Crowley J H, Lorenz R T, Parks L W
Department of Microbiology, North Carolina State University, Raleigh 27695-7615.
Antimicrob Agents Chemother. 1994 May;38(5):1004-7. doi: 10.1128/AAC.38.5.1004.
Fenpropimorph was shown to inhibit the accumulation of the pyrimidine bases uracil and cytosine from the growth media in Saccharomyces cerevisiae. Uracil prototrophs of S. cerevisiae were more resistant to the growth-inhibitory effects of fenpropimorph than were uracil auxotrophs. High concentrations of uracil rescued fenpropimorph-treated uracil auxotrophs, and cytosine, which is accumulated by a separate mechanism, could also support growth of treated uracil auxotrophs. Fenpropimorph caused a significant decrease in the uptake of radiolabeled uracil, which was not due to accumulation of ergosta-8,14-dienol (ignosterol) in the treated cultures. Radiolabeled cytosine uptake was unaffected by drug treatment in a wild-type strain but was inhibited in a sterol mutant, in which ergosterol was absent from the cell. The role of fenpropimorph in causing membrane dysfunction through a mechanism other than altered sterol metabolism is discussed.
已证明粉唑醇可抑制酿酒酵母从生长培养基中积累嘧啶碱基尿嘧啶和胞嘧啶。酿酒酵母的尿嘧啶原养型比尿嘧啶营养缺陷型对粉唑醇的生长抑制作用更具抗性。高浓度的尿嘧啶可挽救经粉唑醇处理的尿嘧啶营养缺陷型,而通过单独机制积累的胞嘧啶也可支持经处理的尿嘧啶营养缺陷型的生长。粉唑醇导致放射性标记尿嘧啶的摄取显著减少,这并非由于处理过的培养物中麦角甾 -8,14-二烯醇(异甾醇)的积累所致。在野生型菌株中,放射性标记胞嘧啶的摄取不受药物处理的影响,但在缺乏麦角甾醇的甾醇突变体中受到抑制。本文讨论了粉唑醇通过改变甾醇代谢以外的机制导致膜功能障碍的作用。