bims-aporos Biomed news
on Apoptosis and reactive oxygen species
Issue of 2018‒09‒09
four papers selected by
Gavin McStay
Staffordshire University


  1. Int J Biol Macromol. 2018 Aug 29. pii: S0141-8130(18)32872-1. [Epub ahead of print]
    Li W, Cai ZN, Mehmood S, Wang Y, Pan WJ, Zhang WN, Lu YM, Chen Y.
      Oxidative stress is considered to involve cell death in severe pulmonary diseases like idiopathic pulmonary fibrosis (IPF). Polysaccharide FMP-1 from Morchella esculenta can exert significant antioxidant activity. However, its effects on alveolar epithelial cells remain unperceived. Herein, the effects of FMP-1 against H2O2-induced oxidative damage in human alveolar epithelial A549 cells were investigated. FMP-1 could inhibit H2O2-induced cytochrome C and Caspase-3 release to prevent cell apoptosis via attenuation of MDA and ROS levels, and enhancement the enzymatic activities of SOD and T-AOC. Furthermore, the underlying molecular mechanisms were clarified. The phosphorylation of AKT and the nuclear translocation of Nrf2 were observed to be promoted by FMP-1 as well as the level of HO-1. These findings suggested that FMP-1 attenuate cellular oxidative stress through PI3K/AKT pathway, and FMP-1 could be explored as natural potential antioxidants to lower oxidative stress relevant to the progression of IPF.
    Keywords:  Idiopathic pulmonary fibrosis (IPF); Morchella esculenta; Oxidative stress; PI3K/AKT signaling pathway; Polysaccharide
    DOI:  https://doi.org/10.1016/j.ijbiomac.2018.08.148
  2. Mol Cell Biochem. 2018 Sep 01.
    Zhang W, Hou X, Huang M, Zeng X, He X, Liao Y.
      Tris (1, 3-dichloro-2-propyl) phosphate (TDCPP) is a major type of organophosphorus flame retardants, and long-term exposure to TDCPP to normal cells or tissues under physiological conditions can induce toxic effects. But how TDCPP leads to the adverse effects is not yet clear, and the effect of TDCPP under pathological conditions such as reactive oxygen species assault is not well understood. The present study aimed to explore the potential effect of TDCPP against H2O2-induced oxidative stress in H9c2 cardiomyoblasts and rat neonatal cardiomyocytes. We found that H2O2-treatment decreased cell viability and increased lactate dehydrogenase and malondialdehyde generation of H9c2 cells. However, TDCPP could alleviate these effects. TDCPP alleviated Ca2+-overload caused by H2O2 through decreasing store-operated calcium entry. More importantly, TDCPP remarkably decreased H2O2-induced dephosphorylation of Akt and GSK3β, and through this pathway TDCPP mitigated the H2O2-induced apoptosis and detrimental autophagy. Collectively, via mitigating Ca2+-overload and activating the Akt/GSK3β signaling pathway, TDCPP may have a role in protecting cardiomyocytes from oxidative stress.
    Keywords:  Apoptosis; Calcium overload; Cardiomyocytes; Oxidative stress; TDCPP
    DOI:  https://doi.org/10.1007/s11010-018-3431-8
  3. Colloids Surf B Biointerfaces. 2018 Aug 20. pii: S0927-7765(18)30570-8. [Epub ahead of print]172 152-160
    Ahamed M, Akhtar MJ, Majeed Khan MA, Alhadlaq HA.
      Due to unique optical and electronic properties tin oxide nanoparticles (SnO2 NPs) have shown potential for various applications including solar cell, catalyst, and biomedicine. However, there is limited information concerning the interaction of SnO2 NPs with human cells. In this study, we explored the potential mechanisms of cytotoxicity of SnO2 NPs in human breast cancer (MCF-7) cells. Results demonstrated that SnO2 NPs induce cell viability reduction, lactate dehydrogenase leakage, rounded cell morphology, cell cycle arrest and low mitochondrial membrane potential in dose- and time-dependent manner. SnO2 NPs were also found to provoke oxidative stress evident by generation of reactive oxygen species (ROS), hydrogen peroxide (H2O2) and lipid peroxidation, while depletion of glutathione (GSH) level and lower activity of several antioxidant enzymes. Remarkably, we observed that ROS generation, GSH depletion, and cytotoxicity induced by SnO2 NPs were effectively abrogated by antioxidant N-acetylcycteine. Our data have shown that SnO2 NPs induce toxicity in MCF-7 cells via oxidative stress. This study warrants further research to explore the genotoxicity of SnO2 NPs in different types of cancer cells.
    Keywords:  Antioxidants; Biointeraction; Biomedical application; Cytotoxicity; Human health; Redox homeostasis; SnO(2)nanoparticles
    DOI:  https://doi.org/10.1016/j.colsurfb.2018.08.040
  4. Free Radic Biol Med. 2018 Aug 30. pii: S0891-5849(18)31184-5. [Epub ahead of print]
    Liu D, Ma Z, Di S, Yang Y, Yang J, Xu L, Reiter RJ, Qiao S, Yuan J.
      Doxorubicin (DOX) is a highly effective anticancer anthracycline drug, but its side effects at the level of the heart has limited its widespread clinical application. Melatonin is a documented potent antioxidant, nontoxic and cardioprotective agent, and it is involved in maintaining mitochondrial homeostasis and function. The present study established acute DOX-induced cardiotoxicity models in both H9c2 cells incubated with 1μM DOX and C57BL/6 mice treated with DOX (20mg/kg cumulative dose). Melatonin markedly alleviated the DOX-induced acute cardiac dysfunction and myocardial injury. Both in vivo and in vitro studies verified that melatonin inhibited DOX-induced mitochondrial dysfunction and morphological disorders, apoptosis, and oxidative stress via the activation of AMPK and upregulation of PGC1α with its downstream signaling (NRF1, TFAM and UCP2). These effects were reversed by the use of AMPK siRNA or PGC1α siRNA in H9c2 cells, and were also negated by the cotreatment with AMPK inhibitor Compound C in vivo. Moreover, PGC1α knockdown was without effect on the AMPK phosphorylation induced by melatonin in the DOX treated H9c2 cells. Therefore, AMPK/PGC1α pathway activation may represent a new mechanism for melatonin exerted protection against acute DOX cardiotoxicity through preservation of mitochondrial homeostasis and alleviation of oxidative stress and apoptosis.
    Keywords:  AMPK; Melatonin; PGC1α; apoptosis; cardiotoxicity; doxorubicin; mitochondria
    DOI:  https://doi.org/10.1016/j.freeradbiomed.2018.08.032