Publications by authors named "Wanyue Huang"

18 Publications

  • Page 1 of 1

AFB-induced mice liver injury involves mitochondrial dysfunction mediated by mitochondrial biogenesis inhibition.

Ecotoxicol Environ Saf 2021 Apr 7;216:112213. Epub 2021 Apr 7.

Key Laboratory of the Provincial Education Department of Heilongjiang for Common Animal Disease Prevention and Treatment, College of Veterinary Medicine, Northeast Agricultural University, Harbin 150030, China.

Aflatoxin B1 (AFB) pollutes foodstuffs and feeds, causing a food safety problem and seriously endangering human and animal health. Liver is the principal organ for AFB accumulation and biotransformation, during which AFB can cause acute and chronic liver damage, however, the specific mechanism is not completely clear. Mitochondria are the primary organelle of cellular bio-oxidation, providing 95% energy for liver to execute its multiple functions. Therefore, we speculated that mitochondrial dysfunction is involved in AFB-induced liver injury. To verify the hypothesis, a total of eighty healthy male mice were randomly divided into four groups on average, and exposed with 0, 0.375, 0.75 and 1.5 mg/kg body weight AFB by intragastric administration for 30 d. The results displayed that AFB triggered liver injury accompanied by oxidative stress. AFB exposure also damaged mitochondria structure, decreased mitochondrial membrane potential (MMP), as well as increased cytoplasmic cytochrome c (Cyt-c) protein expression, Bax, p53, Caspase-3/9 protein and/or mRNA expression levels and terminal deoxynucleotidyl transferase-mediated 2'-deoxyuridine-5'-triphosphate (dUTP) nick end labeling (TUNEL) staining positive cells in mice liver. Meanwhile, AFB exposure elevated pyruvate content, inhibited tricarboxylic acid (TCA) cycle rate-limiting enzymes and electron transport chain (ETC) complexes I-V activities, disturbed ETC complexes I-V subunits mRNA expression levels and reduced adenosine triphosphate (ATP) level in mice liver. These results indicated that AFB destroyed mitochondrial structure, activated mitochondrion-dependent apoptosis and induced mitochondrial dysfunction. In addition, AFB disrupted mitochondrial biogenesis, presented as the abnormalities of protein and/or gene expression levels of voltage dependent anion channel protein 1 (VDAC1), peroxisome proliferator-activated receptor γ coactivator-1α (PGC-1α), nuclear respiratory factor 1 (Nrf1) and mitochondrial transcription factor A (Tfam). This may contribute to hepatic and mitochondrial lesions induced by AFB. These results provide a new perspective for elucidating the mechanisms of AFB hepatotoxicity.
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http://dx.doi.org/10.1016/j.ecoenv.2021.112213DOI Listing
April 2021

The nephrotoxicity of T-2 toxin in mice caused by oxidative stress-mediated apoptosis is related to Nrf2 pathway.

Food Chem Toxicol 2021 Mar 27;149:112027. Epub 2021 Jan 27.

Key Laboratory of the Provincial Education, Department of Heilongjiang for Common Animal Disease Prevention and Treatment, College of Veterinary Medicine, Northeast Agricultural. University, Harbin, 150030, China. Electronic address:

T-2 toxin is an inevitable environmental and grain pollutant, which can cause kidney damage, but the mechanism is not clear. In this study, male mice were administered with T-2 toxin at 0, 0.5, 1.0, 2.0 mg/kg body weight (BW) for 28 days. We found that T-2 toxin induced renal structural damage, downregulated BW and kidney coefficient, impaired renal function accompanied by oxidative stress and apoptosis. Meanwhile, T-2 toxin increased nuclear Nrf2 protein expression and the mRNA expressions of its downstream target genes. The correlation analysis indicated that apoptosis and Nrf2 pathway were positively correlated with oxidative stress. These results suggested that the nephrotoxicity of T-2 toxin in mice caused by oxidative stress-mediated apoptosis is related to Nrf2 pathway.
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http://dx.doi.org/10.1016/j.fct.2021.112027DOI Listing
March 2021

Aflatoxin B disrupts blood-testis barrier integrity by reducing junction protein and promoting apoptosis in mice testes.

