• 제목/요약/키워드: glucose-induced acidification

검색결과 5건 처리시간 0.021초

중급 지방산 항진균 활성과 진균의 Plasma membrane H+-ATPase에 대한 저해작용 (Antifungal Activity of Medium-chain Saturated Fatty Acids and Their Inhibitory Activity to the Plasma Membrane H+-ATPase of Fungi)

  • 이상화;김창진
    • 한국미생물·생명공학회지
    • /
    • 제27권5호
    • /
    • pp.354-358
    • /
    • 1999
  • In order to know the antifungal characteristics of saturated fatty acids having 6 to 12 carbons, their minimum inhibitory concentrations (MICs) and minimum fungicidal concentrations (MFCs) were estimated against Saccharomyces cerevisiae. Fatty acids from C6 to C11 exhibited increasing activity with chain length, but C12 fatty acid did not show activity at all. In relation to antifungal modes of actions, fatty acids investigated showed on inhibitory activity toward the plasma membrane H+-ATPase of Saccharomyces cerevisiae. Their inhibitions to the glucose-induced acidification and ATP hydrolysis caused by the proton pump were found to be in common wiht antifungal activities. At the test concentration of 1mM, hexanoic acid (C6) showed the lowest inhibition of about 30%, while undecanoic acid(C11) showed the strongest inhibition of over 90%. In addition, as seen with antifungal activity, the inhibitory activity of dodecanoic acid (C12) was suddenly reduced to less than 50%.

  • PDF

Lysosome Inhibition Reduces Basal and Nutrient-Induced Fat Accumulation in Caenorhabditis elegans

  • Lu, Rui;Chen, Juan;Wang, Fangbin;Wang, Lu;Liu, Jian;Lin, Yan
    • Molecules and Cells
    • /
    • 제45권9호
    • /
    • pp.649-659
    • /
    • 2022
  • A long-term energy nutritional imbalance fundamentally causes the development of obesity and associated fat accumulation. Lysosomes, as nutrient-sensing and lipophagy centers, critically control cellular lipid catabolism in response to nutrient deprivation. However, whether lysosome activity is directly involved in nutrient-induced fat accumulation remains unclear. In this study, worm fat accumulation was induced by 1 mM glucose or 0.02 mM palmitic acid supplementation. Along with the elevation of fat accumulation, lysosomal number and acidification were also increased, suggesting that lysosome activity might be correlated with nutrient-induced fat deposition in Caenorhabditis elegans. Furthermore, treatments with the lysosomal inhibitors chloroquine and leupeptin significantly reduced basal and nutrient-induced fat accumulation in C. elegans. The knockdown of hlh-30, which is a critical gene in lysosomal biogenesis, also resulted in worm fat loss. Finally, the mutation of aak-2, daf-15, and rsks-1 showed that mTORC1 (mechanistic target of rapamycin complex-1) signaling mediated the effects of lysosomes on basal and nutrient-induced fat accumulation in C. elegans. Overall, this study reveals the previously undescribed role of lysosomes in overnutrition sensing, suggesting a new strategy for controlling body fat accumulation.

Antifungal Activity of Medium-Chain ($C_{6}-C_{13}$) Alkenals against, and Their Inhibitory Effect on the Plasma Membrane $H^{+}$-ATPase of Saccharomyces cerevisiae

  • Lee, Jae-Ran;Lee, Sang-Hwa;Kubo, Isao;Hong, Soon-Duck
    • Journal of Microbiology and Biotechnology
    • /
    • 제8권3호
    • /
    • pp.197-202
    • /
    • 1998
  • Aliphatic alkenals having 6 to 13 carbons were evaluated for antifungal activity against Saccharomyces cerevisiae. The activity was gradually increased with chain length, e.g., (E)-2-decenal and (E)-2-undecenal exhibited maximum potency, while (E)-2-dodecenal and (E)-2-tridecenal were completely inactive. Alkenals showed increasing inhibitory activity with chain length, as in the case of antifungal activity, towards glucose-induced medium acidification by the plasma membrane $H^+$-ATPase of S. cerevisiae. The group including (E)-2-nonenal, (E)-2-decenal, and (E)-2-undecenal exhibited maximum potency, but the potency of (E)-2-dodecenal and (E)-2-tridecenal demonstrated a sudden drop with respect to the former group. (E)-2-Nonenal revealed dose-responsive inhibition to the medium acidification and inhibited over 90% at a concentration of 1.25 mM ($175.3{\mu}g$/ml). In contrast to (E)-2-undecenal whose inhibitory efficiency increased with incubation time, inhibition by (E)-2-dodecenal was reversed with time. Of the tested alkenals, (E)-2-heptenal and (E)-2-octenal most highly inhibited ATP hydrolytic activity by the plasma membrane $H^+$ ATPase, while (E)-2-heptenal at 10 mM ($1121.8{\mu}g$/ml) showed an inhibitory efficacy of 93.2%.

