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Arch Environ Contam Toxicol (2012) 62:154164 DOI 10.1007/s00244-011-9672-0
Liver Injury and Its Molecular Mechanisms in Mice Caused by Exposure to Cerium Chloride
Haiquan Zhao Jie Cheng Jingwei Cai Zhe Cheng
Yaling Cui Guodong Gao Renping Hu
Xiaolan Gong Ling Wang Fashui Hong
Received: 30 October 2010 / Accepted: 4 April 2011 / Published online: 19 April 2011 Springer Science+Business Media, LLC 2011
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 signicantly 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 cyto-chrome p450 1A. It implied that CeCl3 resulted in apoptosis and alteration of expression levels of the genes related with metal detoxication/metabolism regulation and radical scavenging action in mice.
The lanthanide (Ln) series of elements comprises the elements between lanthanum and lutetium in the periodic table. Because of their diverse physical, chemical, and biological effects, Ln has been used in pharmacological
and electronic industries. Ln-enriched fertilizers (mainly consisting of lanthanum, cerium, and neodymium nitrates) are known to be able to increase the yields of crops in China (Hu et al. 2004; Ni 2002). Because plants can accumulate Ln (Xu et al. 2002; Zhang et al. 1999; Zhang and Shan 2001), this group of biologically non-necessary elements therefore can be inevitably accumulated in the environment and then transferred to the human body through food chains. Clearly, interests in the potential benets of Ln and a greater production of the material have already led to an increased concern about the potential toxic effects resulting from their uses or unintentional releases into the environment (Basu et al. 1984; Fan et al. 2004; Feng et al. 2006a, b; Sabbioni et al. 1982; Zhu et al. 1996, 1997).