Food Chem Toxicol 2021 Feb 6;148:111972. Epub 2021 Jan 6.

Key Laboratory of the Provincial Education, Department of Heilongjiang for Common Animal Disease Prevention and Treatment, College of Veterinary Medicine, Northeast Agricultural University, Harbin, 150030, China. Electronic address:

Aflatoxin B (AFB) is an unavoidable food and environmental contaminant, which can lead to disorders in spermatogenesis and its mechanism remains unclear. The blood-testis barrier (BTB) is responsible for ensuring normal spermatogenesis in testes. Therefore, we hypothesized that disruption of the BTB was involved in AFB-induced spermatogenesis disorders. To confirm our hypothesis, male Kunming mice were orally gavaged AFB (0, 0.375, 0.75, or 1.5 mg/kg) for 30 days. Primarily, we first proved that AFB disrupted the BTB integrity. Then, AFB decreased BTB-related junction protein expression and elevated Sertoli cell apoptosis, which were associated with oxidative stress. Additionally, AFB upregulated the p-p38 MAPK/p38 MAPK ratio. These results collectively indicated that AFB disrupted the BTB via reducing the expression of BTB-related junction protein and promoting apoptosis in mice testes, which were associated with the oxidative stress-mediated p38 MAPK signaling pathway.
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http://dx.doi.org/10.1016/j.fct.2021.111972DOI Listing
February 2021

Deoxynivalenol induced spermatogenesis disorder by blood-testis barrier disruption associated with testosterone deficiency and inflammation in mice.

Environ Pollut 2020 Sep 7;264:114748. Epub 2020 May 7.

Key Laboratory of the Provincial Education, Department of Heilongjiang for Common Animal Disease Prevention and Treatment, College of Veterinary Medicine, Northeast Agricultural University, Harbin, 150030, China. Electronic address:

Deoxynivalenol (DON) is an unavoidable cereal crops contaminants and environmental pollutants, which seriously threated the health of human and animal. DON has been reported to exert significant toxicity effects on spermatogenesis, but the underlying mechanisms remain largely inconclusive. The blood-testis barrier (BTB) provides a specialized biochemical microenvironment for maintaining spermatogenesis. Thus, we hypothesized that DON could impair BTB and lead to spermatogenesis disorder. To confirm this hypothesis, sixty male mice were intragastrically administered with 0, 1.2, 2.4 and 4.8 mg/kg body weight DON for 28 days, and several important observations were obtained in present study. First, we found that DON induced spermatogenesis disorder, reflected by the declines of sperm concentration and quality, sperm ultrastructural damage as well as seminiferous tubular damage. Then, we proved that DON induced BTB disruption as well as decreased the expressions of BTB junction proteins, including Occludin, Connexin 43 and N-cadherin. Finally, the present study showed that DON induced inflammation and inhibited T biosynthesis in testis of mice. These results revealed that DON induced spermatogenesis disorder by BTB disruption associated with testosterone deficiency and inflammation in mice, which shed a new light on the potential mechanisms of reproductive toxicity induced by DON.
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http://dx.doi.org/10.1016/j.envpol.2020.114748DOI Listing
September 2020

Protective effects of lycopene against AFB-induced erythrocyte dysfunction and oxidative stress in mice.

Res Vet Sci 2020 Apr 13;129:103-108. Epub 2020 Jan 13.

