TY - JOUR
T1 - Zinc, copper, iron, and selenium levels in brain and liver of mice exposed to acrylonitrile
AU - Rongzhu, Lu
AU - Suhua, Wang
AU - Guangwei, Xing
AU - Chunlan, Ren
AU - Fangan, Han
AU - Junjie, Jing
AU - Aschner, Michael
N1 - Funding Information:
Acknowledgments We are grateful to Drs. John Duffus (Edinburgh Centre for Toxicology), Peter Spencer (Oregon Health & Science University), Frederick Benz (University of Louisville Medical School), Larry Fechter (Jerry Pettis Memorial Veterans Medical Center), and Jordi Llorens (University of Barcelona) for their critical reading and constructive criticism of this manuscript. This work was in part supported by Natural Science Foundation of China (No. 30872139), the Fund of Jiangsu University for Advanced Scholars (No. 04JDG006; to Lu Rongzhu) and Junior Scientists (No JDQ03026; to Wang Suhua), the Natural Science Foundation of Jiangsu Province (No. BK2004061; to Lu Rongzhu), NIEHS ES07331 (to Michael Aschner), SCI-TECH Team of Jiangsu University (2008-012-02) and Nutrition and Diseases Team of Jiangsu University (2008-012-02) (To Lu Rongzhu, Wang Suhua and Xing Guangwei) and the Social Development Foundation of Jiangsu Province (No. BS 2005049; to Han Fangan).
PY - 2009/7
Y1 - 2009/7
N2 - The mechanism of toxicity of acrylonitrile (AN) has not been fully defined. The research described herein was undertaken to investigate the possible effects of AN on the levels of metallic elements in liver and brain of mice. Thirty-two mice were randomly assigned to four separate groups and treated intraperitoneal (i.p.) once daily for 1 week. Mice in the control group received normal saline, and mice in the three exposure groups received 5, 10, or 20 mg AN/kg b.w. Samples of brain and liver were collected immediately after decapitation. Tissue levels of trace elements (zinc, copper, iron) were determined with flame atomic absorption spectrophotometer or double channel atomic fluorescence absorption spectrophotometer (selenium). Mean brain weights of AN-treated mice were increased as a function of dose compared to controls, but there was no significant change in the ratio of liver/body weight in the four groups. While mean brain zinc decreased as a function of AN dosage, mean liver zinc of the low-dose group significantly increased (p<0.05); mean liver copper in the medium-dose AN group was significantly higher compared to controls (p<0.05); however, mean brain copper was increased, but the difference did not attain statistical significance in the three AN groups when compared with the controls (p>0.05). Mean brain iron levels were significantly decreased in the middle-dose AN group (p<0.05), but there were no consistent changes inliver iron. Tissue levels of selenium in brain and liver were similar for the control and AN treatment groups. AN induces significant and differential changes in the levels of zinc, copper, and iron in brain and liver. These changes likely play a pivotal role in mediating AN toxicity, most likely via changes in cellular redox status.
AB - The mechanism of toxicity of acrylonitrile (AN) has not been fully defined. The research described herein was undertaken to investigate the possible effects of AN on the levels of metallic elements in liver and brain of mice. Thirty-two mice were randomly assigned to four separate groups and treated intraperitoneal (i.p.) once daily for 1 week. Mice in the control group received normal saline, and mice in the three exposure groups received 5, 10, or 20 mg AN/kg b.w. Samples of brain and liver were collected immediately after decapitation. Tissue levels of trace elements (zinc, copper, iron) were determined with flame atomic absorption spectrophotometer or double channel atomic fluorescence absorption spectrophotometer (selenium). Mean brain weights of AN-treated mice were increased as a function of dose compared to controls, but there was no significant change in the ratio of liver/body weight in the four groups. While mean brain zinc decreased as a function of AN dosage, mean liver zinc of the low-dose group significantly increased (p<0.05); mean liver copper in the medium-dose AN group was significantly higher compared to controls (p<0.05); however, mean brain copper was increased, but the difference did not attain statistical significance in the three AN groups when compared with the controls (p>0.05). Mean brain iron levels were significantly decreased in the middle-dose AN group (p<0.05), but there were no consistent changes inliver iron. Tissue levels of selenium in brain and liver were similar for the control and AN treatment groups. AN induces significant and differential changes in the levels of zinc, copper, and iron in brain and liver. These changes likely play a pivotal role in mediating AN toxicity, most likely via changes in cellular redox status.
KW - Acrylonitrile
KW - Brain
KW - Liver
KW - Redistribution
KW - Trace elements
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U2 - 10.1007/s12011-008-8310-9
DO - 10.1007/s12011-008-8310-9
M3 - Article
C2 - 19165426
AN - SCOPUS:68349105166
SN - 0163-4984
VL - 130
SP - 39
EP - 47
JO - Biological Trace Element Research
JF - Biological Trace Element Research
IS - 1
ER -