Oxidative stress‐induced renal telomere shortening as a mechanism of cyclosporine‐induced nephrotoxicity |
| |
Authors: | Sina Raeisi Amir Ghorbanihaghjo Hassan Argani Siavoush Dastmalchi Morteza Seifi Babollah Ghasemi Teimour Ghazizadeh Mehran Mesgari Abbasi Pouran Karimi |
| |
Affiliation: | 1. Pediatric Health Research Center, Tabriz University of Medical Sciences, Tabriz, Iran;2. Drug Applied Research Center, Tabriz University of Medical Sciences, Tabriz, Iran;3. Biotechnology Research Center, Tabriz University of Medical Sciences, Tabriz, Iran;4. Urology and Nephrology Research Center, Shahid Beheshti University of Medical Sciences, Tehran, Iran;5. Department of Medical Genetics, Faculty of Medicine & Dentistry, University of Alberta, Edmonton, Alberta, Canada;6. Division of Clinical Laboratory, Tabriz Children Hospital, Tabriz University of Medical Sciences, Tabriz, Iran;7. Department of Biochemistry and Clinical Laboratories, Faculty of Medicine, Tabriz University of Medical Sciences, Tabriz, Iran;8. Neurosciences Research Center, Tabriz University of Medical Sciences, Tabriz, Iran |
| |
Abstract: | Due to the association of oxidative stress and telomere shortening, it was aimed in the present study to investigate the possibility whether cyclosporine‐A exerts its nephrotoxic side effects via induction of oxidative stress‐induced renal telomere shortening and senescent phenotype in renal tissues of rats. Renal oxidative stress markers, 8‐hydroxydeoxyguanosine, malondialdehyde, and protein carbonyl groups were measured by standard methods. Telomere length and telomerase activity were also evaluated in kidney tissue samples. Results showed that cyclosporine‐A treatment significantly (P < 0.05) enhanced renal malondialdehyde, 8‐hydroxydeoxyguanosine, and protein carbonyl groups levels, decreased renal telomere length, and deteriorated renal function compared with the controls. Renal telomerase activity was not affected by cyclosporine‐A. Renal telomere length could be considered as an important parameter of both oxidative stress and kidney function. Telomere shortening and accelerated kidney aging may be caused by cyclosporine‐induced oxidative stress, indicating the potential mechanism of cyclosporine‐induced nephrotoxicity. |
| |
Keywords: | cyclosporine‐A nephrotoxicity oxidative stress telomerase telomere length |
|
|