Literature DB >> 24483236

Rapamycin inhibits acrolein-induced apoptosis by alleviating ROS-driven mitochondrial dysfunction in male germ cells.

X He1, W Song, C Liu, S Chen, J Hua.   

Abstract

OBJECTIVES: Acrolein (Acr) is a highly reactive α, β-unsaturated aldehyde, which can induce reactive oxygen species (ROS) generation. Several factors, including lipid peroxidation, clinical use of cyclophosphamide, fried foods, automobile exhausts, smoking and aging can increase its concentration in blood serum. Mounting evidence has suggested that Acr-induced ROS might reduce quality of sperm. Thus, the aim of this study was to examine reproductive toxicity of Acr-caused ROS in vitro and find a means to alleviate it.
MATERIALS AND METHODS: We investigated the effects of Acr on male germ cell (MGC)-derived GC-1 cells in vitro. Dihydroethidium and DCFH-DA fluorescent dyes were used to determine generation of intracellular ROS.
RESULTS: We found that Acr induced ROS generation, which was accompanied by reduced Bcl2/Bax ratio, substantial decline in mitochondrial membrane potential, and further promoted apoptosis of MGCs. Furthermore, Rapamycin was capable of alleviating Acr-induced ROS, reducing ROS-induced apoptosis by increasing ratio of Bcl2/Bax mRNA and proteins, and protecting MGC mitochondrial membranes.
CONCLUSION: Rapamycin inhibited Acr-induced apoptosis by alleviating ROS-driven mitochondrial dysfunction in MGCs.
© 2014 John Wiley & Sons Ltd.

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Year:  2014        PMID: 24483236      PMCID: PMC6496251          DOI: 10.1111/cpr.12091

Source DB:  PubMed          Journal:  Cell Prolif        ISSN: 0960-7722            Impact factor:   6.831


  39 in total

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5.  Testicular gametogenic and steroidogenic activities in cyclophosphamide treated rat: a correlative study with testicular oxidative stress.

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10.  Effects of maternal acrolein exposure during pregnancy on testicular testosterone production in fetal rats.

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