  • PDF

Proteome Changes in Penicillium expansum Grown in a Medium Derived from Host Plant

  • Xia, Xiaoshuang;Li, Huan;Liu, Fei;Zhang, Ye;Zhang, Qi;Wang, Yun;Li, Peiwu
    • Journal of Microbiology and Biotechnology
    • /
    • 제27권3호
    • /
    • pp.624-632
    • /
    • 2017
  • Penicillium expansum causes blue mold rot, a prevalent postharvest disease of pome fruit, and is also the main producer of the patulin. However, knowledge on the molecular mechanisms involved in this pathogen-host interaction remains largely unknown. In this work, a two-dimensional gel electrophoresis-based proteomic approach was applied to probe changes in P. expansum 3.3703 cultivated in apple juice medium, which was used to mimic the in planta condition. The results showed that the pH value and reducing sugar content in the apple juice medium decreased whereas the patulin content increased with the growing of P. expansum. A total of 28 protein spots that were up-regulated in P. expansum when grown in apple juice medium were identified. Functional categorization revealed that the identified proteins were mainly related to carbohydrate metabolism, secondary metabolism, protein biosynthesis or degradation, and redox homeostasis. Remarkably, several induced proteins, including glucose dehydrogenase, galactose oxidase, and FAD-binding monooxygenase, which might be responsible for the observed medium acidification and patulin production, were also detected. Overall, the experimental results provide a comprehensive interpretation of the physiological and proteomic responses of P. expansum to the host plant environment, and future functional characterization of the identified proteins will deepen our understanding of fungi-host interactions.

Ginsenoside compound K protects against cerebral ischemia/ reperfusion injury via Mul1/Mfn2-mediated mitochondrial dynamics and bioenergy

  • Qingxia Huang;Jing Li;Jinjin Chen;Zepeng Zhang;Peng Xu;Hongyu Qi;Zhaoqiang Chen;Jiaqi Liu;Jing Lu;Mengqi Shi;Yibin Zhang;Ying Ma;Daqing Zhao;Xiangyan Li
    • Journal of Ginseng Research
    • /
    • 제47권3호
    • /
    • pp.408-419
    • /
    • 2023
  • Background: Ginsenoside compound K (CK), the main active metabolite in Panax ginseng, has shown good safety and bioavailability in clinical trials and exerts neuroprotective effects in cerebral ischemic stroke. However, its potential role in the prevention of cerebral ischemia/reperfusion (I/R) injury remains unclear. Our study aimed to investigate the molecular mechanism of ginsenoside CK against cerebral I/R injury. Methods: We used a combination of in vitro and in vivo models, including oxygen and glucose deprivation/reperfusion induced PC12 cell model and middle cerebral artery occlusion/reperfusion induced rat model, to mimic I/R injury. Intracellular oxygen consumption and extracellular acidification rate were analyzed by Seahorse multifunctional energy metabolism system; ATP production was detected by luciferase method. The number and size of mitochondria were analyzed by transmission electron microscopy and MitoTracker probe combined with confocal laser microscopy. The potential mechanisms of ginsenoside CK on mitochondrial dynamics and bioenergy were evaluated by RNA interference, pharmacological antagonism combined with co-immunoprecipitation analysis and phenotypic analysis. Results: Ginsenoside CK pretreatment could attenuate mitochondrial translocation of DRP1, mitophagy, mitochondrial apoptosis, and neuronal bioenergy imbalance against cerebral I/R injury in both in vitro and in vivo models. Our data also confirmed that ginsenoside CK administration could reduce the binding affinity of Mul1 and Mfn2 to inhibit the ubiquitination and degradation of Mfn2, thereby elevating the protein level of Mfn2 in cerebral I/R injury. Conclusion: These data provide evidence that ginsenoside CK may be a promising therapeutic agent against cerebral I/R injury via Mul1/Mfn2 mediated mitochondrial dynamics and bioenergy.