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Oxidative stress‐induced renal telomere shortening as a mechanism of cyclosporine‐induced nephrotoxicity
Author(s) -
Raeisi Sina,
Ghorbanihaghjo Amir,
Argani Hassan,
Dastmalchi Siavoush,
Seifi Morteza,
Ghasemi Babollah,
Ghazizadeh Teimour,
Abbasi Mehran Mesgari,
Karimi Pouran
Publication year - 2018
Publication title -
journal of biochemical and molecular toxicology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.526
H-Index - 58
eISSN - 1099-0461
pISSN - 1095-6670
DOI - 10.1002/jbt.22166
Subject(s) - nephrotoxicity , malondialdehyde , oxidative stress , telomere , telomerase , kidney , renal function , medicine , endocrinology , chemistry , senescence , biochemistry , dna , gene
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.