Oxidative injury in the mouse spleen caused by lanthanides

Liu, Jie; Li, Na; Ma, Li; Duan, Yanmei; Wang, Jue; Zhao, Xiaoyang; Wang, Sisi; Wang, Han; Hong, Fashui

doi:10.1016/j.jallcom.2009.09.158

Cited by 28 publications

(14 citation statements)

References 29 publications

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“…This breaks down the balance of the oxidative/antioxidative system in the brain, resulting in lipid peroxidation, which increased the permeability of mitochondrial membrane [49]. In our previous studies, Ln 3+ was also shown to mediate apoptosis in the spleen, liver in mice through the induction of ROS [13], [17]. However, the apoptotic mechanism in Ln 3+ -induced neurotoxicity remains unclear.…”

Section: Discussionmentioning

confidence: 98%

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Gene-Expression Changes in Cerium Chloride-Induced Injury of Mouse Hippocampus

Cheng

Zhao

et al. 2013

PLoS ONE

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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.

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Section: Discussionmentioning

confidence: 98%

“…These authors suggested that Ce 3+ at high doses damaged a specific region of the liver. A recent study showed that exposure to Ce 3+ damaged the spleen [12], [13], lung [14]), and liver [15]–[17] of mice. In addition, La 3+ , Ce 3+ and Nd 3+ were demonstrated to result in brain injuries in mice [18]–[20].…”

Section: Introductionmentioning

confidence: 99%

Gene-Expression Changes in Cerium Chloride-Induced Injury of Mouse Hippocampus

Cheng

Zhao

et al. 2013

PLoS ONE

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“…In our present study, the activities of antioxidase, including GSH-Px, SOD, GR and CAT were all markedly decreased in AFB 1 groups compared with those of the control group. These enzymatic antioxidants have been recognized to play an important role in the anti-oxidant mechanism of the body, which can eliminate ROS from cell, for instance, SOD converts O 2 · − into H 2 O 2 and O 2 ; CAT and GSH-Px reduces H 2 O 2 into H 2 O and O 2 [29]. If their activities decreased, the oxygen free radical would induce harmful effects to biological systems.…”

Section: Discussionmentioning

confidence: 99%

Protective Effects of Sodium Selenite against Aflatoxin B1-Induced Oxidative Stress and Apoptosis in Broiler Spleen

Wang

Shu

Peng

et al. 2013

IJERPH

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The aim of this study was to investigate the possible protective role of sodium selenite on aflatoxin B1-induced oxidative stress and apoptosis in spleen of broilers. Two hundred one-day-old male broilers, divided into five groups, were fed with basal diet (control group), 0.3 mg/kg AFB1 (AFB1 group), 0.3 mg/kg AFB1 + 0.2 mg/kg Se (+Se group I), 0.3 mg/kg AFB1 + 0.4 mg/kg Se (+Se group II) and 0.3 mg/kg AFB1 + 0.6 mg/kg Se (+Se group III), respectively. According to biochemical assays, AFB1 significantly decreased the activities of glutathione peroxidase, total superoxide dismutase, glutathione reductase, catalase and the level of glutathione hormone, while it increased the level of malondialdehyde. Moreover, AFB1 increased the percentage of apoptosis cells by flow cytometry and the occurrence of apoptotic cells by TUNEL assay. Simultaneous supplementation with sodium selenite restored these parameters to be close to those in control group. In conclusion, sodium selenite exhibited protective effects on AFB1-induced splenic toxicity in broilers by inhibiting oxidative stress and excessive apoptosis.

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“…However, whether 4f electronic shell and alterable valence characteristics of Ln exert special toxicity on animals has not been carefully investigated. Recently, our researches showed that exposure to Ln damaged spleen, lung, liver, and brain of mice, which was greatest in Ce 3+ treatment, medium in Nd 3+ treatment, and least in La 3+ treatment [11][12][13][14][15]. However, little is known about the effects of Ln on several organs damages simultaneously.…”

Section: Introductionmentioning

confidence: 99%

Organ Histopathological Changes and its Function Damage in Mice Following Long-term Exposure to Lanthanides Chloride

Cheng

Cai

et al. 2011

Biol Trace Elem Res

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Due to increasing applications of lanthanides (Ln) in industry and daily life, numerous studies confirmed that Ln exposure may result in organ damages in mice and rats, while very few studies focused on several organs damages simultaneously. In order to compare the toxicity of Ln on organs, mice were exposed to LaCl(3), CeCl(3), and NdCl(3) of a dose of 20 mg/kg body weight for consecutive 60 days, respectively, then histopathological changes of liver, kidney, and heart, and their function were investigated. The results showed that long-term exposure to Ln caused cell necrosis and basophilia of liver, ambiguity of renal tubule architecture, congestion of blood vessel and capillary of kidney, and heart hemorrhage. The histopathological changes of liver, kidney, and heart in mice caused by Ce(3+) was most severe; the effect by Nd(3+) was slighter than Ce(3+) but more severe than La(3+). The assay of serum biochemical parameters suggested that Ln exposure severely impaired the functions of liver, kidney, and myocardium in mice. These findings suggested that long-term exposure to Ln resulted in histopathological changes of liver, kidney, and heart, and their function damages. Therefore, we thought that long-term application of the products containing Ln on human should be cautious.

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Oxidative injury in the mouse spleen caused by lanthanides

Cited by 28 publications

References 29 publications

Gene-Expression Changes in Cerium Chloride-Induced Injury of Mouse Hippocampus

Gene-Expression Changes in Cerium Chloride-Induced Injury of Mouse Hippocampus

Protective Effects of Sodium Selenite against Aflatoxin B1-Induced Oxidative Stress and Apoptosis in Broiler Spleen

Organ Histopathological Changes and its Function Damage in Mice Following Long-term Exposure to Lanthanides Chloride

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