Second messenger and cAMP-dependent protein kinase responses to dehydration and anoxia stresses in frogs
Second messenger and cAMP-dependent protein kinase responses to dehydration and anoxia stresses in frogs
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DOI：
10.1007/s003600050078
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发表时间：
1997-05-01
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影响因子：
--
通讯作者：
Storey, KB
中科院分区：
文献类型：
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作者：
Holden, CP;Storey, KB
全身脱水的影响（高达40%的总身体水分流失）或缺氧暴露（在N-2气体下长达2天）对腺苷3 '-5'环一磷酸（cAMP）的组织水平和作为游离催化亚基（PKAc）存在的cAMP依赖性蛋白激酶的百分比，以及蛋白激酶C（PKC）第二信使肌醇1，4，5-三磷酸盐（IP 3），在两个无尾类动物，抗冻林蛙，林蛙林，和不耐冻豹蛙，蛙pipiens。林蛙脱水导致肝脏cAMP和PKAc的快速升高; cAMP是对照值的3.4倍，而PKAc在20%脱水的青蛙中升高了3倍。这些结果表明，蛋白激酶A介导的肝糖原分解和高血糖症，这是诱导脱水在这个物种。骨骼肌PKAc含量也随着脱水而上升，但在豹蛙组织中，cAMP和PKAc都不受脱水的影响。缺氧暴露对信号转导系统有不同程度的影响。缺氧1h后，R. sylvatica大脑中的酶，并持续随着时间的推移，但在其他器官中的酶不受影响; pipiens表现出不同的反应PKAc缺氧在三个器官。这两个物种都表现出快速（30分钟内）和大（3至7.8倍）增加，在缺氧青蛙的肝脏中，随着持续缺氧缓慢下降。缺氧暴露的林蛙心脏IP 3也迅速增加。这表明PKC可能介导多种代谢调节，促进缺氧/缺氧抗性，如协调代谢率降低。在林蛙脱水过程中肝脏IP 3的逐步上升（在40%脱水动物中达到比对照高四倍）也可能介导类似的耐缺氧适应，因为无尾两栖动物在失水达到高值时由于血液粘度增加而经历渐进性缺氧。第二信使和PKAc的变化在林蛙肝脏脱水过程中的模式密切平行的变化，在这些相同的参数，在自然冷冻过程中，这表明选择terrestrially冬眠的无尾两栖动物的抗冻性可能已经演变出各种无尾两栖动物的脱水抗性机制。
The effects of whole body dehydration (up to 40% of total body water lost) or anoxia exposure (up to 2 days under N-2 gas) at 5 OC on tissue levels of adenosine 3'-5' cyclic monophosphate (cAMP) and the percentage of cAMP-dependent protein kinase present as the free catalytic subunit (PKAc), as well as the levels of the protein kinase C (PKC) second messenger, inositol 1,4,5-trisphosphate (IP3), were assessed in two anurans, the freeze-tolerant wood frog, Rana sylvatica, and the freeze-intolerant leopard frog, Rana pipiens. Dehydration of wood frogs resulted in a rapid elevation of liver cAMP and PKAc; cAMP was 3.4-fold greater than control values in animals that had lost 5% of total body water, whereas PKAc was elevated threefold in 20% dehydrated frogs. These results indicate protein kinase A mediation of the liver glycogenolysis and hyperglycemia that is induced by dehydration in this species. Skeletal muscle PKAc content also rose with dehydration but neither cAMP nor PKAc was affected by dehydration in leopard frog tissues. Anoxia exposure had different effects on signal transduction systems. PKAc was elevated after I h anoxia in R. sylvatica brain and was sustained over time but the enzyme was unaffected in other organs; by contrast, R. pipiens showed variable responses by PKAc to anoxia in three organs. Both species showed rapid (within 30 min) and large (3 to 7.8-fold) increases in IP3 in liver of anoxic frogs that decreased slowly with continued anoxia. IP3 also increased quickly in heart of anoxia-exposed wood frogs. This suggests that PKC may mediate various metabolic adjustments that promote hypoxia/anoxia resistance such as coordinating metabolic rate depression. A progressive rise in liver IP3 during dehydration in wood frogs (reaching fourfold higher than controls in 40% dehydrated animals) may also mediate similar hypoxia resistance adaptations under this stress since anurans experience progressive hypoxia due to increased blood viscosity when water loss reaches high values. The patterns of second messenger and PKAc changes in wood frog liver during dehydration closely parallel the changes seen in these same parameters during natural freezing suggesting that the freeze tolerance of selected terrestrially hibernating anurans may have evolved out of various anuran mechanisms of dehydration resistance.