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The organ toxicity of lanthanides (Ln) on organisms had been recognized, but very little is known about the oxidative injury of brain caused by Ln. In order to study the mechanisms underlying the effects of Ln on the brain, ICR mice were injected with a single 20 mg/kg body weight dose of LaCl 3 , CeCl 3 , and NdCl 3 into the abdominal cavity daily for 14 days. We then examined the coefficient of the brain, the brain pathological changes and oxidative stress-mediated responses, and the accumulation of Ln and levels of neurochemicals in the brain. The results showed that CeCl 3 and NdCl 3 could induce some neurons to turn inflammatory cells and slight edema but did not observe the brain pathological changes from LaCl 3 -treated group. The concentrations of La, Ce, and Nd in the brain were significantly different and ranked in the order of Ce, Nd, and La. The injury of the brain and oxidative stress occurred as Ln appeared to trigger a cascade of reactions such as lipid peroxidation, the decreases of the total antioxidation capacity and activities of antioxidative enzymes, the excessive release of nitric oxide, the increase of glutamic acid, and the downregulated level of acetylcholinesterase activities. Furthermore, both Ce 3+ and Nd 3+ exhibited higher oxidative stress and toxicity on brain than La 3+ , and Ce 3+ caused more severe brain injuries and oxidative stress than Nd 3+ , implying that the differences in the brain injuries caused by Ln might be related to the number of 4f electrons of Ln.

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Magnesium (Mg) deficiency has been reported to affect plant photosynthesis and growth, and cerium (Ce) was considered to be able to improve plant growth. However, the mechanisms of Mg deficiency and Ce on plant growth remain poorly understood. The main aim of this work is to identify whether or not Mg deprivation affects the interdependent nitrogen and carbon assimilations in the maize leaves and whether or not Ce modulates the assimilations in the maize leaves under Mg deficiency. Maize plants were cultivated in Hoagland’s solution. They were subjected to Mg deficiency and to cerium chloride administration in the Mg-present Hoagland’s media and Mg-deficient Hoagland’s media.After 2 weeks,we measured chlorophyll (Chl) a fluorescence and the activities of nitrate reductase (NR), sucrose-phosphate synthase(SPS), and phosphoenolpyruvate carboxylase (PEPCase)in metabolic checkpoints coordinating primary nitrogen and carbon assimilations in the maize leaves. The results showed that Mg deficiency significantly inhibited plant growth and decreased the activities of NR, SPS, and PEPCase and the synthesis of Chl and protein. Mg deprivation in maize also significantly decreased the oxygen evolution, electron transport,and efficiency of photochemical energy conversion by photosystem II (PSII). However, Ce addition may promote nitrogen and carbon assimilations, increase PSII activities,and improve maize growth under Mg deficiency. Moreover,our findings would help promote usage of Mg or Ce fertilizers in maize production.

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Cerium is widely used in many aspects of modern society, including agriculture, industry and medicine. It has been demonstrated to enter the ecological environment, is then transferred to humans through food chains, and causes toxic actions in several organs including the brain of animals. However, the neurotoxic molecular mechanisms are not clearly understood. In this study, mice were exposed to 0.5, 1, and 2 mg/kg BW cerium chloride (CeCl3) for 90 consecutive days, and their learning and memory ability as well as hippocampal gene expression profile were investigated. Our findings suggested that exposure to CeCl3 led to hippocampal lesions, apoptosis, oxidative stress and impairment of spatial recognition memory. Furthermore, microarray data showed marked alterations in the expression of 154 genes involved in learning and memory, immunity and inflammation, signal transduction, apoptosis and response to stress in the 2 mg/kg CeCl3 exposed hippocampi. Specifically, the significant up-regulation of Axud1, Cdc37, and Ube2v1 caused severe apoptosis, and great suppression of Adcy8, Fos, and Slc5a7 expression led to impairment of mouse cognitive ability. Therefore, Axud1, Cdc37, Ube2v1, Adcy8, Fos, and Slc5a7 may be potential biomarkers of hippocampal toxicity caused by CeCl3 exposure.

Cerium (Ce) compounds are now widely applied in medicine, agriculture, animal breeding, and daily life; however, the effects of Ce on human body, especially on the central nervous system, are still unclear. In order to investigate whether Ce exposure cause neurotoxicological effects, ICR mice were exposed to CeCl(3) through intragastric administration at 0, 2, 10, and 20 mg/kg body weight doses everyday for 60 days. The behaviors of spatial recognition memory, brain histopathology, the brain elements and neurochemicals, as well as enzymes activities in mice were determined. The Y-maze test showed that CeCl(3) exposure could significantly impair the behaviors of spatial recognition memory. Specifically, in these Ln(3+)-treated mice, the contents of Ca, Mg, Na, K, Fe, and Zn in brain were significantly altered, the activities of Na(+)/K(+)-ATPase, Ca(2+)-ATPase, Ca(2+)/Mg(2+)-ATPase, acetylcholine esterase, and nitric oxide synthase were significantly inhibited; monoamines neurotransmitters such as norepinephrine, dopamine, and 5-hydroxytryptamine were significantly decreased, while the contents of acetylcholine, glutamate, and nitric oxide were significantly increased. These results indicated that CeCl(3) exposure could impair the learning ability, which is attributed to the disturbance of the homeostasis of trace elements, enzymes, and neurotransmitter systems in the mouse brain. Therefore, our study aroused the attention of Ln application and long-term exposure effects.