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d ‐phenothrin‐induced oxidative DNA damage in rat liver and kidney determined by HPLC‐ECD/DAD
Author(s) -
Atmaca Enes,
Aksoy Abdurrahman
Publication year - 2015
Publication title -
environmental toxicology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.813
H-Index - 77
eISSN - 1522-7278
pISSN - 1520-4081
DOI - 10.1002/tox.21938
Subject(s) - chemistry , high performance liquid chromatography , deoxyguanosine , oxidative stress , alkaline phosphatase , genotoxicity , dimethyl sulfoxide , 8 hydroxy 2' deoxyguanosine , chromatography , kidney , comet assay , dna damage , medicine , biochemistry , enzyme , dna oxidation , dna , toxicity , oxidative damage , organic chemistry
ABSTRACT 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)/10 6 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/10 6 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/10 6 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.