative stress in iron‑overloaded mice, attenuated liver lipid peroxidation, elevated antioxidant enzyme activities and maintained reduced glutathione levels. These results indicate that taurine reduces iron‑induced hepatic oxidative stress, preserves liver function and inhibits hepatocyte apoptosis. Therefore, taurine may be a potential therapeutic drug to reduce liver damage caused by iron overload.
authors.affiliation: State Key Laboratory of Food Science and Technology, Nanchang University, Nanchang, Jiangxi 330047, P.R. China.
authors.forename: Zeyu
authors.initials: Z
authors.lastname: Zhang
authors.affiliation: Department of Pharmacology and Molecular Therapeutics, Nanchang University School of Pharmaceutical Science, Nanchang, Jiangxi 330006, P.R. China.
authors.forename: Dan
authors.initials: D
authors.lastname: Liu
authors.affiliation: Second Abdominal Surgery Department, Jiangxi Province Tumor Hospital, Nanchang, Jiangxi 330029, P.R. China.
authors.forename: Bo
authors.initials: B
authors.lastname: Yi
authors.affiliation: Department of Pharmacology and Molecular Therapeutics, Nanchang University School of Pharmaceutical Science, Nanchang, Jiangxi 330006, P.R. China.
authors.forename: Zhangping
authors.initials: Z
authors.lastname: Liao
authors.affiliation: Department of Pharmacology and Molecular Therapeutics, Nanchang University School of Pharmaceutical Science, Nanchang, Jiangxi 330006, P.R. China.
authors.forename: Lei
authors.initials: L
authors.lastname: Tang
authors.affiliation: Jiangxi Provincial Key Laboratory of Molecular Medicine at the Second Affiliated Hospital, Nanchang University, Nanchang, Jiangxi 330006, P.R. China.
authors.forename: Dong
authors.initials: D
authors.lastname: Yin
authors.affiliation: State Key Laboratory of Food Science and Technology, Nanchang University, Nanchang, Jiangxi 330047, P.R. China.
authors.forename: Ming
authors.initials: M
authors.lastname: He
mesh_terms: D000410:Alanine Transaminase / Q000097:blood; D000818:Animals; D017209:Apoptosis / Q000187:drug effects; D001219:Aspartate Aminotransferases / Q000097:blood; D002374:Catalase / Q000378:metabolism; D004195:Disease Models, Animal; D005979:Glutathione Peroxidase / Q000378:metabolism; D022781:Hepatocytes / Q000378:metabolism; D019190:Iron Overload / Q000188:drug therapy*; D015227:Lipid Peroxidation; D008099:Liver / Q000187:drug effects* / Q000201:enzymology / Q000473:pathology; D008297:Male; D008315:Malondialdehyde / Q000097:blood; D053078:Membrane Potential, Mitochondrial; D051379:Mice; D008930:Mitochondria, Liver / Q000502:physiology; D008933:Mitochondrial Swelling; D018384:Oxidative Stress; D020011:Protective Agents / Q000008:administration & dosage*; D013654:Taurine / Q000008:administration & dosage*
chemical_list: D020011:Protective Agents; D013654:Taurine; D008315:Malondialdehyde; D002374:Catalase; D005979:Glutathione Peroxidase; D001219:Aspartate Aminotransferases; D000410:Alanine Transaminase