scholarly journals Dimeric Histidine as a Novel Free Radical Scavenger Alleviates Non-Alcoholic Liver Injury

Antioxidants ◽  
2021 ◽  
Vol 10 (10) ◽  
pp. 1529
Author(s):  
Zizhen Zhao ◽  
Chen Fu ◽  
Yuping Zhang ◽  
Ailing Fu

Non-alcoholic liver injury (NLI) is a common disease worldwide. Since free radical damage in the liver is a crucial initiator leading to diseases, scavenging excess free radicals has become an essential therapeutic strategy. To enhance the antioxidant capacity of histidine, we synthesized a protonated dimeric histidine, H-bihistidine, and investigated its anti-free radical potential in several free-radical-induced NLI. Results showed that H-bihistidine could strongly scavenge free radicals caused by H2O2, fatty acid, and CCl4, respectively, and recover cell viability in cultured hepatocytes. In the animal model of nonalcoholic fatty liver injury caused by high-fat diet, H-bihistidine reduced the contents of transaminases and lipids in serum, eliminated the liver’s fat accumulation, and decreased the oxidative damage. Moreover, H-bihistidine could rescue CCl4-induced liver injury and recover energy supply through scavenging free radicals. Moreover, liver fibrosis prepared by high-fat diet and CCl4 administration was significantly alleviated after H-bihistidine treatment. This study suggests a novel nonenzymatic free radical scavenger against NLI and, potentially, other free-radical-induced diseases.

1990 ◽  
Vol 258 (3) ◽  
pp. C429-C435 ◽  
Author(s):  
E. Zerba ◽  
T. E. Komorowski ◽  
J. A. Faulkner

We tested the hypotheses that 1) muscles of old mice are more susceptible to injury than muscles of young and adult mice, and 2) secondary or delayed onset injury results from free radical damage. Extensor digitorum longus muscles were injured in situ by lengthening contractions. Injury was assessed by measurement of maximum isometric tetanic force (Po) expressed as a percentage of the control value and by morphological damage. Mice were treated with a free radical scavenger, polyethylene glycol-superoxide dismutase (PEG-SOD). Three days postinjury, the Po of 44% for muscles of nontreated old mice was significantly lower than the Po of 58 and 61% for those of young and adult mice. In each group, the secondary injury at 3 days was alleviated by treatment with PEG-SOD. For treated muscles of young, adult, and old mice, values for Po were 88, 80, and 70%, respectively. We conclude that muscles of old mice are more susceptible to injury than muscles of young or adult mice and that free radicals contribute to the secondary or delayed onset injury.


2002 ◽  
Vol 88 (6) ◽  
pp. 2909-2918 ◽  
Author(s):  
Richard Kovács ◽  
Sebastian Schuchmann ◽  
Siegrun Gabriel ◽  
Oliver Kann ◽  
Julianna Kardos ◽  
...  

Generation of free radicals may have a key role in the nerve cell damage induced by prolonged or frequently recurring convulsions (status epilepticus). Mitochondrial function may also be altered due to production of free radicals during seizures. We therefore studied changes in field potentials (fp) together with measurements of extracellular, intracellular, and intramitochondrial calcium concentration ([Ca2+]e, [Ca2+]i, and [Ca2+]m, respectively), mitochondrial membrane potential (ΔΨ), NAD(P)H auto-fluorescence, and dihydroethidium (HEt) fluorescence in hippocampal slice cultures by means of simultaneous electrophysiological and microfluorimetric measurements. As reported previously, each seizure-like event (SLE) resulted in mitochondrial depolarization associated with a delayed rise in oxidation of HEt to ethidum, presumably indicating ROS production. We show here that repeated SLEs led to a decline in intracellular and intramitochondrial Ca2+ signals despite unaltered Ca2+ influx. Also, mitochondrial depolarization and the NAD(P)H signal became smaller during recurring SLEs. By contrast, the ethidium fluorescence rises remained constant or even increased from SLE to SLE. After about 15 SLEs, activity changed to continuous afterdischarges with steady depolarization of mitochondrial membranes. Staining with a cell death marker, propidium iodide, indicated widespread cell damage after 2 h of recurring SLEs. The free radical scavenger, α-tocopherol, protected the slice cultures against this damage and also reduced the ongoing impairment of NAD(P)H production. These findings suggest involvement of reactive oxygen species (ROS) of mitochondrial origin in the epileptic cell damage and that free radical scavenging may prevent status epilepticus–induced cell loss.


2000 ◽  
Vol 34 (2) ◽  
pp. 167-174 ◽  
Author(s):  
Emmanuel J. Diamantopoulos ◽  
Dionisios Charitos ◽  
Vassilios Georgopoulos ◽  
Emmanuel Economou ◽  
Michael Sfakianakis ◽  
...  

2010 ◽  
Vol 29 (8) ◽  
pp. 627-633 ◽  
Author(s):  
Seol-Hee Jeon ◽  
Hye-Min Park ◽  
Shang-Jin Kim ◽  
Mun-Young Lee ◽  
Gi-Beum Kim ◽  
...  

The immunosuppressive compound FK506 has been successfully used in kidney and liver transplant recipients. However, the compound can induce significant side effects on kidney function. Taurine is a potent free radical scavenger that attenuates a variety of renal diseases that are the consequence of excessive oxygen free radical damage. The purpose of this study was to investigate FK506-mediated death of Madin Darby canine kidney (MDCK) cells, in relation to reactive oxygen species (ROS) production. We determined the calcium (Ca2+) and magnesium (Mg2+) concentration in cultured MDCK cells by microfluorescence techniques and the level of activation of c-Jun-N-terminal kinase (JNK), extracellular signal regulated kinases (ERK), Bcl-2 and Bax proteins by Western blot. Treatment with 10 μM FK506 induced apoptosis in MDCK cells by increasing the level of intracellular ROS and Ca2+ and by decreaseing the level of intracellular Mg2+. This increase in intracellular ROS promoted JNK and Bax activation, which increased FK506-induced MDCK cell death. Taurine reduced the FK506-induced generation of ROS and activation of JNK and Bax. The results indicate that taurine can prevent FK506-induced kidney toxicity.


2003 ◽  
Vol 307 (1) ◽  
pp. 74-82 ◽  
Author(s):  
Hiroshi Kono ◽  
Masami Asakawa ◽  
Hideki Fujii ◽  
Akira Maki ◽  
Hidetake Amemiya ◽  
...  

2019 ◽  
Vol 12 (1) ◽  
pp. 273-280 ◽  
Author(s):  
Yue Ma ◽  
Kai Chen ◽  
Jun Ma ◽  
Gaojie Xu ◽  
Shanmu Dong ◽  
...  

A lignin binder has been introduced to high voltage lithium-ion batteries to suppress electrolyte decomposition by scavenging free radicals.


2007 ◽  
Vol 0 (0) ◽  
pp. 070901025723001-??? ◽  
Author(s):  
Koji Ito ◽  
Hisashi Ozasa ◽  
Yumi Noda ◽  
Shigeki Arii ◽  
Saburo Horikawa

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