alexa Renal Protection Through CBS/H2S Pathway In Mammalian Hibernation: A Natural Model Of Hypothermic Organ Preservation During Cold Ischemia And Reperfusion
ISSN: 2161-0959

Journal of Nephrology & Therapeutics
Open Access

Like us on:
OMICS International organises 3000+ Global Conferenceseries Events every year across USA, Europe & Asia with support from 1000 more scientific Societies and Publishes 700+ Open Access Journals which contains over 50000 eminent personalities, reputed scientists as editorial board members.

Open Access Journals gaining more Readers and Citations

700 Journals and 15,000,000 Readers Each Journal is getting 25,000+ Readers

This Readership is 10 times more when compared to other Subscription Journals (Source: Google Analytics)

Share This Page

Additional Info

Loading Please wait..

3rd International Conference on Nephrology & Therapeutics
June 26-27, 2014 Valencia Conference Centre, Valencia, Spain

George J Dugbartey, Leo E Deelman and Rob H Henning
ScientificTracks Abstracts: J Nephrol Ther
DOI: 10.4172/2161-0959.S1.013
Background: Hibernation represents the most radical example of hypometabolism among mammalian species and is characterized by repetitive cycles of cooling (torpor) and rewarming, which resembles several clinically relevant conditions such as deep hypothermia, organ storage for transplantation, major surgery and ischemia-reperfusion. Therefore mechanisms applied by hibernators to undergo hibernation without reperfusion injury or other ill effects may have potential application to human medicine. Recently, we have shown that cultured hamster cells are protected from cooling induced apoptotic cell death by an increased production of endogenous H2S through upregulation of cystathionine-β-synthase (CBS). This study aimed at investigating the role of CBS enzyme and H2S in the induction of torpor and kidney preservation during hibernation. Method: Male Syrian golden hamsters ( Mesocricetus auratus ) were housed in cages in a climate controlled chamber at 5?C under dim red light to induce torpor. Movement of all animals was continuously monitored with passive infrared detectors. Osmotic mini-pumps filled with saline or CBS inhibitor aminooxyacetic acid (AOAA; 100 mg/kg/day) were implanted i.p. during torpor following a bolus injection of AOAA (70 mg/kg) under 2.5% isoflurane anesthesia. At 4 days following implantation of pumps, hamsters which re-entered torpor were aroused by handling for 4 hours and euthanized under pentobarbital anesthesia. Blood samples were taken and kidney of the hamsters was obtained. Summer euthermic hamsters served as controls. Results: Torpid hamsters were aroused during pump implantation. In contrast to saline infusions, infusion of AOAA prevented hamsters from re-entry into torpor. Infusion of AOAA also induced excess renal damage as indicated by high expression of kidney injury marker as well as changes in renal morphology. In contrast, renal morphology was well preserved during hibernation in the saline and non-hibernating summer control groups. Conclusion: Our data show that CBS/H2S pathway is essential in entrance into torpor and preservation of kidney morphology and function during hibernation. These findings might be relevant for a number of clinical conditions such as therapeutic hypothermia or organ preservation for transplantation medicine.
George J Dugbartey is pursuing his PhD at University Medical Center Groningen, Netherlands and will finish in December 2014 after which he intends to do a Postdoctoral research in renal transplantation. He has just submitted four research papers to reputed journals and awaiting reviewers? feedback, and currently writing two review papers
image PDF   |   image HTML

Relevant Topics

Peer Reviewed Journals
Make the best use of Scientific Research and information from our 700 + peer reviewed, Open Access Journals
International Conferences 2017-18
Meet Inspiring Speakers and Experts at our 3000+ Global Annual Meetings

Contact Us

© 2008-2017 OMICS International - Open Access Publisher. Best viewed in Mozilla Firefox | Google Chrome | Above IE 7.0 version