Abstract：
:Cerium has been demonstrated to damage liver of mice, but very little is known about the molecular mechanisms underlying the mouse liver apoptosis. In order to understand the liver injury induced by intragastric administration of cerium chloride (CeCl3) for 60 consecutive days, the hepatocyte ultrasrtucture, various oxidative stress parameters, and the stress-related gene expression levels were investigated for the mouse liver. The results demonstrated that CeCl3 had an obvious accumulation in the mouse liver, leading to a classical laddering cleavage of DNA and hepatocyte apoptosis. CeCl3 significantly promoted the accumulation of reactive oxygen species and inhibited the stress-related gene expression of superoxide dismutase, catalase, glutathione peroxidase, metallothionein, heat-shock protein 70, glutathione-S-transferase, P53, and transferring, and it effectively activated the cytochrome p450 1A. It implied that CeCl3 resulted in apoptosis and alteration of expression levels of the genes related with metal detoxification/metabolism regulation and radical scavenging action in mice.
journal_name
Arch Environ Contam Toxicoljournal_title
Archives of environmental contamination and toxicologyauthors
Zhao H,Cheng J,Cai J,Cheng Z,Cui Y,Gao G,Hu R,Gong X,Wang L,Hong Fdoi
10.1007/s00244-011-9672-0subject
Has Abstractpub_date
2012-01-01 00:00:00pages
154-64issue
1eissn
0090-4341issn
1432-0703journal_volume
62pub_type
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journal_title：Archives of environmental contamination and toxicology
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journal_title：Archives of environmental contamination and toxicology
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