On two rat cell lines, pheochromocytoma PC12 and ascites hepatoma AS-30D, and on rat liver mitochondria we studied action of paxilline (lipophilic mycotoxin from fungus Penicillium paxilli which is blocker of large-conductance potassium channels) against harmful effects of Cd(II) - one of the most dangerous toxic metals and environmental pollutants. We investigated an influence of paxilline on cell viability and mitochondrial function in the presence and in the absence of Cd²⁺. As found, paxilline protected partially from the Cd²⁺-induced cytotoxicity, namely taken in concentration of 1 μM it decreased the Cd²⁺-induced cell necrosis in average by 10–14 or 13–23% for AS-30D and PC12 cells, respectively. Nevertheless, paxilline did not affect the Cd²⁺-induced apoptosis of AS-30D cells. The alleviating concentration of paxilline reduced an intracellular production of reactive oxygen species (ROS) in PC12 cells intoxicated by Cd²⁺ and enhanced the ROS production in control AS-30D cells; however, it weakly affected mitochondrial membrane potential of the cells in the absence and in the presence of Cd²⁺. The ameliorative concentration of paxilline decreased the maximal respiration rates of control cells of both types after short-term (3–5 h) treatment with it while the rates reached their control levels after long-term (24–48 h) incubation with the drug. Paxilline was not protective against the Cd²⁺-induced membrane permeability and respiration rate changes in isolated rat liver mitochondria. As result, the mitochondrial electron transport chain was concluded to contribute in the mitigating effect of paxilline against the Cd²⁺-produced cell injury.

在两种大鼠嗜铬细胞瘤PC12和腹水性肝癌AS-30D细胞系中，以及在大鼠肝线粒体上，我们研究了Paxilline（真菌的青霉菌Paxilli的亲脂性真菌毒素，它是大传导性钾通道的阻滞剂）对Cd（II）有害作用的作用。 -最危险的有毒金属和环境污染物之一。我们研究了在存在和不存在Cd ²⁺的情况下，paxilline对细胞活力和线粒体功能的影响。如发现的那样，paxilline部分保护了Cd ²⁺诱导的细胞毒性，即浓度为1μM时，对于AS-30D和PC12细胞，Cd ²⁺诱导的细胞坏死平均减少了10–14或13–23％。 ， 分别。尽管如此，帕克西林并没有影响镉²⁺诱导AS-30D细胞凋亡。降低的paxilline浓度减少了被Cd ²⁺致毒的PC12细胞的细胞内活性氧（ROS）的产生，并增加了AS-30D对照细胞的ROS产生。然而，在不存在和存在Cd ²⁺的情况下，它对细胞线粒体膜电位的影响微弱。短期（3-5h）治疗后，paxilline的改善浓度降低了两种类型的对照细胞的最大呼吸速率，而与药物长期孵育（24-48h）后，其达到了对照水平。Paxilline对Cd ^2+的保护作用不强诱导的离体大鼠肝线粒体的膜通透性和呼吸速率变化。结果，线粒体电子传输链被认为有助于减轻帕克西林对Cd ²⁺产生的细胞损伤的作用。