This article was summarized from the PhD thesis of Enes ATMACA's. The results of this study were presented in part as an abstract at the 12th International Congress of the European Association for Veterinary Pharmacology and Toxicology (EAVPT), from 8 to 12 July 2012 in Noordwijkerhout, The Netherlands.
d-phenothrin-induced oxidative DNA damage in rat liver and kidney determined by HPLC-ECD/DAD
Article first published online: 12 DEC 2013
© 2013 Wiley Periodicals, Inc.
Volume 30, Issue 5, pages 607–613, May 2015
How to Cite
Atmaca, E. and Aksoy, A. (2015), d-phenothrin-induced oxidative DNA damage in rat liver and kidney determined by HPLC-ECD/DAD. Environ. Toxicol., 30: 607–613. doi: 10.1002/tox.21938
- Issue published online: 24 APR 2015
- Article first published online: 12 DEC 2013
- Manuscript Accepted: 29 NOV 2013
- Manuscript Revised: 28 NOV 2013
- Manuscript Received: 16 JUL 2013
- Commission for Scientific Research Projects of Ondokuz Mayis University, Samsun, Turkey. Grant Number: PYO.VET.1904.10.002
- oxidative DNA damage
The objective of this study was to assess the risk of genotoxicity of d-phenothrin by measuring the oxidative stress it causes in rat liver and kidney. The level of 8-oxo-7,8-dihydro-2′-deoxyguanosine (8-oxodG)/106 2′-deoxyguanosine (dG) was measured by using high performance liquid chromatography (HPLC) with a diode array (DAD) and an electrochemical detector (ECD). Sixty male Wistar albino rats were randomly divided into five experimental groups and one control group of 10 rats/group. d-phenothrin was administered intraperitoneally (IP) to the five experimental groups at 25 mg/kg (Group I), 50 mg/kg (Group II), 66.7 mg/kg (Group III), 100 mg/kg (Group IV), and 200 mg/kg (Group V) for 14 consecutive days, and the control group received only the vehicle, dimethyl sulfoxide (DMSO). DNA from samples frozen in liquid nitrogen was isolated with a DNA isolation kit. Following digestion with nuclease P1 and alkaline phosphatase (ALP), hydrolyzed DNA was subjected to HPLC. The dG and 8-oxodG levels were analyzed with a DAD and ECD, respectively. In the experimental groups, the mean 8-oxodG/106 dG levels were 48.15 ± 7.43, 68.92 ± 20.66, 82.07 ± 14.15, 85.08 ± 28.50, and 89.14 ± 21.73 in livers and 39.06 ± 7.63, 59.69 ± 14.22, 61.13 ± 17.46, 65.13 ± 23.40, and 72.66 ± 19.04 in kidneys of Groups I, II, III, IV, and V, respectively. The mean 8-oxodG/106 dG levels in the control groups were 44.96 ± 12.66 for the liver and 39.07 ± 4.80 for the kidney. A statistically significant (p < 0.05), dose-dependent increase in oxidative DNA damage was observed in both organs of animals exposed to d-phenothrin when compared to controls. Furthermore, the liver showed a significantly higher level of oxidative DNA damage than the kidney (p < 0.01). In conclusion, d-phenothrin administered to rats intraperitoneally for 14 consecutive days generated free radical species in a dose-dependent manner and caused oxidative DNA damage in the liver and kidney. © 2013 Wiley Periodicals, Inc. Environ Toxicol 30: 607–613, 2015.