l -色氨酸摄食对网闭攀鲈脑线粒体离子运输的影响

S. Anupriya, V. S. Peter, M. Peter
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引用次数: 2

摘要

5-羟色胺(5-HT)是一种具有多种生理作用的神经激素,由膳食必需氨基酸色氨酸(TRP)合成。然而,色氨酸对硬骨鱼神经离子转运体的影响及其在应激反应中的作用尚未被确定。研究了不同剂量的TRP对无应激和应激条件下呼吸鱼testudineus Bloch前脑(FB)、中脑(MB)和后脑(HB)段线粒体(m)和细胞质(c)离子转运蛋白活性的影响。用不同剂量的TRP(1、2和4 mg g -1饲料)喂养鱼7天,对鱼脑不同区域的Na +、K + - atp酶和H + - atp酶活性产生剂量依赖性。TRP治疗7天后,FB和MB的Na +、K + - atp酶活性降低(P<0.001)。TRP降低了FB的H + - atp酶活性(P<0.001),但增加了脑内所有三个区域的Na +、K + atp酶活性。在非应激鱼中,喂食20 mg g -1 TRP 2天后,鱼FB和HB中cH + - atp酶活性显著升高(P<0.001)。而mH + - atp酶则对TRP的摄食表现出相反的反应。与之相反,TRP使网闭鱼FB和HB的cH + - atp酶活性降低(P<0.001),而使MB的cH + - atp酶活性升高(P<0.001)。在非应激鱼中,TRP饲喂后FB和MB的胞质和线粒体ca2 + - atp酶活性降低(P<0.001)。应激鱼饲喂TRP降低了线粒体ccca2 + - atp酶活性(P<0.001),提高了线粒体ccca2 + - atp酶活性(P<0.001)。在非应激鱼中,TRP摄食降低了FB和MB段的mMg 2+ - atp酶活性(P<0.001)。然而,在应激鱼中,TRP处理降低了MB中Mg 2+ - atp酶的活性(P<0.001),而在其他脑段中没有。上述数据表明,TRP可以调节脑线粒体离子转运,应激诱导可能会改变TRP诱导的呼吸鱼线粒体离子转运反应。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Effect of L-tryptophan feeding on brain mitochondrial ion transport in net- confined climbing perch (Anabas testudineus Bloch)
Serotonin (5-HT), a neurohormone with many physiological actions, is synthesized from the dietary essential amino acid tryptophan (TRP). However, the effects of TRP on neuronal ion transporters and its role in stress response have not yet been identified in the teleost fish. The effects of varied doses of TRP on the activities of mitochondrial (m) and cytosolic (c) ion transporters were examined in the forebrain (FB), midbrain (MB) and hindbrain (HB) segments of an air-breathing fish Anabas testudineus Bloch kept either in non-stressed or in stressed condition. Feeding the fish with varied doses of TRP (1, 2 and 4 mg g -1 feed) for seven days produced dose-dependent effects on Na + , K + -ATPase and H + -ATPase activities in different regions of fish brain. A decrease in (P<0.001) Na + , K + -ATPase activity was found in FB and MB after seven days of TRP treatment. TRP decreased (P<0.001) H + -ATPase activity in the FB but increased Na + , K + ATPase activity in all the three regions of the brain. In non-stressed fish, feeding 20 mg g -1 TRP for two days produced a substantial rise (P<0.001) in cH + -ATPase activity in the FB and HB of the fish. But mH + -ATPase showed a reversed response to TRP feeding. On the contrary, TRP treatment in net-confined fish showed a decrease (P<0.001) in the cH + -ATPase activity in the FB and HB, whereas it produced an increase (P<0.001) in the MB. In non-stressed fish, cytosolic and mitochondrial Ca 2+ -ATPase activities in FB and MB decreased (P<0.001) after TRP feeding. Feeding TRP in stressed fish reduced (P<0.001) cCa 2+ - ATPase activity in the MB but produced an increase (P<0.001) in its activity in mitochondria. In non-stressed fish, TRP feeding decreased (P<0.001) mMg 2+ -ATPase activity in the FB and MB segments. TRP treatment, in stressed fish, however decreased (P<0.001) Mg 2+ -ATPase activity in the MB but not in other brain segments. The data indicate that TRP can regulate brain mitochondrial ion transport, and induction of stress may modify the TRP-induced mitochondrial ion transport response of air-breathing fish.
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