Development of a rapid and sensitive bioassay device using human cells immobilized in macroporous microcarriers for the on-site evaluation of environmental waters

2000 ◽  
Vol 54 (3) ◽  
pp. 432-438 ◽  
Author(s):  
R. Shoji ◽  
Y. Sakai ◽  
A. Sakoda ◽  
M. Suzuki
2002 ◽  
Vol 46 (11-12) ◽  
pp. 355-362 ◽  
Author(s):  
R. Shoji ◽  
Y. Sakai ◽  
A. Sakoda ◽  
M. Suzuki

We have already developed a novel disposable bioassay device based on the low-density lipoprotein (LDL) uptaking activity of human hepatoblastoma Hep G2 cells in our previous work. However, this device is not readily applicable to evaluate river water toxicity on-site because it cannot be preserved for more than one week. In this work, we developed the method for preservation of the device to enable it to be preserved for at least one month. The device can be supplied to individual environmental sites without any facilities for cell culture. We can evaluate river water toxicity by 2 hours of exposure after thawing. Therefore, this kind of device could be a promising tool for daily water quality management.


2002 ◽  
Vol 72 (3) ◽  
pp. 147-153 ◽  
Author(s):  
Kei-Ichi Hirai ◽  
Jie-Hong Pan ◽  
Ying-Bo Shui ◽  
Eriko Simamura ◽  
Hiroki Shimada ◽  
...  

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.


2003 ◽  
Vol 104 ◽  
pp. 289-292 ◽  
Author(s):  
R. Ortega ◽  
B. Fayard ◽  
M. Salomé ◽  
G. Devès ◽  
J. Susini

2004 ◽  
Vol 36 (05) ◽  
Author(s):  
U Henning ◽  
K Krieger ◽  
S Loeffler ◽  
A Klimke
Keyword(s):  

2015 ◽  
Author(s):  
Gerard Ruiz Babot ◽  
Irene Hadjidemetriou ◽  
Sharon Jane Ajodha ◽  
David Taylor ◽  
Norman Taylor ◽  
...  

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