The effects of β-estradiol on SHSY5Y neuroblastoma cells during heavy metal induced oxidative stress, neurotoxicity and β-amyloid secretion

Olivieri, Gianfranco; Novaković﻿﻿﻿, Marko; Savaskan, Egemen; Meier, Fides; Baysang, Ginette; Brockhaus, Manfred; Müller‐Spahn, F.

doi:10.1016/s0306-4522(02)00211-7

Cited by 97 publications

(52 citation statements)

References 56 publications

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“…In vitro studies produced the following results: Mercury interferes with polymerization of microtubules [122,123], increases secretion of both 1-40 and 1-42 forms of Aβ and promotes hyperphosphorylation of tau protein [9,[124][125][126][127], changes mitochondrial structure inducing a stress-response in astrocytes [128], and interferes with cell-maturation [129] or other aspects of cell functioning, such as DNA repair, glutathione level, or linkage and structure of microtubules [119,130,131]. Mercury disturbs the interaction between tubulin and GTP [132], and the chelator DMSA can reverse this process [133], while amalgam exposure is toxic for nerve cells in vitro [134].…”

Section: Experimental Animal and In Vitro Studiesmentioning

confidence: 99%

Does Inorganic Mercury Play a Role in Alzheimer's Disease? A Systematic Review and an Integrated Molecular Mechanism

Mutter¹,

Curth

Naumann³

et al. 2010

JAD

147

113

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Abstract. Mercury is one of the most toxic substances known to humans. It has been introduced into the human environment and has also been widely used in medicine. Since circumstantial evidence exists that the pathology of Alzheimer's disease (AD) might be in part caused or exacerbated by inorganic mercury, we conducted a systematic review using a comprehensive search strategy. Studies were screened according to a pre-defined protocol. Two reviewers extracted relevant data independent of each other. One thousand and forty one references were scrutinized, and 106 studies fulfilled the inclusion criteria. Most studies were case control or comparative cohort studies. Thirty-two studies, out of 40 testing memory in individuals exposed to inorganic mercury, found significant memory deficits. Some autopsy studies found increased mercury levels in brain tissues of AD patients. Measurements of mercury levels in blood, urine, hair, nails, and cerebrospinal fluid were inconsistent. In vitro models showed that inorganic mercury reproduces all pathological changes seen in AD, and in animal models inorganic mercury produced changes that are similar to those seen in AD. Its high affinity for selenium and selenoproteins suggests that inorganic mercury may promote neurodegenerative disorders via disruption of redox regulation. Inorganic mercury may play a role as a co-factor in the development of AD. It may also increase the pathological influence of other metals. Our mechanistic model describes potential causal pathways. As the single most effective public health primary preventive measure, industrial, and medical usage of mercury should be eliminated as soon as possible.

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Section: Experimental Animal and In Vitro Studiesmentioning

confidence: 99%

Does Inorganic Mercury Play a Role in Alzheimer's Disease? A Systematic Review and an Integrated Molecular Mechanism

Mutter¹,

Curth

Naumann³

et al. 2010

JAD

147

113

View full text Add to dashboard Cite

show abstract

“…Additional protection against oxidative stress is provided by estrogen, which has antioxidant effects by acting as a scavenger or by inducing the synthesis of protective molecules via activation of estrogen receptors (ERs) (Olivieri et al, 2002;Kluxen et al, 2012). These hormones play a critical role in the gender differences reported in the pathophysiology and outcome of acute neurological injuries where oxidative stress is clearly involved.…”

Section: Gender Differencesmentioning

confidence: 99%

Effects of Metallic Elements on Reproduction and Development

Apostoli¹,

Catalani²

2015

Handbook on the Toxicology of Metals

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“…They retain many properties of human neuronal cells and can be easily maintained under culture conditions [8,[38][39][40]42]. The SK-N-MC cells selectively express the NPY-Y1 receptors [1,42], and the SH-SY5Y cells selectively express the Y2 receptors [38,39].…”

Section: Animals and Cell Linesmentioning

confidence: 99%

“…The stock vial of SK-N-MC or SH-SY5Y cell line was kept above the level of liquid nitrogen. The vial of cells was thawed at 37°C for 2 min by gentle agitation before the vial contents were transferred to a 75-cm 2 culture flask containing 12-15 ml of culture medium and cultured for 1-2 weeks [21,39,40]. When the cells became confluent, they were dissociated using trypsin-EDTA and subcultured at a dilution of 1:10.…”

Section: Animals and Cell Linesmentioning

confidence: 99%

“…Cellular viability was assessed using the mitochondrial assay kit [26,37,39,40]. Briefly, 10 Ìl of the MTT labeling reagent at a final concentration of 0.5 mg/ml was added into each well at 24 h after the termination of OGD before incubation in a humidified incubator at 37°C with 5% CO 2 and 95% air (v/v) at 90% humidity for 4 h to allow formation of purple formazan crystals.…”

Section: Assessment Of Cell Viabilitymentioning

confidence: 99%

See 1 more Smart Citation

Neuropeptide Y-Y1 Receptor Agonist Worsens while Antagonist Improves Survival of Cultured Y1-Expressing Neuronal Cells following Oxygen and Glucose Deprivation

Chen

Cheung

2004

J Biomed Sci

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In this in vitro study, we investigated the influence of neuropeptide Y (NPY) Y1 receptor activation or inhibition on the viability of cultured neuronal or glial cells following oxygen glucose deprivation (OGD). Viability of cultured cells was assessed using 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide. When compared to the vehicle-treated control group, treatment with NPY or [Leu³¹,Pro³⁴]-NPY (Y1 agonist) reduced viability of cultured SK-N-MC (Y1-expressing) human neuronal cells at 24 h after 1 h of OGD, while BIBP3226 (Y1 antagonist) improved viability. Except at the highest concentration of NPY used in the study, treatment with NPY or NPY3-36 (Y2 agonist) did not influence viability of cultured SH-SY5Y (Y2-expressing) human neuronal cells at 24 h after 1 h of OGD. In addition, treatment with NPY, [Leu³¹,Pro³⁴]-NPY, NPY3-36, or BIBP3226 did not affect viability of cultured primary astrocytes at 24 h after 4 h of OGD. The present results agree with those of a recent in vivo study. Activation of NPY-Y1 receptors may mediate ischemic pathophysiological processes, and inhibiting the Y1 receptors may be protective. The combination of OGD and cultured neuronal cells may be useful in future studies on the neuroprotective and harmful mechanisms of NPY-Y1 receptor inhibition and activation during ischemia, respectively.

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The effects of β-estradiol on SHSY5Y neuroblastoma cells during heavy metal induced oxidative stress, neurotoxicity and β-amyloid secretion

Cited by 97 publications

References 56 publications

Does Inorganic Mercury Play a Role in Alzheimer's Disease? A Systematic Review and an Integrated Molecular Mechanism

Does Inorganic Mercury Play a Role in Alzheimer's Disease? A Systematic Review and an Integrated Molecular Mechanism

Effects of Metallic Elements on Reproduction and Development

Neuropeptide Y-Y1 Receptor Agonist Worsens while Antagonist Improves Survival of Cultured Y1-Expressing Neuronal Cells following Oxygen and Glucose Deprivation

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