Zinc, copper, iron, and selenium levels in brain and liver of mice exposed to acrylonitrile

Lu Rongzhu, Wang Suhua, Xing Guangwei, Ren Chunlan, Han Fangan, Jing Junjie, Michael Aschner

Research output: Contribution to journalArticle

9 Citations (Scopus)

Abstract

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.

Original languageEnglish (US)
Pages (from-to)39-47
Number of pages9
JournalBiological Trace Element Research
Volume130
Issue number1
DOIs
StatePublished - Jul 2009
Externally publishedYes

Fingerprint

Acrylonitrile
Selenium
Liver
Zinc
Copper
Brain
Iron
Spectrophotometers
Toxicity
Tissue
Decapitation
Trace Elements
Oxidation-Reduction
Fluorescence
Body Weight
Weights and Measures

Keywords

  • Acrylonitrile
  • Brain
  • Liver
  • Redistribution
  • Trace elements

ASJC Scopus subject areas

  • Biochemistry
  • Clinical Biochemistry
  • Inorganic Chemistry
  • Biochemistry, medical
  • Endocrinology, Diabetes and Metabolism

Cite this

Zinc, copper, iron, and selenium levels in brain and liver of mice exposed to acrylonitrile. / Rongzhu, Lu; Suhua, Wang; Guangwei, Xing; Chunlan, Ren; Fangan, Han; Junjie, Jing; Aschner, Michael.

In: Biological Trace Element Research, Vol. 130, No. 1, 07.2009, p. 39-47.

Research output: Contribution to journalArticle

Rongzhu, Lu ; Suhua, Wang ; Guangwei, Xing ; Chunlan, Ren ; Fangan, Han ; Junjie, Jing ; Aschner, Michael. / Zinc, copper, iron, and selenium levels in brain and liver of mice exposed to acrylonitrile. In: Biological Trace Element Research. 2009 ; Vol. 130, No. 1. pp. 39-47.
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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.

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