Heilongjiang Key Laboratory for Laboratory Animals and Comparative Medicine, College of Veterinary Medicine, Northeast Agricultural University, Harbin 150030, China. Electronic address:

To evaluate the protective role of lycopene (LYC) against aflatoxin B (AFB)-induced erythrocyte dysfunction and oxidative stress, male kunming mice were treated with LYC (5 mg/kg) and/or AFB (0.75 mg/kg) by intragastric administration for 30 d. Hematological indices were detected to assess erythrocyte function. The erythrocytes C3b receptor rate (E-C3bRR) and erythrocytes C3b immune complex rosette rate (E-ICRR) were detected to assess erythrocyte immune function. Hydrogen peroxide (HO) and malondialdehyde (MDA) contents and superoxide dismutase (SOD) and catalase (CAT) activities were determined to evaluate erythrocyte oxidative stress. The results showed that LYC administration significantly relieved AFB-induced erythrocyte dysfunction by increasing the levels of red blood cell count (RBC), hemoglobin (HGB) and hematocrit (HCT), as well as reducing red blood cell volume distribution width (RDW) level, while the levels of mean corpuscular volume (MCV), mean corpuscular hemoglobin (MCH), mean corpuscular hemoglobin concentration (MCHC) and mean platelet volume (MPV) had no significant differences among the four groups. Besides, LYC ameliorated AFB1-induced erythrocyte immune dysfunction by increasing E-C3bRR and decreasing E-ICRR. Furthermore, LYC also alleviated AFB-induced erythrocyte oxidative stress by decreasing HO and MDA contents and increasing SOD and CAT activities. These results indicated that LYC protected against AFB-induced erythrocyte dysfunction and oxidative stress in mice. The findings could lead a possible therapeutics for the management of AFB-induced erythrocyte toxicity.
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http://dx.doi.org/10.1016/j.rvsc.2020.01.015DOI Listing
April 2020

Review of the Reproductive Toxicity of T-2 Toxin.

J Agric Food Chem 2020 Jan 8;68(3):727-734. Epub 2020 Jan 8.

Key Laboratory of the Provincial Education Department of Heilongjiang for Common Animal Disease Prevention and Treatment, College of Veterinary Medicine , Northeast Agricultural University , 600 Changjiang Road , Xiangfang District, Harbin , Heilongjiang 150030 , People's Republic of China.

T-2 toxin, an inevitable environmental pollutant, is the most toxic type A trichothecene mycotoxin. Reproductive disruption is a key adverse effect of T-2 toxin. Herein, this paper reviews the reproductive toxicity of T-2 toxin and its mechanisms in male and female members of different species. The reproductive toxicity of T-2 toxin is evidenced by decreased fertility, disrupted structures and functions of reproductive organs, and loss of gametogenesis in males and females. T-2 toxin disrupts the reproductive endocrine axis and inhibits reproductive hormone synthesis. Furthermore, exposure to T-2 toxin during pregnancy results in embryotoxicity and the abnormal development of offspring. We also summarize the research progress in counteracting the reproductive toxicity of T-2 toxin. This review provides information toward a comprehensive understanding of the reproductive toxicity mechanisms of T-2 toxin.
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http://dx.doi.org/10.1021/acs.jafc.9b07880DOI Listing
January 2020

Iron Dyshomeostasis Participated in Rat Hippocampus Toxicity Caused by Aluminum Chloride.

Biol Trace Elem Res 2020 Oct 17;197(2):580-590. Epub 2019 Dec 17.

Key Laboratory of the Provincial Education, Department of Heilongjiang for Common Animal Disease Prevention and Treatment, College of Veterinary Medicine, Northeast Agricultural University, Harbin, 150030, China.

Aluminum (Al) alters iron regulatory factors content and leads to the changes in iron-related proteins causing iron accumulation. But limited evidence ascertains this hypothesis. Therefore, our experiment was conducted and four groups of male Wistar rats were orally administrated of 0, 50, 150, and 450 mg/kg BW/d aluminum chloride (AlCl) for 90 days by drinking water, respectively. The cognitive function, pathological lesion of hippocampus, oxidative stress, as well as iron-related proteins and iron regulatory factors expression were detected. The results showed that AlCl remarkably induced the oxidative stress and pathological lesion in the hippocampus and impaired the learning-memory ability. The contents of Al and iron increased in all AlCl-exposed groups. Meanwhile, the increased divalent metal transporter 1 (DMT1) expression enhanced iron import and the decreased ferroportin 1 (Fpn1) expression reduced iron export in AlCl-exposed groups. The iron accumulated and ferritin heavy chains (Fth) expression decreased in all AlCl-exposed groups led to an increase in free iron. The study also showed that iron regulatory factor iron regulatory protein 2 (IRP2) was decreased and hepcidin was increased in AlCl-exposed groups. The results indicated that AlCl induces iron dyshomeostasis presenting as iron accumulation, the disordered expression of iron import, export, store, and regulatory proteins in rat hippocampus accompanied with oxidative stress, pathological lesion, and impaired learning-memory ability.
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http://dx.doi.org/10.1007/s12011-019-02008-7DOI Listing
October 2020

