Nickel induced structural and functional alterations in mouse Leydig cells in vitro

Kročková, Jiřina; Massányi, Péter; Sirotkin, Alexander V.; Pivko, J.; Makarevich, Alexander V.; Lukáč, Norbert; Capcarová, Marcela; Toman, R.; Poláková, Zuzana

doi:10.1016/j.jtemb.2010.11.003

Cited by 33 publications

(20 citation statements)

References 13 publications

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“…Kročková et al [55] H295R cell culture 3.9-500 µM NiCl 2 (48 h) decreased progesterone and testosterone production at 3.9 µM or higher dose of Ni 2+…”

Section: Discussionmentioning

confidence: 96%

“…These observed changes of cell shape may be related to changes of cadherin-catenin based cell contacts and/or a direct effect of toxic metal on cytoskeletal system. Kročková et al [55] investigated nickel-induced structural and functional alterations in mouse Leydig cell culture. The cell viability was assessed by MTT assay, quantification of apoptotic cells was performed by TUNEL assay and the ultrastructural changes were analyzed by transmission electron microscopy.…”

Section: Effects On Primary Gonadal Cellsmentioning

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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“…Kročková et al [55] H295R cell culture 3.9-500 µM NiCl 2 (48 h) decreased progesterone and testosterone production at 3.9 µM or higher dose of Ni 2+…”

Section: Discussionmentioning

confidence: 96%

Section: Effects On Primary Gonadal Cellsmentioning

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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“…In fact, an increasing number of studies suggest that chemicals and pollutants in the environment, such as those arising from the traffic which are caused and spread by human activities, can affect the male reproductive system [106,107,108,109,110,111,112,113,114,115,116] and act as an endocrine disruptor because of their adverse effects on reproduction [117,118] and disruption of steroidogenesis and spermatogenesis [119,120]. Nickel pollution, taken as water-soluble, sulfidic, oxidic or metallic form, is known to modify the function of proteins in mammalian testes in terms of fertility and/or hormone production [119].…”

Section: Discussionmentioning

confidence: 99%

Effect of Chronic Cabergoline Treatment and Testosterone Replacement on Metabolism in Male Patients with Prolactinomas

et al. 2015

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Introduction: Hyperprolactinemia and hypogonadism are reportedly associated with an impaired metabolic profile. The current study aimed at investigating the effects of testosterone replacement and cabergoline (CAB) treatment on the metabolic profile in male hyperprolactinemic patients. Patients and Methods: Thirty-two men with prolactinomas, including 22 with total testosterone (TT) <8 nmol/l (HG, 69%) and 10 with TT >8 nmol/l (non-HG, 31%), were entered in the study. In all patients, metabolic parameters were assessed at diagnosis and after 12- and 24-month treatment. Results: Compared to non-HG patients, at baseline the HG patients had higher waist circumference (WC). TT significantly correlated with body mass index (BMI). Twelve-month CAB induced PRL normalization in 84%. HG prevalence significantly decreased (28%) and non-HG prevalence significantly increased (72%). Anthropometric and lipid parameters, fasting insulin (FI), insulin sensitivity index (ISI₀), homeostatic model assessment of insulin secretion (HOMA-β) and homeostatic model assessment of insulin resistance (HOMA-IR) significantly improved compared to baseline. TT was the best predictor for FI. Percent change (Δ) of TT significantly correlated with ΔCholesterol, ΔWeight and ΔBMI. Compared to non-HG patients, the HG patients had a higher weight, BMI, WC and HOMA-β. In HG, testosterone replacement was started. After 24 months, PRL normalized in 97%. HG prevalence significantly decreased (6%) and non-HG prevalence significantly increased (94%). Anthropometric and lipid parameters, FI, ISI₀, HOMA-β and HOMA-IR significantly improved compared to baseline, with FI, ISI₀, HOMA-β and HOMA-IR further ameliorating compared to the 12-month evaluation. Compared to non-HG patients, the HG patients still had a higher weight, BMI and WC. Conclusions: In hyperprolactinemic hypogonal men, proper testosterone replacement induces a significant improvement in the metabolic profile, even though the amelioration in the lipid profile might reflect the direct action of CAB.

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“…To determine the effects of Ni-smelting fumes on signal transduction in NIH/3T3 cells, we assessed whether Ni-smelting fumes changed the expression of the PI3K and ERK signaling pathways and their downstream signaling molecule HIF-1α. NIH/3T3 cells were exposed to 50.00 μg/mL Ni-smelting fumes for different periods of time (6,12,24, and 48 h). A negative control without cells and a positive control (Ni powder at 50.00 μg/mL for 24 h) were also included.…”

Section: Time-dependent Alterations In Pi3k P-akt P70s6k1 Erk Andmentioning

confidence: 99%

“…Occupational exposure to Ni compounds occurs mainly in Ni ore mining, ore dressing, smelting of Ni and Ni alloy production plating and welding processes 4) . Ni compounds are absorbed into the respiratory tract, the digestive system and through skin contact [5][6][7] . Of the different levels of damage to human health following exposure to Ni compounds, the most serious is carcinogenesis 8,9) .…”

Section: Introductionmentioning

confidence: 99%

Nickel‐smelting fumes increased the expression of HIF‐1α through PI3K/ERK pathway in NIH/3T3 cells

Han

Yang

Zhang

et al. 2016

Journal of Occupational Health

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Objective: The purpose of this study was to investigate the effects of Nickel (Ni) -smelting fumes on oncogenic proteins in vivo and in vitro. Methods: Ni fallout beside a Ni smelting furnace in a factory was sampled to study its toxic effect. The effects of Ni-smelting fumes on the regulation of PI3K and ERK signaling pathways and the important downstream hypoxia inducible factor, HIF-1α, were studied both in NIH/3T3 cells and in the lung tissue of rats. NIH/3T3 cell transformation induced by Ni-smelting fumes was also observed. Results: Ni-smelting fumes activated PI3K, p-AKT, p70S6K1, and ERK proteins and increased HIF-1α expression in a time- and dose-dependent manner. However, activation was suppressed when NIH/3T3 cells were pretreated with PI3K/AKT or ERK inhibitors. Ni-smelting fumes caused malignant transformation of NIH/3T3 cells. Conclusions: Ni-smelting fumes increased the expression of HIF-1α through the PI3K/ERK pathway in NIH/3T3 cells and induced malignant transformation in these cells indicating that Ni-smelting fumes may be a potential carcinogen in mammalian cells.

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Nickel induced structural and functional alterations in mouse Leydig cells in vitro

Cited by 33 publications

References 13 publications

Reproductive toxicology of nickel – Review

Reproductive toxicology of nickel – Review

Effect of Chronic Cabergoline Treatment and Testosterone Replacement on Metabolism in Male Patients with Prolactinomas

Nickel‐smelting fumes increased the expression of HIF‐1α through PI3K/ERK pathway in NIH/3T3 cells

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