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巯基试剂对大鼠比目鱼肌糖转运的多种影响。

Multiple effects of sulphydryl reagents on sugar transport by rat soleus muscle.

作者信息

Kozka I J, Gould M K

出版信息

Biochim Biophys Acta. 1982 Jul 28;689(2):210-8. doi: 10.1016/0005-2736(82)90253-x.

Abstract

Iodoacetate, over the range 0.2-2 mM, stimulated the uptake of D-xylose by rat soleus muscle and inhibited anaerobic lactate production by soleus muscle. Stimulation of sugar transport is considered to be due to the resultant fall in ATP. p-Chloromercuribenzene sulphonate (0.5-2 mM) stimulated xylose uptake to a lesser extent than iodoacetate and induced a proportionately smaller fall in ATP, consistent with the inhibitory effect of p-chloromercuribenzene sulphonate on lactate production. Under certain conditions, p-chloromercuribenzene sulphonate stimulated sugar transport without affecting the ATP level. This suggests that whereas p-chloromercuribenzene sulphonate can be expected to stimulate sugar transport through the lowering of muscle ATP, it may also act through some other mechanism. No stimulatory effect on xylose uptake was observed when muscles were exposed to N-ethylmaleimide (0.02-2 mM) either for brief (1 min) or more prolonged (30 min) periods. Because N-ethylmaleimide induced a marked fall in muscle ATP, it is surprising that N-ethylmaleimide did not stimulate sugar transport; in most experiments this inhibitor actually inhibited sugar transport. N-Ethylmaleimide inhibited the stimulation of sugar transport by 2,4-dinitrophenol and anoxia; this inhibitory effect appears to explain why N-ethylmaleimide itself did not stimulate sugar transport. p-Chloromercuribenzene sulphonate also inhibited 2,4-dinitrophenol-stimulated xylose uptake by a mechanism which seems similar to that of N-ethylmaleimide; this could explain in part the modest stimulatory effect of this inhibitor on muscle sugar transport.

摘要

在0.2 - 2 mM范围内,碘乙酸盐刺激大鼠比目鱼肌对D - 木糖的摄取,并抑制比目鱼肌的无氧乳酸生成。糖转运的刺激被认为是由于ATP含量下降所致。对氯汞苯磺酸盐(0.5 - 2 mM)刺激木糖摄取的程度小于碘乙酸盐,且导致ATP下降幅度相应较小,这与对氯汞苯磺酸盐对乳酸生成的抑制作用一致。在某些条件下,对氯汞苯磺酸盐刺激糖转运而不影响ATP水平。这表明,虽然预期对氯汞苯磺酸盐可通过降低肌肉ATP来刺激糖转运,但它也可能通过其他机制起作用。当肌肉暴露于N - 乙基马来酰亚胺(0.02 - 2 mM)短时间(1分钟)或较长时间(30分钟)时,未观察到对木糖摄取的刺激作用。由于N - 乙基马来酰亚胺导致肌肉ATP显著下降,令人惊讶的是N - 乙基马来酰亚胺并未刺激糖转运;在大多数实验中,这种抑制剂实际上抑制了糖转运。N - 乙基马来酰亚胺抑制2,4 - 二硝基苯酚和缺氧对糖转运的刺激作用;这种抑制作用似乎可以解释为什么N - 乙基马来酰亚胺本身不刺激糖转运。对氯汞苯磺酸盐也通过一种似乎与N - 乙基马来酰亚胺相似的机制抑制2,4 - 二硝基苯酚刺激的木糖摄取;这可以部分解释这种抑制剂对肌肉糖转运的适度刺激作用。

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