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( Suel Kee Kim ),( Ho Joon Lee ),( Su Yeon An ),( Chang Joo Lee ),( Yong Dal Yoon ) 한국환경생물학회 2004 환경생물 : 환경생물학회지 Vol.22 No.4
N/A This study was focused on the risk assessment of whether radiofrequency electromagnetic fields generated by mobile phone is cytogenetically toxic or not. We conducted the effects of 835-MHz electromagnetic field (EMF) on DNA strand breaks in mouse thymic lymphoma L5178Y Tk^(+/-) cells using alkaline comet assay. EMF frequency 835-MHz we chosen is one of the most popular communication frequency bands in Korean code-division multiple-access (CDMA) mobile phone system. The cells were exposed to 835-MHz EMF alone or 835-MHz EMF combined with cyclophosamide (CPA) or 4-nitroquinoline-l-oxide (4NQO) at specific absorption rate (SAR) of 4.0 W kg^(-1) for 24 and 48 hrs. DNA damage expressed as tail moment was increased more than two-fold after exposure to 835-MHz EMF for 24 and 48 hr. In particular, CPA for 48 hr and 4NQO for 24 hr enhanced notably the tail moment to 9-fold and 16-fold in the presence of 835-MHz EMF, respectively, compared to each single treatment. From these results, it appears that exposure to CDMA-mobile phone radiation at 835-MHz frequency may potentiate DNA strand breaks of mouse thymic lymphoma L5178Y Tk^(+/-) cells under the defined conditions of this study.
Suel Ki Lim,Byeong Cheol Yoon,Dong IL Kim,Seong Soo Kang,Ho Jae Han,Soo Hyun Park 한국실험동물학회 2007 Laboratory Animal Research Vol.23 No.3
Liver transplantation is essential for patients with liver failure. Pig is known to be a most suitable species in xeno-transplantation of human organs. Hepatocytes are important sites in the body's metabolism and function. Glucose transporter in hepatocytes plays a role in regulation of blood glucose homeostasis. Epidermal growth factor (EGF) is known to be a regulator of physiological function in various cell systems. However, the effect of EGF on glucose activity in pig hepatocytes was not clearly elucidated. Thus, this study investigated the effect of EGF on glucose transporter and its related signal cascades in primary cultured pig hepatocytes. EGF inhibited glucose uptake in a dose (> 1 ng/㎖) dependent manner. EGF-induced decrease of [³H]-deoxyglucose uptake was blocked by AG 1478 (10-⁶ M, an EGF receptor antagonist) genistein and herbymycin A (tyrosine kinase inhibitors, 10⁻⁶ M), suggesting the role of activation and tyrosine phosphorylation of EGF receptor. In addition, EGF-induced decrease of [³H]-deoxyglucose uptake was prevented by mepacrine, AACOCF₃ (phospholipase A₂ inhibitors), indomethacin and ibuprofen (cyclooxygenase inhibitors). Indeed, EGF increased [³H]-arachidonic acid release and cyclooxygenase-2 (COX-2) expression. Moreover, EGF-induced stimulation of [³H]-arachidonic acid release was blocked by PD 98059 (a p44/42 mitogen activated protein kinase [MAPK] inhibitor) and SB 203580 (a p38 MAPK inhibitor). EGF-induced decrease of [³H]-deoxyglucose uptake was also prevented by these two MAPKs. However, EGF-induced stimulation of p44/42 MAPK and p38 MAPK was not blocked by mepacrine and indomethacin. In conclusion, EGF decreases glucose uptake via MAPK-COX-2 signal cascades in cultured pig hepatocytes.
Suel Ki Lim,Min Jung Park,Byeong Cheol Yoon,Su Young Jung,Kyung Chul Yoon,Chun Sik Bae,Ho Jae Han,Soo-hyun Park 한국실험동물학회 2007 Laboratory Animal Research Vol.23 No.4
The development of diabetic nephropathy is associated with the dysfunction of proximal tubule cells. High glucose has also been considered to play an important role in alteration of Na⁺/glucose cotransporter in proximal tubule cells. Ginsenosides have been used as a remedy for diabetes in Asian countries. Therefore, we examined the preventive effect of ginsenosides against high glucose-induced alteration of Na⁺/glucose cotransporter and its related signal pathways in the primary cultured proximal tubule cells. In present study, high glucose inhibited Na⁺/glucose cotransporter (α-MG uptake) in proximal tubule cells. Ginsenosides total saponin (GTS), penoxatriol (PT) and penoxadiol (PD) blocked high glucose-induced inhibition of α-MG uptake in proximal tubule cells. In addition, high glucose stimulated cAMP formation and PKC activity from cytosolic to membrane fraction. GTS, PT and PD prevented high glucose-induced stimulation of cAMP and PKC activity. Moreover, high glucose stimulated TGF-β1 secretion, which was completely blocked by the treatment of GTS, PD and PT in proximal tubule cells. In conclusion, GTS prevented high glucose-induced dysfunction of proximal tubule cells via inhibition of cAMP, PKC, and TGF-β1 signaling cascades.