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10.1016/j.lssr.2014.02.006 http://scihub22266oqcxt.onion/10.1016/j.lssr.2014.02.006 C4111269!4111269!25072018     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=25072018&cmd=llinks): Failed to open stream: HTTP request failed! 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Mitochondria regulate DNA damage and genomic instability induced by high LET radiation |pdf=|usr=}}{{25072018}} gab.com Text Mitochondria regulate DNA damage and genomic instability induced by high LET radiation JO: Life Sci Space Res (Amst) http://www.kidney.de/pget.php?&tw=1&pmid=25072018 #FOAvip High linear energy transfer (LET) radiation including ? particles and heavy ions is the major type of radiation find in space and is considered a potential health risk for astronauts. Even though the chance that these high LET particles traversing through the cytoplasm of cells is higher than that through the nuclei, the contribution of targeted cytoplasmic irradiation, to the induction of genomic instability and other chromosomal damages induced by high LET radiation is not known. In the present study, we investigated whether mitochondria are the potential cytoplasmic target of high LET radiation in mediating cellular damage using a mitochondrial DNA (mtDNA) depleted (?0) human small airway epithelial (SAE) cell model and a precision charged particle microbeam with a beam width of merely one micron. Targeted cytoplasmic irradiation by high LET ? particles induced DNA oxidative damage and double strand breaks in wild type ?+ SAE cells. Furthermore, there was a significant increase in autophagy, micronuclei, which is an indication of genomic instability, together with the activation of nuclear factor kappa-B (NF-?B) and mitochondrial inducible nitric oxide synthase (iNOS) signaling pathways in ?+ SAE cells. In contrast, ?0 SAE cells exhibited a significantly lower response to these same endpoints examined after cytoplasmic irradiation with high LET ? particles. The results indicate that mitochondria are essential in mediating cytoplasmic radiation induced genotoxic damage in mammalian cells. Furthermore, the findings may shed some light in the design of countermeasures for space radiation. Twit Text FOAVip Mitochondria regulate DNA damage and genomic instability induced by high LET radiation ????Life Sci Space Res (Amst) http://www.kidney.de/pget.php?&tw=1&pmid=25072018 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=25072018 #FOAvip English Wikipedia <ref>{{Cite pmid|25072018}}</ref> Mitochondria regulate DNA damage and genomic instability induced by high LET radiation #MMPMID25072018 Zhang B; Davidson MM; Hei TK Life Sci Space Res (Amst) 2014[Apr]; 1 (ä): 80-8 PMID25072018show ga High linear energy transfer (LET) radiation including ? particles and heavy ions is the major type of radiation find in space and is considered a potential health risk for astronauts. Even though the chance that these high LET particles traversing through the cytoplasm of cells is higher than that through the nuclei, the contribution of targeted cytoplasmic irradiation, to the induction of genomic instability and other chromosomal damages induced by high LET radiation is not known. In the present study, we investigated whether mitochondria are the potential cytoplasmic target of high LET radiation in mediating cellular damage using a mitochondrial DNA (mtDNA) depleted (?0) human small airway epithelial (SAE) cell model and a precision charged particle microbeam with a beam width of merely one micron. Targeted cytoplasmic irradiation by high LET ? particles induced DNA oxidative damage and double strand breaks in wild type ?+ SAE cells. Furthermore, there was a significant increase in autophagy, micronuclei, which is an indication of genomic instability, together with the activation of nuclear factor kappa-B (NF-?B) and mitochondrial inducible nitric oxide synthase (iNOS) signaling pathways in ?+ SAE cells. In contrast, ?0 SAE cells exhibited a significantly lower response to these same endpoints examined after cytoplasmic irradiation with high LET ? particles. The results indicate that mitochondria are essential in mediating cytoplasmic radiation induced genotoxic damage in mammalian cells. Furthermore, the findings may shed some light in the design of countermeasures for space radiation. äMitochondria regulate DNA damage and genomic instability induced by hi(epmc).pdf DeepDyve Pubget Overpricing