TY - JOUR
T1 - Iron release and oxidative DNA damage in splenic toxicity of aniline
AU - Wu, Xiaohong
AU - Kannan, Subburaj
AU - Ramanujam, V. M.Sadagopa
AU - Khan, M. Firoze
N1 - Funding Information:
Received 27 August 2004; accepted 31 October 2004. This publication was made possible by a grant (ES 06476) from the National Institute of Environmental Health Sciences (NIEHS), NIH, and its contents are solely the responsibility of the authors and do not necessarily represent the official views of the NIEHS, NIH. Address correspondence to M. Firoze Khan, PhD, Associate Professor, Department of Pathology, University of Texas Medical Branch, Galveston, TX 77555-0609, USA. E-mail: [email protected]
PY - 2005/4/23
Y1 - 2005/4/23
N2 - Mechanisms by which aniline produces selective toxicity to the spleen are not well understood. Previously, studies showed that aniline exposure induces lipid peroxidation and protein oxidation in the spleen. The present study was aimed to determine the release of free iron and oxidative DNA damage in the spleen following aniline exposure. To achieve this, male SD rats were orally administered 1 mmol/kg/d aniline for 7 d, while controls received the vehicle only. Total splenic iron content showed a significant increase of 200% in the aniline-treated rats, whereas free iron (low-molecular-weight chelatable iron) showed a marked increase of 375% in comparison to controls. Oxidative DNA damage, measured in terms of 8-hydroxy-2′-deoxyguanosine (8-OHdG) levels, showed a remarkable increase of 83% in the aniline-treated rats. These results suggest an association between release of free iron and oxidative DNA damage, which could lead to mutagenic and/or carcinogenic responses in the spleen. Copyright
AB - Mechanisms by which aniline produces selective toxicity to the spleen are not well understood. Previously, studies showed that aniline exposure induces lipid peroxidation and protein oxidation in the spleen. The present study was aimed to determine the release of free iron and oxidative DNA damage in the spleen following aniline exposure. To achieve this, male SD rats were orally administered 1 mmol/kg/d aniline for 7 d, while controls received the vehicle only. Total splenic iron content showed a significant increase of 200% in the aniline-treated rats, whereas free iron (low-molecular-weight chelatable iron) showed a marked increase of 375% in comparison to controls. Oxidative DNA damage, measured in terms of 8-hydroxy-2′-deoxyguanosine (8-OHdG) levels, showed a remarkable increase of 83% in the aniline-treated rats. These results suggest an association between release of free iron and oxidative DNA damage, which could lead to mutagenic and/or carcinogenic responses in the spleen. Copyright
UR - http://www.scopus.com/inward/record.url?scp=17444398085&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=17444398085&partnerID=8YFLogxK
U2 - 10.1080/15287390590921757
DO - 10.1080/15287390590921757
M3 - Article
C2 - 15901093
AN - SCOPUS:17444398085
SN - 1528-7394
VL - 68
SP - 657
EP - 666
JO - Journal of Toxicology and Environmental Health - Part A
JF - Journal of Toxicology and Environmental Health - Part A
IS - 8
ER -