Sulfated lentinan induced mitochondrial dysfunction leads to programmed cell death of tobacco BY-2 cells.
Pestic Biochem Physiol
; 137: 27-35, 2017 Apr.
Article
em En
| MEDLINE
| ID: mdl-28364801
ABSTRACT
Sulphated lentinan (sLTN) is known to act as a resistance inducer by causing programmed cell death (PCD) in tobacco suspension cells. However, the underlying mechanism of this effect is largely unknown. Using tobacco BY-2 cell model, morphological and biochemical studies revealed that mitochondrial reactive oxygen species (ROS) production and mitochondrial dysfunction contribute to sLNT induced PCD. Cell viability, and HO/PI fluorescence imaging and TUNEL assays confirmed a typical cell death process caused by sLNT. Acetylsalicylic acid (an ROS scavenger), diphenylene iodonium (an inhibitor of NADPH oxidases) and protonophore carbonyl cyanide p-trifluoromethoxyphenyl hydrazone (a protonophore and an uncoupler of mitochondrial oxidative phosphorylation) inhibited sLNT-induced H2O2 generation and cell death, suggesting that ROS generation linked, at least partly, to a mitochondrial dysfunction and caspase-like activation. This conclusion was further confirmed by double-stained cells with the mitochondria-specific marker MitoTracker RedCMXRos and the ROS probe H2DCFDA. Moreover, the sLNT-induced PCD of BY-2 cells required cellular metabolism as up-regulation of the AOX family gene transcripts and induction of the SA biosynthesis, the TCA cycle, and miETC related genes were observed. It is concluded that mitochondria play an essential role in the signaling pathway of sLNT-induced ROS generation, which possibly provided new insight into the sLNT-mediated antiviral response, including PCD.
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Texto completo:
1
Base de dados:
MEDLINE
Assunto principal:
Nicotiana
/
Apoptose
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Lentinano
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Mitocôndrias
Tipo de estudo:
Prognostic_studies
Idioma:
En
Revista:
Pestic Biochem Physiol
Ano de publicação:
2017
Tipo de documento:
Article
País de afiliação:
China