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Oxidative stress-induced renal telomere shortening as a mechanism of cyclosporine-induced nephrotoxicity.
- Source :
-
Journal of biochemical and molecular toxicology [J Biochem Mol Toxicol] 2018 Aug; Vol. 32 (8), pp. e22166. Date of Electronic Publication: 2018 Jul 05. - Publication Year :
- 2018
-
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.<br /> (© 2018 Wiley Periodicals, Inc.)
- Subjects :
- Aging genetics
Animals
Biomarkers metabolism
Body Weight
Creatinine blood
Kidney enzymology
Kidney metabolism
Kidney physiology
Male
Rats, Wistar
Telomerase metabolism
Urea blood
Cyclosporine toxicity
Immunosuppressive Agents toxicity
Kidney drug effects
Oxidative Stress drug effects
Telomere Shortening
Subjects
Details
- Language :
- English
- ISSN :
- 1099-0461
- Volume :
- 32
- Issue :
- 8
- Database :
- MEDLINE
- Journal :
- Journal of biochemical and molecular toxicology
- Publication Type :
- Academic Journal
- Accession number :
- 29975447
- Full Text :
- https://doi.org/10.1002/jbt.22166