In VitroComparative Effect of Cd2+, Ni2+, and Co2+on Mouse Postblastocyst Development

Paksy, Katalin; Forgács, Zsolt; Gáti, I

doi:10.1006/enrs.1998.3933

Cited by 19 publications

(11 citation statements)

References 32 publications

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“…Paksy et al [47] Human ovarian granulosa cell culture 15.6-1000 µM NiCl 2 (48 h) concentration-dependent depression in both hGC and db-cAMP stimulated progesterone production at 15.625 µM Ni 2+ or above Révész et al [49] Human ovarian granulosa cell culture 15 µM NiCl 2 (48 h) decreased amounts of cadherins and β-catenin along the surface of the cell-to-cell contacts; alterations of cell shape, changes of distribution of microtubuli Révész et al [50] Rat short-term (3 h) Leydig cell culture 1-5000 µM NiCl 2 (3 h) concentration-dependent depression in both hGC and db-cAMP stimulated testosterone production; elevated HCHOL-and PREG-stimulated testosterone production Laskey and Phelps [51] Mouse primary Leydig cell culture 62.5-1000 µM NiSO 4 (48 h) concentration-dependent depression in hGC stimulated testosterone production at 125 µM or higher dose of Ni 2+…”

Section: Discussionmentioning

confidence: 98%

“…Paksy et al [47] investigated postblastocyst development of mouse preembryos in vitro in order to determine direct effect of Cd 2+ , Ni 2+ , and Co 2+ ions on embryogenesis during the peri-implantation stage. Uterine horns were flushed on Day 4 of pregnancy and expanded blastocysts were cultured for 4 days in the presence of 1.1-26.4 µM Cd 2+ , 0.1-500 µM Ni 2+ or 1-200 µM Co 2+ .…”

Section: Effects On Preimplantation Embryomentioning

confidence: 99%

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Reproductive toxicology of nickel – Review

Forgács¹,

Massányi

Lukáč

et al. 2012

Journal of Environmental Science and Health, Part A

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The goal of this minireview is to summarize our current knowledge on the reproductive toxicity of soluble nickel salts. We made an attempt to present the most relevant data obtained from in vivo and in vitro experiments performed on mammals, mammalian primary cell cultures and cell lines. Nickel has been demonstrated to disturb the mammalian reproductive functions at several levels of regulation. The results of previous investigations indicate that the hormonal effects may play an important role in the reproductive toxicology of nickel both at the neuroendocrine and gonadal levels in the hypothalamic-pituitary-gonadal (HPG) axis. At the molecular level, it may be important that nickel may substitute certain other metals in metal dependent enzymes, leading to an altered protein function. It readily crosses the cell membrane via calcium channels and competes with calcium for specific receptors. Nickel can cross-link aminoacids to DNA, lead to formation of reactive oxygen species (ROS), moreover mimic hypoxia. These changes may lead to the activation of some signaling pathways, subsequent transcription factors and eventually to alterations in gene expression and cellular metabolism. These events are likely to be involved in the reproductive toxicity of nickel.

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Section: Discussionmentioning

confidence: 98%

Section: Effects On Preimplantation Embryomentioning

confidence: 99%

Reproductive toxicology of nickel – Review

Forgács¹,

Massányi

Lukáč

et al. 2012

Journal of Environmental Science and Health, Part A

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“…Absorption through the skin, inhalation, ingestion through eating or drinking of nickel-contaminated foods and water represent the major access pathways of nickel into the body. The lung is the main target organ in workers occupationally exposed to fumes or dusts, but other organs, such as the kidney, liver, spleen, heart and reproductive system may be affected (Paksy et al, 1999).…”

Section: Introductionmentioning

confidence: 99%

A not cytotoxic nickel concentration alters the expression of neuronal differentiation markers in NT2 cells

2015

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“…Cobalt [Co(II)] and Nickel [Ni(II)] are capable of crossing the placenta barrier and exerting their toxicity on the animal reproduction system, thus affecting embryonic development [1], [2]. Exposure of Ni(II) and Co(II) at a high concentration (100 µM) significantly reduced proliferation of inner cell mass and trophoblast cells [3].…”

Section: Introductionmentioning

confidence: 99%

Cobalt and Nickel Stabilize Stem Cell Transcription Factor OCT4 through Modulating Its Sumoylation and Ubiquitination

Yao

Chen

et al. 2014

PLoS ONE

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Stem cell research can lead to the development of treatments for a wide range of ailments including diabetes, heart disease, aging, neurodegenerative diseases, spinal cord injury, and cancer. OCT4 is a master regulator of self-renewal of undifferentiated embryonic stem cells. OCT4 also plays a crucial role in reprogramming of somatic cells into induced pluripotent stem (iPS) cells. Given known vivo reproductive toxicity of cobalt and nickel metals, we examined the effect of these metals on expression of several stem cell factors in embryonic Tera-1 cells, as well as stem cells. Cobalt and nickel induced a concentration-dependent increase of OCT4 and HIF-1α, but not NANOG or KLF4. OCT4 induced by cobalt and nickel was due primarily to protein stabilization because MG132 stabilized OCT4 in cells treated with either metals and because neither nickel nor cobalt significantly modulated its steady-state mRNA level. OCT4 stabilization by cobalt and nickel was mediated largely through reactive oxygen species (ROS) as co-treatment with ascorbic acid abolished OCT4 increase. Moreover, nickel and cobalt treatment increased sumoylation and mono-ubiquitination of OCT4 and K123 was crucial for mediating these modifications. Combined, our observations suggest that nickel and cobalt may exert their reproductive toxicity through perturbing OCT4 activity in the stem cell compartment.

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In VitroComparative Effect of Cd2+, Ni2+, and Co2+on Mouse Postblastocyst Development

Cited by 19 publications

References 32 publications

Reproductive toxicology of nickel – Review

Reproductive toxicology of nickel – Review

A not cytotoxic nickel concentration alters the expression of neuronal differentiation markers in NT2 cells

Cobalt and Nickel Stabilize Stem Cell Transcription Factor OCT4 through Modulating Its Sumoylation and Ubiquitination

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