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Mohammad Mehdi Ommati

Researcher at Shanxi Agricultural University

Publications -  114
Citations -  2627

Mohammad Mehdi Ommati is an academic researcher from Shanxi Agricultural University. The author has contributed to research in topics: Oxidative stress & Mitochondrion. The author has an hindex of 23, co-authored 91 publications receiving 1488 citations. Previous affiliations of Mohammad Mehdi Ommati include Shiraz University & Shiraz University of Medical Sciences.

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Taurine treatment preserves brain and liver mitochondrial function in a rat model of fulminant hepatic failure and hyperammonemia.

TL;DR: Taurine was found to be a potential protective agent with therapeutic capability against hepatic encephalopathy and hyperammonemia-induced mitochondrial dysfunction and energy crisis and restored brain and liver mitochondrial ATP.
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Effect of taurine on chronic and acute liver injury: Focus on blood and brain ammonia.

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.
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Betaine treatment protects liver through regulating mitochondrial function and counteracting oxidative stress in acute and chronic animal models of hepatic injury

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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The nephroprotective properties of taurine in colistin-treated mice is mediated through the regulation of mitochondrial function and mitigation of oxidative stress.

TL;DR: The data obtained from the current study suggest mitochondrial dysfunction and oxidative stress as fundamental mechanisms of renal injury induced by COL and taurine supplementation protected kidney through decreasing oxidative stress and regulating mitochondrial function.
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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.