Mitochondrial damage are involved in Aflatoxin B-induced testicular damage and spermatogenesis disorder in mice.

Sci Total Environ 2020 Jan 1;701:135077. Epub 2019 Nov 1.

Key Laboratory of the Provincial Education, Department of Heilongjiang for Common Animal Disease Prevention and Treatment, College of Veterinary Medicine, Northeast Agricultural University, Harbin 150030, China. Electronic address:

Aflatoxin B (AFB) is an unavoidable environmental pollutants, which seriously endangers human and animal health. AFB has male reproductive toxicity, yet the underlying mechanisms remain inconclusive. Mitochondra are a kind of crucial organelle for maintaining spermatogenesis in testis. Thus, we hypothesized that AFB can impair mitochondria to aggravate testicular damage and spermatogenesis disorder. To verify this hypothesis, 48 male mice were intragastrically administered with 0, 0.375, 0.75 or 1.5 mg/kg body weight AFB for 30 days, respectively. In this study, we found AFB caused testicular histopathological lesions and spermatogenesis abnormalities, with the elevation of oxidative stress (increased HO, whereas decreased SOD and GSH). Significant mitochondria structure damage of germ cells and Leydig cells, MMP loss, ATP contents reduction, and inhibited activities of mitochondrial complexes I-IV in mice testis were found in AFB treatment groups. Besides, AFB inhibited mitochondrial biogenesis and mitochondrial dynamics, presenting as the decreased mRNA and protein expressions of PGC-1α, Nrf1, Tfam, Drp1, Fis1, Mfn1 and Opa1. The results revealed that the mitochondrial damage were involved in AFB-induced testicular damage and spermatogenesis disorder, providing a considerable direction to clarify potential mechanisms of AFB reproductive toxicity.
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http://dx.doi.org/10.1016/j.scitotenv.2019.135077DOI Listing
January 2020

Aflatoxin B promotes autophagy associated with oxidative stress-related PI3K/AKT/mTOR signaling pathway in mice testis.

Environ Pollut 2019 Dec 3;255(Pt 2):113317. Epub 2019 Oct 3.

Key Laboratory of the Provincial Education, Department of Heilongjiang for Common Animal Disease Prevention and Treatment, College of Veterinary Medicine, Northeast Agricultural University, Harbin 150030, China. Electronic address:

Aflatoxin B (AFB) is a hazard environmental pollutants and the most toxic one of all the aflatoxins. AFB can cause a serious impairment to testicular development and spermatogenesis, yet the underlying mechanisms remain inconclusive. Oxidative stress acts as a master mechanism of AFB toxicity, and can promote autophagy. Abnormal autophagy resulted in testicular damage and spermatogenesis disorders. The objective of this study was to explore the effect of AFB on autophagy in mice testis and its potential mechanisms. In this study, male mice were intragastrically administered with 0, 0.375, 0.75 or 1.5 mg/kg body weight AFB for 30 days. We found that AFB induced testicular damage, reduced serum testosterone level and impaired sperm quality accompanied with the elevation of oxidative stress and germ cell apoptosis. Interestingly, we observed increasing numbers of autophagosomes in AFB-exposed mice testis. Meanwhile, AFB caused testis abnormal autophagy with the characterization of increased expressions of LC3, Beclin-1, Atg5 and p62. Furthermore, AFB downregulated the expressions of PI3K, p-AKT and p-mTOR in mice testis. Taken together, our data indicated AFB induced testicular damage and promoted autophagy, which were associated with oxidative stress-related PI3K/AKT/mTOR signaling pathway in mice testis.
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http://dx.doi.org/10.1016/j.envpol.2019.113317DOI Listing
December 2019

Spermatogenesis disorder caused by T-2 toxin is associated with germ cell apoptosis mediated by oxidative stress.

