In Vitro Assessment of the Impact of Nickel on the Viability and Steroidogenesis in the Human Adrenocortical Carcinoma (NCI-H295R) Cell Line (original) (raw)
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Reproductive toxicology of nickel – Review
Journal of Environmental Science and Health, Part A, 2012
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.
Advanced Chemicobiology Research
Nickel has been known to adversely affect the female reproductive system and pregnancy, and cause teratogenesis. This review aims to analyse these effects of nickel. The implications of maternal oxidative stress and hormonal perturbations caused due nickel exposure have been discussed. Increased placental permeability, unidirectional foetal exposure through blood and milk leading to defects during organogenesis are analysed, along with post parturition eventualities such as stillbirth and altered sex ratios. Efforts are made to understand the ameliorative effects of selenium and possible future directions of research in the broad area are enumerated.
Effect of Nickel Chloride on Cell Proliferation
The Open Dentistry Journal, 2012
Objective: Metal alloys used in dentistry and in other biomedical fields may release nickel ions in the oral environment. The release of nickel might influence the normal biological and physiological processes, including tissue wound healing, cell growth and proliferation. The aim of this study was to evaluate in vitro the effects of nickel ions on cell cycle, viability and proliferation.
Nickel toxicology with reference to male molecular reproductive physiology
Reproductive Biology, 2020
The toxicity of metals is a known phenomenon. Nickel toxicity is very common since nickel is used extensively both industrially and in items of personal use such as utensils and jewellery. Here we discuss human exposure to nickel and its toxicity in the light of the available scientific evidence to understand its underlying pathophysiology. The ability of Ni +2 to get oxidized to Ni +3 renders it's potential of generating reactive oxygen species (ROS) in the system leading to oxidative stress. Carcinogenesis, apoptosis induction, contact dermatitis, epigenetic changes, and alteration in gene regulation are a result of overexposure of nickel. Our focus is on how nickel affects the male reproductive physiology. Nickel primarily drives ROS mediated perturbations in the male reproductive system. It influences zinc metabolism, which is critical for sperm stability and affects the structure of DNA binding proteins, including protamines, thereby affecting sperm function.
Reviews on Environmental Health, 2011
Nickel, a naturally occurring element that exists in various mineral forms, is mainly found in soil and sediment, and its mobilization is influenced by the physicochemical properties of the soil. Industrial sources of nickel include metallurgical processes such as electroplating, alloy production, stainless steel, and nickel-cadmium batteries. Nickel industries, oil-and coal-burning power plants, and trash incinerators have been implicated in its release into the environment. In humans, nickel toxicity is influenced by the route of exposure, dose, and solubility of the nickel compound. Lung inhalation is the major route of exposure for nickel-induced toxicity. Nickel may also be ingested or absorbed through the skin. The primary target organs are the kidneys and lungs. Other organs such as the liver, spleen, heart and testes may also be affected to a lesser extent. Although the most common health effect is an allergic reaction, research has also demonstrated that nickel is carcinogenic to humans. The focus of the present review is on recent research concerning the molecular mechanisms of nickel-induced genotoxicity and carcinogenicity. We first present a background on the occurrence of nickel in the environment, human exposure, and human health effects.
Hormonal Perturbations in Occupationally Exposed Nickel Workers
Open Access Macedonian Journal of Medical Sciences, 2016
BACKGROUND: Nickel exposure is recognized as an endocrine disruptor because of its adverse effects on reproduction.AIM: This study was designed to investigate the possible testiculo-hormonal perturbations on workers occupationally exposed to nickel and to assess its effects on human male sexual function. METHODS: Cross-sectional comparative study, comprising 105 electroplating male non-smoker, non-alcoholic workers exposed to soluble nickel and 60 controls was done. Serum luteinizing hormone, follicle stimulating hormone, testosterone levels and urinary nickel concentrations were determined for the studied groups. RESULTS: Serum luteinizing hormone, follicle stimulating hormone, urinary nickel and the simultaneous incidence of more than one sexual disorder were significantly higher in the exposed workers compared to controls. The occurrence of various types of sexual disorders (decreased libido, impotence and premature ejaculation) in the exposed workers was 9.5, 5.1 and 4.4 folds r...
