High Frequency Electromagnetic Field Induces Lipocalin 2 Expression in Mouse Liver
(ندگان)پدیدآور
Mohammadi Roushandeh, AmanehHalabian, RahelehSoleimani Rad, JafarSadeghzadeh Oskouei, BehnazMehdipour, AhmadNourani, Mohammad RezaHabibi Roudkenar, Mehryarنوع مدرک
TextOriginal Article
زبان مدرک
Englishچکیده
Objective(s)
Neutrophil gelatinase-associated lipocalin (NGAL/Lcn2), comprise a group of small extracellular proteins with a common P-sheet-dominated 3-dimensional structure. In the past, it was assumed that the predominant role of lipocalin was acting as transport proteins. Recently it has been found that oxidative stress induces Lcn2 expression. It has been also proved that electromagnetic field (EMF) produces reactive oxygen species (ROS) in different tissues. Expression of Lcn2 following exposure to electromagnetic field has been investigated in this study.
Materials and Methods
Balb/c mice (8 weeks old) were exposed to 3 mT, 50 HZ EMF for 2 months, 4 hr/day. Afterwards, the mice were sacrificed by cervical dislocation and livers were removed. The liver specimens were stained with Haematoxylin- Eosin (H&E) and analyzed under an optical microscope. Total RNA was extracted from liver and reverse transcription was performed by Superscript III reverse transcriptase with 1 pg of total RNA. Assessment of Lcn2 expression was performed by semiquantitative and real time- PCR.
Results
The light microscopic studies revealed that the number of lymphocyte cells was increased compared to control and dilation of sinosoids was observed in the liver. Lcn2 was up-regulated in the mice exposed to EMF both in mRNA and protein levels.
Conclusion
To the extent of our knowledge, this is the first report dealing with up-regulation of Lcn2 in liver after exposure to EMF. The up-regulation might be a compensatory response that involves cell defense pathways and protective effects against ROS. However, further and complementary studies are required in this regards.
کلید واژگان
Electromagnetic FieldLiver
Lipocalin 2
Reactive Oxygen Species
شماره نشریه
3تاریخ نشر
2010-07-011389-04-10
ناشر
Mashhad University of Medical Sciencesسازمان پدید آورنده
Anatomical Sciences Department, Medicine Faculty, Medical University of Tabriz, Tabriz, IranResearch Center, Iranian Blood Transfusion Organization (IBTO), Tehran, Iran
Anatomical Sciences Department, Medicine Faculty, Medical University of Tabriz, Tabriz, Iran
Anatomical Sciences Department, Medicine Faculty, Medical University of Tabriz, Tabriz, Iran
Anatomical Sciences Department, Medicine Faculty, Medical University of Tabriz, Tabriz, Iran
Chemical Injury Research Center, Baqiyatallah Medical Science University, Tehran Iran
Research Center, Iranian Blood Transfusion Organization (IBTO), Tehran, Iran
شاپا
2008-38662008-3874




