Repression of transient expression by DNA methylation in transcribed regions of reporter genes introduced into cultured human cells

1995 ◽  
Vol 1260 (1) ◽  
pp. 73-78 ◽  
Author(s):  
Jun-ichiro Komura ◽  
Takaho Okada ◽  
Tetsuya Ono
Keyword(s):  
Dna Methylation ◽  
Transient Expression ◽  
Reporter Genes ◽  
Human Cells ◽  
Cultured Human Cells

Alpha-Tocopherol Protects Cultured Human Cells from the Acute Lethal Cytotoxicity of Dioxin

2002 ◽  
Vol 72 (3) ◽  
pp. 147-153 ◽  
Author(s):  
Kei-Ichi Hirai ◽  
Jie-Hong Pan ◽  
Ying-Bo Shui ◽  
Eriko Simamura ◽  
Hiroki Shimada ◽  
...  
Keyword(s):  
Cell Death ◽  
Cell Damage ◽  
Smooth Endoplasmic Reticulum ◽  
Dehydroascorbic Acid ◽  
Human Cells ◽  
Alpha Tocopherol ◽  
Cervical Cancer Cells ◽  
Cultured Human Cells ◽  
Nuclear Damage ◽  
Conjunctival Epithelial Cells

The possible protection of cultured human cells from acute dioxin injury by antioxidants was investigated. The most potent dioxin, 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD), caused vacuolization of the smooth endoplasmic reticulum and Golgi apparatus in cultured human conjunctival epithelial cells and cervical cancer cells. Subsequent nuclear damage included a deep irregular indentation resulting in cell death. A dosage of 30–40 ng/mL TCDD induced maximal intracellular production of H2O2 at 30 minutes and led to severe cell death (0–31% survival) at two hours. A dose of 1.7 mM alpha-tocopherol or 1 mM L-dehydroascorbic acid significantly protected human cells against acute TCDD injuries (78–97% survivals), but vitamin C did not provide this protection. These results indicate that accidental exposure to fatal doses of TCDD causes cytoplasmic free radical production within the smooth endoplasmic reticular systems, resulting in severe cytotoxicity, and that vitamin E and dehydroascorbic acid can protect against TCDD-induced cell damage.

Cytotoxic, genotoxic and cell-cycle disruptive effects of thio-dimethylarsinate in cultured human cells and the role of glutathione

2008 ◽  
Vol 228 (1) ◽  
pp. 59-67 ◽  
Author(s):  
Takafumi Ochi ◽  
Kayoko Kita ◽  
Toshihide Suzuki ◽  
Alice Rumpler ◽  
Walter Goessler ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Human Cells ◽  
Cultured Human Cells

scholarly journals Multiple Fates of L1 Retrotransposition Intermediates in Cultured Human Cells

2005 ◽  
Vol 25 (17) ◽  
pp. 7780-7795 ◽  
Author(s):  
Nicolas Gilbert ◽  
Sheila Lutz ◽  
Tammy A. Morrish ◽  
John V. Moran
Keyword(s):  
Genetic Instability ◽  
Noncoding Rnas ◽  
Human Cells ◽  
Genomic Rearrangements ◽  
U6 Snrna ◽  
Human Dna ◽  
Cultured Human Cells ◽  
Repair Pathways ◽  
Genomic Locations ◽  
Host Parasite

ABSTRACT LINE-1 (L1) retrotransposons comprise ∼17% of human DNA, yet little is known about L1 integration. Here, we characterized 100 retrotransposition events in HeLa cells and show that distinct DNA repair pathways can resolve L1 cDNA retrotransposition intermediates. L1 cDNA resolution can lead to various forms of genetic instability including the generation of chimeric L1s, intrachromosomal deletions, intrachromosomal duplications, and intra-L1 rearrangements as well as a possible interchromosomal translocation. The L1 retrotransposition machinery also can mobilize U6 snRNA to new genomic locations, increasing the repertoire of noncoding RNAs that are mobilized by L1s. Finally, we have determined that the L1 reverse transcriptase can faithfully replicate its own transcript and has a base misincorporation error rate of ∼1/7,000 bases. These data indicate that L1 retrotransposition in transformed human cells can lead to a variety of genomic rearrangements and suggest that host processes act to restrict L1 integration in cultured human cells. Indeed, the initial steps in L1 retrotransposition may define a host/parasite battleground that serves to limit the number of active L1s in the genome.

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