H
Hossein Niknahad
Researcher at Shiraz University of Medical Sciences
Publications - 115
Citations - 2748
Hossein Niknahad is an academic researcher from Shiraz University of Medical Sciences. The author has contributed to research in topics: Oxidative stress & Liver injury. The author has an hindex of 28, co-authored 106 publications receiving 2044 citations. Previous affiliations of Hossein Niknahad include University of Toronto & Shiraz University.
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Journal ArticleDOI
Effect of taurine on chronic and acute liver injury: Focus on blood and brain ammonia.
Reza Heidari,Akram Jamshidzadeh,Hossein Niknahad,Elnaz Mardani,Mohammad Mehdi Ommati,Negar Azarpira,Forouzan Khodaei,Azita Zarei,Maryam Ayarzadeh,Somayeh Mousavi,Narges Abdoli,Babak Shirazi Yeganeh,Arastoo Saeedi,Asma Najibi +13 more
TL;DR: In this article, the role of taurine (TA) administration on plasma and brain ammonia and its consequent events in different models of chronic and acute liver injury and hyperammonemia was evaluated.
Journal ArticleDOI
Betaine treatment protects liver through regulating mitochondrial function and counteracting oxidative stress in acute and chronic animal models of hepatic injury
Reza Heidari,Hossein Niknahad,Ala Sadeghi,Hamidreza Mohammadi,Vahid Ghanbarinejad,Mohammad Mehdi Ommati,Arghavan Hosseini,Negar Azarpira,Forouzan Khodaei,Omid Farshad,Elaheh Rashidi,Asma Siavashpour,Asma Najibi,Asrin Ahmadi,Akram Jamshidzadeh +14 more
TL;DR: Betaine supplementation ameliorated hepatic injury as judged by decreased liver tissue histopathological alterations, a significant decrease in tissue markers of oxidative stress, and mitigation of serum biomarkers of hepatotoxicity.
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Ammonia-induced mitochondrial dysfunction and energy metabolism disturbances in isolated brain and liver mitochondria, and the effect of taurine administration: relevance to hepatic encephalopathy treatment
TL;DR: It was found that ammonia inhibited mitochondrial dehydrogenases activity caused collapse of mitochondrial membrane potential (MMP), induced mitochondrial swelling (MPP), and increased reactive oxygen species (ROS) in isolated liver and brain mitochondria, and taurine administration mitigated ammonia-induced mitochondrial dysfunction.
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Mechanism of sulfite cytotoxicity in isolated rat hepatocytes.
TL;DR: These findings suggest that cytotoxicity of sulfite is mediated by free radicals as ROS formation increases by sulfite and antioxidants prevent its toxicity.
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Mechanism of valproic acid-induced Fanconi syndrome involves mitochondrial dysfunction and oxidative stress in rat kidney
TL;DR: The current investigation was designed to evaluate the role of mitochondrial dysfunction and oxidative stress in VPA‐induced renal injury.