Environ Pollut 2019 Aug 6;251:372-379. Epub 2019 May 6.

Key Laboratory of the Provincial Education Department of Heilongjiang for Common Animal Disease Prevention and Treatment, Northeast Agricultural University, Harbin, 150030, China. Electronic address:

T-2 toxin is an unavoidable contaminant in human food, animal feeds, and agricultural products. T-2 toxin has been found to impair male reproductive function. But, few data is available that reveals the reproductive toxicity mechanism. In the study, male Kunming mice were orally administrated with T-2 toxin at the doses of 0, 0.5, 1 or 2 mg/kg body weight for 28 days. The body and reproductive organs weight, the concentration, malformation rate and ultrastructure of sperm in cauda epididymis were detected. Oxidative stress biomarkers and apoptosis were also measured in testes. Histological change of testes was performed by H&E and TUNEL staining. T-2 toxin down-regulated body and reproductive organs (testis, epididymis and seminal vesicle) weight, sperm concentration, increased sperm malformation rate and damaged the ultrastructure of sperm and structure of testes. T-2 toxin treatment increased the reactive oxygen species (ROS) and malondialdehyde content, while, decreased the total anti-oxidation capacity (T-AOC) and the superoxide dismutase activity in testes. T-2 toxin exposure increased the TUNEL-positive germ cells, the activities and mRNA expressions of caspase-3, caspase-8 and caspase-9, the mRNA expression of Bax, and inhibited the Bcl-2 mRNA expression. Furthermore, the expressions of caspase-3, caspase-8 caspase-9 and Bax were positively correlated with ROS level, but negatively correlated with T-AOC in testis. In summary, T-2 toxin caused spermatogenesis disorder associated with the germ cell apoptosis medicated by oxidative stress, impairing the male reproductive function.
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http://dx.doi.org/10.1016/j.envpol.2019.05.023DOI Listing
August 2019

AlCl inhibits LPS-induced NLRP3 inflammasome activation and IL-1β production through suppressing NF-κB signaling pathway in murine peritoneal macrophages.

Chemosphere 2018 Oct 28;209:972-980. Epub 2018 Jun 28.

College of Veterinary Medicine, Northeast Agricultural University, Harbin 150030, China; Key Laboratory of the Provincial Education, Department of Heilongjiang for Common Animal Disease Prevention and Treatment, Northeast Agricultural University, Harbin 150030, China. Electronic address:

Aluminum (Al), a common environmental pollutant, has been reported to inhibit the immune functions of macrophage. However, the mechanisms involved remain unclear. In this study, murine peritoneal macrophages were exposed to 0, 0.27, 0.54, and 1.08 mg/mL of aluminium chloride (AlCl) for 24 h, and then treated with 1 μg/mL lipopolysaccharide (LPS) for another 6 h. No addition of both AlCl and LPS serviced as control group. We observed that AlCl has cytotoxicity in murine peritoneal macrophages, showing a decrease in cell viability and an increase in lactate dehydrogenase release. Besides, AlCl exposure restrained the LPS-induced NLR pyrin domain containing 3 (NLRP3) inflammasome activation presented as NLRP3 expressions reduction, caspase-1 cleavage inhibition and interleukin 1 beta (IL-1β) maturation lessened. Meanwhile, AlCl exposure decreased LPS-induced IKKβ activity, IκBα phosphorylation, the phosphorylation and mRNA expression of NF-κB p65, as well the genes expression and concentration in medium supernatant of tumor necrosis factor alpha (TNF-α) and interleukin 6 (IL-6). The results suggested that AlCl inhibited the activation of NF-κB signaling pathway induced by LPS, which maybe one of the upstream signals involved in the inhibition of NLRP3 inflammasome activation by AlCl. This research can provide theoretical basis for understanding the immune toxicity of Al, and deepening the cognition of Al exposure hazards to immune response.
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http://dx.doi.org/10.1016/j.chemosphere.2018.06.171DOI Listing
October 2018

Hyperforin attenuates aluminum-induced Aβ production and Tau phosphorylation via regulating Akt/GSK-3β signaling pathway in PC12 cells.

