完整的鼠类圆线虫感染性（L3）幼虫对呼吸电子传递底物和抑制剂的反应

The response of intact Strongyloides ratti infective (L3) larvae to substrates and inhibitors of respiratory electron transport.

作者信息

Mendis A H, Armson A, Thompson R C, Grubb W B

机构信息

School of Biomedical Sciences, Curtin University of Technology, Perth, Australia.

出版信息

Int J Parasitol. 1991 Dec;21(8):965-8. doi: 10.1016/0020-7519(91)90174-6.

DOI:10.1016/0020-7519(91)90174-6

PMID:1787040

Abstract

Live, intact third-stage larvae (L3s) of Strongyloides ratti in the absence of exogenous substrates consumed oxygen at a rate (E-QO2) of 181.8 +/- 12.4 ng atoms min-1 mg dry weight-1 at 35 degrees C. Respiratory electron transport (RET) Complex I inhibitor rotenone (2 microM) produced 33 +/- 6.5% inhibition of the E-QO2. Unusually the rotenone-induced inhibition was not relieved by 5 mM-succinate. The E-QO2 of intact L3s was refractory to RET Complex III inhibitor antimycin A at 2 microM; 4 microM-antimycin inhibited less than or equal to 10% of the E-QO2. The electron donor couple ascorbate/TMPD augmented the E-QO2 in the presence of rotenone (2 microM) and antimycin A (4 microM) by 110%. Azide (1 mM) stimulated the antimycin A refractory QO2 by 36.6 +/- 7.2% which was only partially inhibited by 1.0 mM-KCN (IC50 = 0.8 mM). The data suggest the presence of classical (CPW) and alternate (APW) electron transport pathways in S. ratti L3s.

摘要

在无外源底物的情况下，活的完整的鼠类圆线虫第三期幼虫（L3s）在35℃时以181.8±12.4纳摩尔原子每分钟每毫克干重的速率（E-QO2）消耗氧气。呼吸电子传递（RET）复合体I抑制剂鱼藤酮（2微摩尔）对E-QO2产生了33±6.5%的抑制作用。不同寻常的是，5毫摩尔琥珀酸并不能缓解鱼藤酮诱导的抑制作用。完整L3s的E-QO2对2微摩尔的RET复合体III抑制剂抗霉素A不敏感；4微摩尔抗霉素对E-QO2的抑制作用小于或等于10%。在存在鱼藤酮（2微摩尔）和抗霉素A（4微摩尔）的情况下，电子供体对Ascorbate/TMPD使E-QO2增加了110%。叠氮化物（1毫摩尔）使对抗霉素A不敏感的QO2增加了36.6±7.2%，而1.0毫摩尔氰化钾仅部分抑制了该增加（IC50 = 0.8毫摩尔）。数据表明鼠类圆线虫L3s中存在经典（CPW）和交替（APW）电子传递途径。