Oxidative DNA damage in cultured cells and rat lungs by carcinogenic nickel compounds
Free Radical Biology and Medicine, 2001
DNA damage in cultured cells and in lungs of rats induced by nickel compounds was investigated to clarify the mechanism of nickel carcinogenesis. DNA strand breaks in cultured cells exposed to nickel compounds were measured by using a pulsed field gel electrophoresis technique. Among nickel compounds (Ni 3 S 2 , NiO (black), NiO (green), and NiSO 4 ), only Ni 3 S 2 , which is highly carcinogenic, induced lesions of both double-and single-stranded DNA in cultured human cells (Raji and HeLa cells). Treatment of cultured HeLa cells with Ni 3 S 2 (10 g/ml) induced a 1.5-fold increase in 8-hydroxy-2Ј-deoxyguanosine (8-OH-dG) compared with control, whereas NiO (black), NiO (green), and NiSO 4 did not enhance the generation of 8-OH-dG. Intratracheal instillation of Ni 3 S 2 , NiO(black), and NiO(green) to Wistar rats increased 8-OH-dG in the lungs significantly. NiSO 4 induced a smaller but significant increase in 8-OH-dG. Histological studies showed that all the nickel compounds used induced inflammation in lungs of the rats. Nitric oxide (NO) generation in phagocytic cells induced by Ni 3 S 2 , NiO(black), and NiO(green) was examined using macrophage cell line RAW 264.7 cells. NO generation in RAW 264.7 cells stimulated with lipopolysaccharide was enhanced by all nickel particles. Two mechanisms for nickel-induced oxidative DNA damage have been proposed as follows: all the nickel compounds used induced indirect damage through inflammation, and Ni 3 S 2 also showed direct oxidative DNA damage through H 2 O 2 formation. This double action may explain relatively high carcinogenic risk of Ni 3 S 2 .
Effect of Nickel Sulfate on Testicular Steroidogenesis in Rats during Protein Restriction
Environmental Health Perspectives, 2002
Nickel, a widely used heavy metal, exerts potent toxic effects on peripheral tissues as well as on the reproductive system. Low dietary protein coupled with exposure to this metal induces more severe changes, including biochemical defects, structural disorders, and altered physiologic functions. This study was designed to assess the effects of nickel sulfate on testicular steroidogenesis and to ascertain whether such alterations are reversible with normal protein and protein-restricted dietary regime. Nickel sulfate [2 mg/100 g body weight (bw)] dissolved in double-distilled water was administered on alternate days for 10 doses in a normal protein diet (18% casein) and a proteinrestricted diet (5% casein) to Wistar male albino rats (bw 160 ± 5 g). Two groups, one with a normal protein diet and the other with a protein-restricted diet, served as controls. Twenty-four hours after the last treatment, all the animals except those in withdrawal groups were sacrificed by decapitation. We observed a significant reduction in the activities of the testicular steroidogenic enzymes and plasma testosterone concentration accompanied by a significant elevation in cholesterol and ascorbic acid level in both dietary groups. After 15 days of withdrawal from the nickel sulfate treatment, the testicular steroidogenic enzymes, along with plasma testosterone level, improved significantly in both normal protein-fed and protein-restricted dietary groups. The effects of nickel on testicular cholesterol and ascorbic acid concentration were also reduced after withdrawal. Our results indicate that nickel sulfate affects the steroidogenic enzymes, causing alteration in the formation of testosterone in both dietary groups, which was manifested in the elevated cholesterol and ascorbic acid level with decreased activities of steroidogenic enzymes in adult rats testes. However, these alterations were reversible in both groups of animals fed normal protein diets and protein-restricted diets. Key words: hydroxysteroid dehydrogenase, nickel sulfate, protein restriction, testes, testosterone. Environ Health Perspect 110:923-926 (2002). [Online 13 August 2002] http://ehpnet1.niehs.nih.gov/docs/2002/110p923-926das/abstract.html
Oxidative Stress Level in the Testes of Mice and Rats during Nickel Intoxication
The Scientific World Journal, 2012
The genotioxic and carcinogenic effect of nickel probably results from its capacity to produce reactive oxygen species (ROS) and disturb the redox balance. The aim of the study was to find out if rats lacking spermatic protamine 2 are less susceptible to Ni(II) than mice. Consequently, the levels of malondialdehyde + 4 hydroxynonenal (MDA+4HDA) − markers of lipid peroxidation, as well as the level of reduced glutathione (GSH) were measured within the rat and mouse testes. Our results showed that the levels of lipid peroxidation markers were elevated in testicular homogenates of intoxicated mice without any changes in rats. GSH level was lower in the group of intoxicated mice comparing to the control without statistically significant changes in rats' homogenates. Moreover, the level of GSH in the testes of intoxicated mice was lower than in rats. On the basis of our results, it appears that Ni(II) can initiate oxidative stress in the testes of mice but not of rats and can reduce GSH level. Consequently, the antioxidative defense of the testes is reduced. Ni(II) that causes oxidative stress in the testes may also contribute to infertility.