Abstract
Marine mammals are exposed to ischemia/reperfusion and hypoxia/reoxygenation during diving. During oxygen deprivation, adenosine triphosphate (ATP) breakdown implies purine metabolite accumulation, which in humans is associated with pathological conditions. Purine recycling in seals increases in response to prolonged fasting and ischemia. Concentrations of metabolites and activities of key enzymes in purine metabolism were examined in plasma and red blood cells from bottlenose dolphins (Tursiops truncatus) and humans. Hypoxanthine and inosine monophosphate concentrations were higher in plasma from dolphins than humans. Plasma hypoxanthine-guanine phosphoribosyl transferase (HGPRT) activity in dolphins suggests an elevated purine recycling rate, and a mechanism for avoiding accumulation of non-recyclable purines (xanthine and uric acid). Red blood cell concentrations of hypoxanthine, adenosine diphosphate, ATP and guanosine triphosphate were lower in dolphins than in humans; adenosine monophosphate and nicotinamide adenine dinucleotide concentrations were higher in dolphins. HGPRT activity in red blood cells was higher in humans than in dolphins. The lower concentrations of purine catabolism and recycling by-products in plasma from dolphins could be beneficial in providing substrates for recovery of ATP depleted during diving or vigorous swimming. These results suggest that purine salvage in dolphins could be a mechanism for delivering nucleotide precursors to tissues with high ATP and guanosine triphosphate requirements.
Highlights
Purine bases and nucleotides are essential for the appropriate performance of metabolic functions, such as cellular signaling and energy transfer, and as constituents of nucleic acids in all living organisms (Traut, 1994; Baranowska-Bosiacka et al, 2004)
In RBC from humans HX, inosine monophosphate (IMP), NAD+, adenosine monophosphate (AMP), adenosine diphosphate (ADP), guanosine triphosphate (GTP), adenosine triphosphate (ATP) were detected; in addition to these, GDP was identified in RBC from dolphins
Determination of HX, xanthine, uric acid, IMP, adenosine, NAD+, AMP, ADP, GDP, GTP, and ATP was achieved in plasma of both species
Summary
Purine bases and nucleotides are essential for the appropriate performance of metabolic functions, such as cellular signaling and energy transfer, and as constituents of nucleic acids in all living organisms (Traut, 1994; Baranowska-Bosiacka et al, 2004). Hyperuricemia and gout are among the common pathologies associated to purine disorders, increased synthesis and decreased excretion of uric acid (the final product of purine metabolism in humans) are the main causes of these conditions (Curto et al, 1998). Accumulation of uric acid and decreased activities of enzymes involved in the purine salvage pathway, such as purine nucleoside phosphorylase (PNP) and hypoxanthine-guanine phosphoribosyl transferase (HGPRT), are related with metabolic disorders including hyperuricemia, gout, immunological disorders, neurologic abnormalities and LeschNyhan syndrome, some of which are known to cause early death in humans (Fox, 1981; Curto et al, 1998; Skinner et al, 2006; Torres and Puig, 2007; Jurecka, 2009). In non-primate mammals, such as seals and dolphins, the enzyme uricase catalyzes uric acid to allantoin (Skinner et al, 2006)
Sign-in/Register to view highlights & summary Sign-in/Register to access full text options 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