Biomed Pharmacother 2017 Dec 24;96:1-6. Epub 2017 Nov 24.

Key Laboratory of the Provincial Education Department of Heilongjiang for Common Animal Disease Prevention and Treatment, Northeast Agricultural University, Harbin, 150030, China. Electronic address:

Aluminum (Al) is a neurotoxicant and cause β-amyloid (Aβ) peptides aggregation and tau hyperphosphorylation. Hyperforin (HF) is one of the major active constituents of the extracts of St. John's Wort (Hypericum perforatum), can treat Alzheimer's disease (AD) and other diseases involving peptide accumulation and cognition impairment. To determine the effects of HF on Al-induced Aβ formation and tau hyperphosphorylation, PC12 cells were cultured and treated with Al-malt (500μM) and/or HF (1μM). The results showed that HF treatment significantly attenuated Al-malt-induced Aβ production by reducing the expressions of APP, BACE1 and PS1, while increasing the expressions of sAPPα, ADAM9/10/17, and tau phosphorylation in PC12 cells. In addition, HF treatment also increased phosphorylation of AKT (Ser473) and inhibited GSK-3β activity by increasing phosphorylation of GSK-3β (Ser9). These results indicated that HF may exert the protection via regulating the AKT/GSK-3β signaling to reduce Aβ production and tau phosphorylation in PC12 cells. Furthermore, these results could lead a possible therapeutics for the management of Al neurotoxicity.
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http://dx.doi.org/10.1016/j.biopha.2017.09.114DOI Listing
December 2017

Inhibition of bone formation in rats by aluminum exposure via Wnt/β-catenin pathway.

Chemosphere 2017 Jun 20;176:1-7. Epub 2017 Feb 20.

Institute of Special Animal and Plant Sciences of Chinese Academy of Agricultural Sciences, Changchun 130112, China. Electronic address:

The previous research found that aluminum trichloride (AlCl) inhibited rat osteoblastic differentiation through inactivation of Wnt/β-catenin signaling pathway in vitro. On that basis, the experiment in vivo was conducted in this study. Rats were orally exposed to 0 (control group) and 0.4 g/L AlCl (AlCl-treated group) for 30, 60, 90 or 120 days, respectively. We found that mRNA expressions of type I collagen and insulin-like growth factor-1, mRNA and protein expressions of Runx2 and survivin, ratio of p-GSK3β/GSK3β and protein expression of β-catenin were all decreased, whereas the mRNA and protein expressions Dkk1 and sFRP1 and the mRNA expressions and activity of Caspase-3 were increased in the AlCl-treated group compared with the control group with time prolonged. These results suggest that AlCl inhibits bone formation and induces bone impairment by inhibiting the Wnt/β-catenin signaling pathway in young growing rats.
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http://dx.doi.org/10.1016/j.chemosphere.2017.02.086DOI Listing
June 2017

Aluminum Trichloride Inhibited Osteoblastic Proliferation and Downregulated the Wnt/β-Catenin Pathway.

Biol Trace Elem Res 2017 Jun 10;177(2):323-330. Epub 2016 Nov 10.

Institute of Special Animal and Plant Sciences, Chinese Academy of Agricultural Sciences, Changchun, 130112, China.

