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耳蜗结构中的三磷酸腺苷和磷酸肌酸水平。水杨酸盐的使用速率及作用。

Adenosine triphosphate and phosphocreatine levels in cochlear structures. Use rate and effect of salicylates.

作者信息

Krzanowski J J, Matschinsky F M

出版信息

J Histochem Cytochem. 1975 Oct;23(10):766-73. doi: 10.1177/23.10.1194666.

Abstract

Guinea pigs were injected with various dosages of salicylate for varying time periods. The temporal bones were removed, frozen quickly, freeze-dried, and the cochlea was dissected into essential auditory component parts and subjected to microchemical analysis for phospho-creatine (P-creatine) and adenosine triphosphate (ATP) levels. It was found that high energy phosphates were not decreased by therapeutic or acutely toxic levels of salicylate. Only when chronic intoxication with salicylate was accomplished was there a reduction in ATP and P-creatine. The data presented do not provide support for the widely held view that uncoupling of oxidative phosphorylation or inhibition of enzymes involved in energy generation in the inner ear structures studied (organ of Corti, stria vascularis, Reissner's membrane, modiolar blood vessels, cochlear nerve and spiral ganglion) are the mechanisms by which salicylates cause reversible hearing loss. The study confirms the existence of a P-creatine gradient opposite to the well known glycogen gradient in the organ of Corti (Krzanowski JJ Jr, Matschinsky M: J Histochem 19:321, 1971) and suggests a relatively uniform energy use rate of this tissue for all four turns (20 mmoles of approximately phosphorus used/kg dry weight/min).

摘要

给豚鼠注射不同剂量的水杨酸盐,并持续不同时长。取出颞骨,迅速冷冻、冻干,将耳蜗解剖成基本的听觉组成部分,然后对磷酸肌酸(P-肌酸)和三磷酸腺苷(ATP)水平进行微量化学分析。结果发现,治疗剂量或急性中毒剂量的水杨酸盐不会降低高能磷酸盐水平。只有当水杨酸盐导致慢性中毒时,ATP和P-肌酸才会减少。所呈现的数据并不支持广泛持有的观点,即氧化磷酸化解偶联或抑制所研究的内耳结构(柯蒂氏器、血管纹、前庭膜、蜗轴血管、蜗神经和螺旋神经节)中参与能量生成的酶是水杨酸盐导致可逆性听力损失的机制。该研究证实了在柯蒂氏器中存在与众所周知的糖原梯度相反的P-肌酸梯度(Krzanowski JJ Jr, Matschinsky M: J Histochem 19:321, 1971),并表明该组织在所有四个螺旋(约20毫摩尔磷/kg干重/分钟)中的能量利用率相对一致。

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