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10.1016/j.redox.2020.101504 http://scihub22266oqcxt.onion/10.1016/j.redox.2020.101504 32182573!7078436!32182573     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=32182573&cmd=llinks): Failed to open stream: HTTP request failed! 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Oral high dose vitamin B12 decreases renal superoxide and post-ischemia/reperfusion injury in mice |pdf=|usr=}}{{32182573}} gab.com Text Oral high dose vitamin B12 decreases renal superoxide and post-ischemia/reperfusion injury in mice JO: Redox Biol http://www.kidney.de/pget.php?&tw=1&pmid=32182573 #FOAvip Renal ischemia/reperfusion injury (IRI) is a leading cause of acute kidney injury (AKI), a potentially fatal syndrome characterized by a rapid decline in kidney function. Excess production of superoxide contributes to the injury. We hypothesized that oral administration of a high dose of vitamin B12 (B12 - cyanocobalamin), which possesses a superoxide scavenging function, would protect kidneys against IRI and provide a safe means of treatment. Following unilateral renal IR surgery, C57BL/6J wild type (WT) mice were administered B12 via drinking water at a dose of 50 mg/L. After 5 days of the treatment, plasma B12 levels increased by 1.2-1.5x, and kidney B12 levels increased by 7-8x. IRI mice treated with B12 showed near normal renal function and morphology. Further, IRI-induced changes in RNA and protein markers of inflammation, fibrosis, apoptosis, and DNA damage response (DDR) were significantly attenuated by at least 50% compared to those in untreated mice. Moreover, the presence of B12 at 0.3 muM in the culture medium of mouse proximal tubular cells subjected to 3 hr of hypoxia followed by 1 hr of reperfusion in vitro showed similar protective effects, including increased cell viability and decreased reactive oxygen species (ROS) level. We conclude that a high dose of B12 protects against perfusion injury both in vivo and in vitro without observable adverse effects in mice and suggest that B12 merits evaluation as a treatment for I/R-mediated AKI in humans. Twit Text FOAVip Oral high dose vitamin B12 decreases renal superoxide and post-ischemia/reperfusion injury in mice ????Redox Biol http://www.kidney.de/pget.php?&tw=1&pmid=32182573 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=32182573 #FOAvip English Wikipedia <ref>{{Cite pmid|32182573}}</ref> Oral high dose vitamin B12 decreases renal superoxide and post-ischemia/reperfusion injury in mice #MMPMID32182573 Li F; Bahnson EM; Wilder J; Siletzky R; Hagaman J; Nickekeit V; Hiller S; Ayesha A; Feng L; Levine JS; Takahashi N; Maeda-Smithies N Redox Biol 2020[May]; 32 (ä): 101504 PMID32182573show ga Renal ischemia/reperfusion injury (IRI) is a leading cause of acute kidney injury (AKI), a potentially fatal syndrome characterized by a rapid decline in kidney function. Excess production of superoxide contributes to the injury. We hypothesized that oral administration of a high dose of vitamin B12 (B12 - cyanocobalamin), which possesses a superoxide scavenging function, would protect kidneys against IRI and provide a safe means of treatment. Following unilateral renal IR surgery, C57BL/6J wild type (WT) mice were administered B12 via drinking water at a dose of 50 mg/L. After 5 days of the treatment, plasma B12 levels increased by 1.2-1.5x, and kidney B12 levels increased by 7-8x. IRI mice treated with B12 showed near normal renal function and morphology. Further, IRI-induced changes in RNA and protein markers of inflammation, fibrosis, apoptosis, and DNA damage response (DDR) were significantly attenuated by at least 50% compared to those in untreated mice. Moreover, the presence of B12 at 0.3 muM in the culture medium of mouse proximal tubular cells subjected to 3 hr of hypoxia followed by 1 hr of reperfusion in vitro showed similar protective effects, including increased cell viability and decreased reactive oxygen species (ROS) level. We conclude that a high dose of B12 protects against perfusion injury both in vivo and in vitro without observable adverse effects in mice and suggest that B12 merits evaluation as a treatment for I/R-mediated AKI in humans. |*Acute Kidney Injury/drug therapy[MESH] |*Reperfusion Injury/drug therapy[MESH] |Animals[MESH] |Apoptosis[MESH] |Ischemia[MESH] |Kidney[MESH] |Mice[MESH] |Mice, Inbred C57BL[MESH] |Superoxides[MESH]Oral high dose vitamin B12 decreases renal superoxide and post-ischem(epmc).pdf DeepDyve Pubget Overpricing