Exposure to swainsonine impairs adult neurogenesis and spatial learning and memory

Wang, Jiutao; Song, Lingzhen; Zhang, Qi; Zhang, Wei; An, Lei; Zhang, Yamei; Tong, Dewen; Zhao, Bin; Chen, Shulin; Zhao, Shanting

doi:10.1016/j.toxlet.2014.11.017

Cited by 10 publications

(6 citation statements)

References 43 publications

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“…Children with higher Pb level may be affected with delayed growth, decreased intelligence, short-term memory and a lower intelligence quotient (IQ) along with learning disabilities, behavioral problems, and school failure. 20 In order to quantify proliferation of the precursor cells, we used the synthetic thymidine analogue BrdU which incorporates into the DNA of dividing cells. Cognitive stimuli promote the survival of newborn cells.…”

Section: Discussionmentioning

confidence: 99%

“…29,30 Our previous work also showed that an interplay seems to exist in the hippocampus between neurogenesis and learning and memory. 20 In order to quantify proliferation of the precursor cells, we used the synthetic thymidine analogue BrdU which incorporates into the DNA of dividing cells. Based upon BrdU uptake and labeling, we assessed the proliferation of precursor cells in the DG.…”

Section: Discussionmentioning

confidence: 99%

“…20 Sections (6 per mouse spaced at 50 mm) were incubated with mixed primary antibodies (rat anti-BrdU, mouse anti-NeuN and rabbit anti-GFAP diluted 1 : 1000 in blocking solution) overnight at 4°C. To evaluate the fate decision (differentiation) of newborn cells, triple-immunofluorescence staining for BrdU, NeuN (marker of mature neurons) and GFAP (marker of astrocytes) was performed as described in our previous study.…”

Section: Cell Survival and Differentiationmentioning

confidence: 99%

“…To evaluate the fate decision (differentiation) of newborn cells, triple-immunofluorescence staining for BrdU, NeuN (marker of mature neurons) and GFAP (marker of astrocytes) was performed as described in our previous study. 20 Sections (6 per mouse spaced at 50 mm) were incubated with mixed primary antibodies (rat anti-BrdU, mouse anti-NeuN and rabbit anti-GFAP diluted 1 : 1000 in blocking solution) overnight at 4 °C. After rinsing (3 × 10 min) with PB at RT the sections were incubated in mixed secondary antibodies (goat anti-rat-488, goat anti-mouse-568 and goat anti-rabbit-647 diluted 1 : 300 in PB) for 3 h in the dark.…”

Section: Cell Survival and Differentiationmentioning

confidence: 99%

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Protective effects of lithium against lead-induced toxicities in multiple systems of adult mouse

Wang

Song

et al. 2015

Toxicol. Res.

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Occupational and environmental exposures to lead (Pb), one of the toxic metal pollutants, is of global concern. The present study aims to investigate the protective effects of lithium (Li) against Pb-induced damage in vivo and in vitro. For this purpose, 3-month-old mice received Li (250 mg per kg body weight, i.p.) and 2 hours later water containing Pb (20 mg per kg body weight, i.p.) for 2-weeks. Treatment of mice with Pb induced remarkable morphological damage in multiple organs, such as swelling and necrosis in the liver, kidney and spleen. Immunohistochemistry demonstrated that the number of newly generated cells and immature neurons in the hippocampus was significantly decreased in mice exposed to Pb when compared with those that received saline for control or Li. Furthermore, in mice exposed to Pb a higher percentage of newly generated cells differentiated into glial cells and fewer into neurons, and less newborn cells survived compared to those in controls and Li-treated mice. In mice exposed to Pb cognitive tests were impaired. Interestingly, pre-administration of Li markedly decreased Pb-induced pathological and neurological lesions in vivo and in vitro. Specifically, the reduction of hippocampal neurogenesis resulting from Pb exposure was prevented by administration of Li. In addition, we found that pretreatment with Li effectively prevented cognitive impairment in mice exposed to Pb. Furthermore, Li pretreatment significantly improved Pb-induced depletion in p-GSK-3β (Ser9) and microRNA-34c levels in the hippocampus. Collectively our findings point to the capacity of Li to attenuate Pb-induced damage.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Section: Cell Survival and Differentiationmentioning

confidence: 99%

Section: Cell Survival and Differentiationmentioning

confidence: 99%

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Protective effects of lithium against lead-induced toxicities in multiple systems of adult mouse

Wang

Song

et al. 2015

Toxicol. Res.

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“…Many lines of evidence have demonstrated that swainsonine (SW) is the main toxin in locoweeds [ 2 , 3 , 4 ]. Pathology studies showed that SW can inhibit cellular alpha-mannosidase and induce lysosomal accumulation of incompletely processed oligosaccharides as vacuoles in many cell types, including liver, renal, and cerebellar cells [ 5 , 6 ]. The pathological changes caused by SW directly or indirectly lead to the clinical symptoms of locoism, including birth defects, reproductive disorders, congestive heart failure, edema, growth retardation, and body weight loss [ 7 , 8 ].…”

Section: Introductionmentioning

confidence: 99%

Degradation of Swainsonine by the NADP-Dependent Alcohol Dehydrogenase A1R6C3 in Arthrobacter sp. HW08

Wang

Zhai

Zhang

et al. 2016

Toxins

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Swainsonine is an indolizidine alkaloid that has been found in locoweeds and some fungi. Our previous study demonstrated that Arthrobacter sp. HW08 or its crude enzyme extract could degrade swainsonie efficiently. However, the mechanism of swainsonine degradation in bacteria remains unclear. In this study, we used label-free quantitative proteomics method based on liquid chromatography-electrospray ionization-tandem mass spectrometry to dissect the mechanism of swainsonine biodegradation by Arthrobacter sp. HW08. The results showed that 129 differentially expressed proteins were relevant to swainsonine degradation. These differentially expressed proteins were mostly related to the biological process of metabolism and the molecular function of catalytic activity. Among the 129 differentially expressed proteins, putative sugar phosphate isomerase/epimerase A1R5X7, Acetyl-CoA acetyltransferase A0JZ95, and nicotinamide adenine dinucleotide phosphate (NADP)-dependent alcohol dehydrogenase A1R6C3 were found to contribute to the swainsonine degradation. Notably, NADP-dependent alcohol dehyrodgenase A1R6C3 appeared to play a major role in degrading swainsonine, but not as much as Arthrobacter sp. HW08 did. Collectively, our findings here provide insights to understand the mechanism of swainsonine degradation in bacteria.

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Developmental exposure of decabromodiphenyl ether impairs subventricular zone neurogenesis and morphology of granule cells in mouse olfactory bulb

Huang

et al. 2017

Arch Toxicol

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Exposure to swainsonine impairs adult neurogenesis and spatial learning and memory

Cited by 10 publications

References 43 publications

Protective effects of lithium against lead-induced toxicities in multiple systems of adult mouse

Protective effects of lithium against lead-induced toxicities in multiple systems of adult mouse

Degradation of Swainsonine by the NADP-Dependent Alcohol Dehydrogenase A1R6C3 in Arthrobacter sp. HW08

Developmental exposure of decabromodiphenyl ether impairs subventricular zone neurogenesis and morphology of granule cells in mouse olfactory bulb

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