Dichlorodiphenyltrichloroethane Specifically Depletes Dopaminergic Neurons in Primary Cell Culture

Leung, Ka Nang; Chan, Ying-Shing; Yung, Kin Lam

doi:10.1159/000074188

Cited by 5 publications

(1 citation statement)

References 29 publications

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“…Voltammetric study for cells viability HEK-293 cells, seeded at 10 5 cells/ml on a peptidecoated Au surface, were grown for 24 h. The fresh (Lang et al 2008) and dichlorodiphenyltrichloroethane (DDT) (Leunga et al 2003) were applied to immobilized cells. Electrochemical measurements were performed after 24 h. Figure 5a shows CV signals for the cells which were treated with BPA: the reduction peak current (I pc ) decreased linearly (R 2 = 0.95) up to 7.5 lM BAP (Fig.…”

Section: Resultsmentioning

confidence: 99%

Nanoscale fabrication of a peptide layer in cell chip to detect effects of environmental toxins on HEK293 cells

et al. 2010

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A cysteine-terminated C(RGD)(4) peptide film was fabricated on a gold electrode for improving the attachment of cells. The electrochemical signals of cyclic voltammogram from cells on a C(RGD)(4) deposited electrode was enhanced from 0.27 to 0.49 μA compared to a bare electrode. The developed cell-based sensor determined the effect of bisphenol-A (BPA) and dichlorodiphenyltrichloroethane (DTT) on the viability of HEK-293 cells by detecting decrease of reduction peaks (1.12-0.15 μA for BPA and 0.81-0.29 μA for DDT) after the treatment of environmental chemicals. This developed system can be a powerful tool for the monitoring of environmental toxicants.

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Section: Resultsmentioning

confidence: 99%

Nanoscale fabrication of a peptide layer in cell chip to detect effects of environmental toxins on HEK293 cells

et al. 2010

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Zebrafish as a model for developmental neurotoxicity testing

Ton

Lin

Willett

2006

Birth Defects Research

186

136

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BACKGROUND:To establish zebrafish as a developmental toxicity model, we used 7 well-characterized compounds to examine several parameters of neurotoxicity during development. METHODS: Embryos were exposed by semistatic immersion from 6 hrs postfertilization (hpf). Teratogenicity was assessed using a modified method previously developed by Phylonix. Dying cells in the brain were assessed by acridine orange staining (these cells are likely to be apoptotic). Motor neurons were assessed by antiacetylated tubulin staining and catecholaminergic neurons were visualized by antityrosine hydroxylase staining. RESULTS: Atrazine, dichlorodiphenyltrichloroethane (DDT), and 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) were primarily teratogenic and not specifically neurotoxic. 2,4-dichlorophenoxyacetic acid (2,4-D), dieldrin, and nonylphenol showed specific neurotoxicity; dieldrin and nonylphenol were specifically toxic to catecholaminergic neurons. Malathion, although not teratogenic, showed some nonspecific toxicity. CONCLUSIONS: Teratogenicity measured in 96-hpf zebrafish is predictive of mammalian teratogenicity and is useful in determining whether a compound causes specific neurotoxicity or general developmental toxicity. Induction of apoptosis or necrosis is an indicator of neurotoxicity. An effect on motor neurons in the caudal third of the embryo correlates with expected defects in motility. Overall, our results showed a strong correlation with mammalian data and suggest that zebrafish is a predictive animal model for neurotoxicity screening. Birth Defects Research (Part A) 76:553-567,

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Development of the human motor‐related thalamic nuclei during the first half of gestation, with special emphasis on GABAergic circuits

Kultas‐Ilinsky

Fallet

Verney

2004

J of Comparative Neurology

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This study analyzed the expression of differentiation markers (Calbindin D28K: CaBP; parvalbumin: PARV; calretinin: CalR), gamma-aminobutyric acid (GABA) markers (GABA, glutamic acid decarboxylases: GAD65, GAD67; and GABA transporters: GAT1, GAT3), and other markers (neurotensin: NT, and neurofilament-specific protein: SMI32) in the human thalamus at 8-23 gestation weeks (g.w.), focusing on the motor-related nuclei. From 8-13 g.w. mainly CaBP was expressed in the cells while fiber bundles traversing the thalamus in addition to CaBP expressed all GABA markers except GAD67. CaBP and PARV expression patterns in different nuclei changed over the time course studied, whereas NT was expressed consistently along the anterior-lateral curvature of the thalamus. CalR and SMI were detectable at 23 g.w. in the ventral parts of the dorsal thalamus. Most remarkably, punctate GAD65 immunoreactivity in the neuropil was confined to the nigro- and pallidothalamic afferent receiving nuclei from 16 to about 21 g.w., overlapping with that of CaBP in some of these nuclei (subdivisions of the ventral anterior and mediodorsal nuclei) and with PARV in others (centromedian nucleus). During this period, GAD65 immunoreactivity can be considered a marker of the basal ganglia afferent receiving territory in the motor thalamus. GAD67-positive local circuit neurons were first detected at 12-13 g.w. in the thalamic nuclei outside the basal ganglia afferent receiving territory. In the ventral anterior and centromedian nuclei, GAD-containing local circuit neurons were not conspicuous even at 22-23 g.w. The cells of the reticular nucleus expressed GAD67 and PARV from 12 g.w. on starting in the lateral-posterior regions. By 23 g.w., both markers were expressed in about two-thirds of the nucleus except for its most medial-anterior part. The results imply spatially and temporally differential expression of GABA and differentiation markers in the developing human thalamus.

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Dichlorodiphenyltrichloroethane Specifically Depletes Dopaminergic Neurons in Primary Cell Culture

Cited by 5 publications

References 29 publications

Nanoscale fabrication of a peptide layer in cell chip to detect effects of environmental toxins on HEK293 cells

Nanoscale fabrication of a peptide layer in cell chip to detect effects of environmental toxins on HEK293 cells

Zebrafish as a model for developmental neurotoxicity testing

Development of the human motor‐related thalamic nuclei during the first half of gestation, with special emphasis on GABAergic circuits

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