Aluminum (Al) exposure inhibits bone formation. Osteoblastic proliferation promotes bone formation. Therefore, we inferred that Al may inhibit bone formation by the inhibition of osteoblastic proliferation. However, the effects and molecular mechanisms of Al on osteoblastic proliferation are still under investigation. Osteoblastic proliferation can be regulated by Wnt/β-catenin signaling pathway. To investigate the effects of Al on osteoblastic proliferation and whether Wnt/β-catenin signaling pathway is involved in it, osteoblasts from neonatal rats were cultured and exposed to 0, 0.4 mM (1/20 IC), 0.8 mM (1/10 IC), and 1.6 mM (1/5 IC) of aluminum trichloride (AlCl) for 24 h, respectively. The osteoblastic proliferation rates; Wnt3a, lipoprotein receptor-related protein 5 (LRP-5), T cell factor 1 (TCF-1), cyclin D1, and c-Myc messenger RNA (mRNA) expressions; and p-glycogen synthase kinase 3β (GSK3β), GSK3β, and β-catenin protein expressions indicated that AlCl inhibited osteoblastic proliferation and downregulated Wnt/β-catenin signaling pathway. In addition, the AlCl concentration was negatively correlated with osteoblastic proliferation rates and the mRNA expressions of Wnt3a, c-Myc, and cyclin D1, while the osteoblastic proliferation rates were positively correlated with mRNA expressions of Wnt3a, c-Myc, and cyclin D1. Taken together, these findings indicated that AlCl inhibits osteoblastic proliferation may be associated with the inactivation of Wnt/β-catenin signaling pathway.
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http://dx.doi.org/10.1007/s12011-016-0880-3DOI Listing
June 2017

Aluminum chloride induced splenic lymphocytes apoptosis through NF-κB inhibition.

Chem Biol Interact 2016 Sep 29;257:94-100. Epub 2016 Jul 29.

College of Veterinary Medicine, Northeast Agricultural University, Harbin 150030, China. Electronic address:

This research investigated the relationship between lymphocytes apoptosis, hypothalamic-pituitary-adrenal (HPA) axis and NF-κB in AlCl3-treated rats. Eighty Wistar rats were orally exposed to 0 (control group, CG), 0.4 mg/mL (low-dose group, LG), 0.8 mg/mL (mid-dose group, MG) and 1.6 mg/mL (high-dose group, HG) AlCl3 for 90 days, respectively. A variety of measurements were taken including lymphocyte apoptosis index, serum corticotropin-releasing hormone (CRH), adrenocorticotrophic hormone (ACTH) and glucocorticoids (GCs) contents, GC receptors (GCR) and NF-κB mRNA and nuclear protein expressions, caspase 3 and 9 mRNA expressions and activities. The results showed that in the AlCl3-treated rats serum CRH, ACTH and GCs contents, lymphocyte GC receptors (GCR) mRNA and nuclear protein expressions, caspase 3 and 9 mRNA expressions and activities increased, while Bcl-2/Bax ratio and NF-κB mRNA and nuclear protein expressions decreased compared with the CG. Furthermore GCR and NF-κB nuclear protein expressions were negatively correlated. And NF-κB mRNA expression was positively correlated with that of Bcl-2, but negatively correlated with that of Bax in AlCl3-treated rats. These findings indicated that AlCl3 activated HPA axis, then induced splenic lymphocytes apoptosis through NF-κB inhibition.
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http://dx.doi.org/10.1016/j.cbi.2016.07.033DOI Listing
September 2016

Effects of Corticosterone on Immune Functions of Cultured Rat Splenic Lymphocytes Exposed to Aluminum Trichloride.

Biol Trace Elem Res 2016 Oct 23;173(2):399-404. Epub 2016 Mar 23.

College of Veterinary Medicine, Northeast Agricultural University, Harbin, 150030, China.

