Summary: | When tissues are deprived of blood (ischemia) there is a progressive reduction of oxygen (hypoxia). Tissue function can be maintained until oxygen and ATP stores are depleted. During breath‐hold diving, blood flow to most tissues is decreased and blood is directed preferentially to the central nervous system. Diving mammals (seals and dolphins) routinely dive as part of their natural history. The hypothesis of this study is that diving mammals have a refined purine salvage system to avoid loss of nucleotides and to maximize ATP recycling during ischemia/reperfusion associated to diving. The goal of this study is to analyze the activities of purine nuceoside phosphorylase (PNP), xanthine oxidase (XO) and hypoxanthine‐guanine phosphorybosil transferase (HGPRT), key enzymes involved in the purine salvage pathway in marine mammals adapted to tolerate repeated cycles of ischemia/reperfusion associated with diving (bottlenose dolphin, northern elephant seal, river otter) and compare with those from non‐diving mammals (human, pig). PNP, XO and HGPRT activities were analyzed by spectrophotometry, purine nucleotide metabolite concentrations was analyzed by HPLC. No clear relationship in circulating PNP or XO activity could be established between diving and non‐diving mammals. Intraerythrocyte PNP activity in bottlenose dolphins could be related to a release of purine nucleotides from the liver. The plasma PNP and XO activities observed in river otters may be due to their precarious energetic balance. Low erythrocyte PNP activity and elevated plasma XO activity in northern elephant seal could be due to fasting and/or sleep‐ and dive‐associated apneas. Grant Funding Source : Supported by CONACYT
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