Aluminum (Al) exposure is toxic to immune system. Studies have implicated that glucocorticoids (GCs) exert the dual regulation effect on the immune function depending on the concentration. However, it is unknown whether a dual effect of GCs exists in the AlCl3-treated lymphocytes. Corticosterone (Cort) is one kind of GCs. To investigate the effect of different concentration Cort on AlCl3-treated lymphocytes, rat splenic lymphocyte was isolated and cultured with 0.55 mmol/L AlCl3, simultaneously administrated Cort at final concentration of 0 (control group, CG), 10(-8) (low-level group, LG), and 10(-6) (high-level group, HG) mol/L, respectively. Another group without AlCl3 and Cort served as the blank group (BG). We found that low concentration Cort increased the T and B lymphocyte proliferation rate, proportions of CD4(+) T lymphocyte subset, IgG, IL-2, and TNF-α contents, whereas high concentration Cort decreased those in AlCl3-treated lymphocytes. In conclusion, the results of this study indicated that low concentration Cort relieves the immunotoxicity of AlCl3 on the splenic lymphocytes, whereas high concentration Cort aggravates it.
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http://dx.doi.org/10.1007/s12011-016-0678-3DOI Listing
October 2016

Aluminum chloride induces neuroinflammation, loss of neuronal dendritic spine and cognition impairment in developing rat.

Chemosphere 2016 May 15;151:289-95. Epub 2016 Mar 15.

College of Veterinary Medicine, Northeast Agricultural University, Harbin, 150030, China. Electronic address:

Aluminum (Al) is present in the daily life of humans, and the incidence of Al contamination increased in recent years. Long-term excessive Al intake induces neuroinflammation and cognition impairment. Neuroinflammation alter density of dendritic spine, which, in turn, influence cognition function. However, it is unknown whether increased neuroinflammation is associated with altered density of dendritic spine in Al-treated rats. In the present study, AlCl3 was orally administrated to rat at 50, 150 and 450 mg/kg for 90d. We examined the effects of AlCl3 on the cognition function, density of dendritic spine in hippocampus of CA1 and DG region and the mRNA levels of IL-1β, IL-6, TNF-α, MHC II, CX3CL1 and BNDF in developing rat. These results showed exposure to AlCl3 lead to increased mRNA levels of IL-1β, IL-6, TNF-α and MCH II, decreased mRNA levels of CX3CL1 and BDNF, decreased density of dendritic spine and impaired learning and memory in developing rat. Our results suggest AlCl3 can induce neuroinflammation that may result in loss of spine, and thereby leads to learning and memory deficits.
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http://dx.doi.org/10.1016/j.chemosphere.2016.02.092DOI Listing
May 2016

Aluminum Trichloride Induces Hypertension and Disturbs the Function of Erythrocyte Membrane in Male Rats.

Biol Trace Elem Res 2016 May 10;171(1):116-23. Epub 2015 Sep 10.

College of Veterinary Medicine, Northeast Agricultural University, Harbin, 150030, China.

Aluminum (Al) is the most abundant metal in the earth's crust. Al accumulates in erythrocyte and causes toxicity on erythrocyte membrane. The dysfunction of erythrocyte membrane is a potential risk to hypertension. The high Al content in plasma was associated with hypertension. To investigate the effect of AlCl3 on blood pressure and the function of erythrocyte membrane, the rats were intragastrically exposed to 0, 64(1/20 LD50), 128(1/10 LD50), and 256(1/5 LD50) mg/kg body weight AlCl3 in double distilled water for 120 days, respectively. Then, we determined the systolic and mean arterial blood pressures of rats, the osmotic fragility, the percentage of membrane proteins, the activities of Na(+)/K(+)-ATPase, Mg(2+)-ATPase, Ca(2+)-ATPase, catalase (CAT), superoxide dismutase (SOD) and glutathione peroxidase (GSH-pX), and malondialdehyde (MDA) content of the erythrocyte membrane in this experiment. The results showed that AlCl3 elevated the systolic and mean arterial blood pressure of rats, increased the osmotic fragility, decreased the percentage of membrane protein, inhibited the activities of Na(+)/K(+)-ATPase, Mg(2+)-ATPase, Ca(2+)-ATPase, CAT, SOD and GSH-pX, and increased the MDA content of erythrocyte membrane. These results indicate that AlCl3 may induce hypertension by disturbing the function of erythrocyte membrane.
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http://dx.doi.org/10.1007/s12011-015-0504-3DOI Listing
May 2016