Chronic Nephrotoxicity of Soluble Nickel in Rots

Vyskočil, Adolf; Viau, Claude; Čížková, Martina

doi:10.1177/096032719401301007

Cited by 35 publications

(32 citation statements)

References 12 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…Decreases or increases in kidney weights were observed in several oral studies in rats or mice (Ambrose et al, 1976;Weischer et al, 1980, Obone et al, 1999. In addition, increased urinary albumin (indicator of diminished kidney function) and mild tubular nephrosis was observed in some studies in rats (Dieter et al, 1988;Vyskocil et al, 1994).…”

Section: Repeat Dose Toxicitymentioning

confidence: 99%

“…In its assessment, TERA derived a RfD for soluble Ni salts of 8 μg/kg b.w. per day based on the lowest LOAEL from Vyskocil et al (1994) study where multiple sensitive endpoints for kidney function were evaluated in rats exposed to soluble Ni compounds in drinking water for 6 months. Kidney weights were significantly increased in the exposed groups but no significant changes were observed in other parameters.…”

Section: Previous Risk Assessmentsmentioning

confidence: 99%

See 1 more Smart Citation

Scientific Opinion on the risks to public health related to the presence of nickel in food and drinking water

Publication¹

2015

EFS2

119

View full text Add to dashboard Cite

EFSA received a request from the Hellenic Food Authority (EFET) for a scientific opinion on the risk to human health from the presence of nickel (Ni) in food, particularly in vegetables. The EFSA Panel on Contaminants in the Food Chain (CONTAM Panel) decided to extend the risk assessment also to drinking water. The reproductive and developmental toxicity in experimental animals was selected as the critical effect for the assessment of chronic effects of Ni. A tolerable daily intake of 2.8 µg Ni/kg body weight (b.w.) per day was derived from a lower 95 % confidence limit for a benchmark dose at 10 % extra risk (BMDL 10 ) of 0.28 mg/kg b.w. for post-implantation fetal loss in rats. The current dietary exposure to Ni raises concern when considering the mean and 95th percentile chronic exposure levels for all different age groups. The systemic contact dermatitis (SCD) elicited in Ni-sensitive humans after oral exposure to Ni was selected as the critical effect suitable for the assessment of acute effects of Ni. A lowest BMDL 10 of 1.1 µg Ni/kg b.w. was derived for the incidence of SCD following oral exposure to Ni of human volunteers. The CONTAM Panel applied a margin of exposure (MOE) approach and considered an MOE of 10 to be indicative of a low health concern. The MOEs calculated considering the estimated mean and the 95th percentile acute exposure levels were considerably below 10 for all age groups. Overall, the CONTAM Panel concluded that, at the current levels of acute dietary exposure to Ni, there is a concern that Ni-sensitized individuals may develop eczematous flare-up skin reactions. The CONTAM Panel noted the need for mechanistic studies to assess the human relevance of the effects on reproduction and development observed in experimental animals and for additional studies on human absorption of nickel from food, for example in combination with duplicate diet studies. Following a call for data on Ni levels in food and drinking water (water intended for human consumption and mineral waters), a total of 18 885 food samples and 25 700 drinking water samples were available in the final dataset to estimate dietary exposure to nickel. No speciation data were provided. Samples were collected between 2003 and 2012 in 15 different European countries, with almost 80 % of the total collected in one Member State. The most reported analytical methods were inductively coupled plasma-mass spectrometry (ICP-MS) and atomic absorption spectrometry (AAS), that represented 54 % and 42 % of the methods reported, respectively. The highest sensitivity was reported for the analysis of drinking water with a limit of quantification (LOQ) of 0.001 µg/L (for both ICP-MS and AAS). In food, ICP-MS showed the lowest LOQ for the analysis of 'Alcoholic beverages' (0.002 µg/kg) while the lowest LOQ reported with AAS was 1 µg/kg for samples of 'Fish and seafood' and 'Sugar and confectionery'. In the final dataset, left-censored data represented 66 % of the analytical results, with 35 % in food samples and 89 % in drinking water sa...

show abstract

Section: Repeat Dose Toxicitymentioning

confidence: 99%

Section: Previous Risk Assessmentsmentioning

confidence: 99%

Scientific Opinion on the risks to public health related to the presence of nickel in food and drinking water

Publication¹

2015

EFS2

119

View full text Add to dashboard Cite

show abstract

“…One-month dietary restriction (lanes 2, 6) did not lead to evident changes of stress protein expression as compared to NF controls (lanes 1, 5). Ni-induced overexpression of 96 and 73 kDa appeared to be similar in NF (lanes 3, 7) and DR rats (lanes 4,8).…”

Section: Expression Pattern Of Stress Proteins In Kidney Of Ni-treatementioning

confidence: 80%

Effects of nickel poisoning on expression pattern of the 72/73 and 94 kDa stress proteins in rat organs and in the COS‐7, HepG2, and A549 cell lines

Hfaïedh

Allagui

Feki

et al. 2005

J Biochem & Molecular Tox

View full text Add to dashboard Cite

The present study deals with the effects of Ni on the expression level of three stress proteins, namely, the cytosolic HSP72 and HSP73, and the reticulum-associated GRP94. Experiments were carried out on "Wistar'' female rats daily injected with 4 mg NiCl2 per kg body weight for 1, 3, 5, and 10 days. Another set of experiments were carried out using cell lines, derived from the monkey kidney (COS-7), and from human tumors of the lung (A549) and liver (HepG2). Cells were cultured for 4 days in the permanent presence of 100, 200, or 400 microM NiCl2. In control rats, stress proteins pattern was found to be tissue specific: two protein bands of 96 and 94 kDa were immunodetected with the anti-GRP94 antibody in kidney and liver extracts, whereas only the 96 kDa band was present in ovary extracts. HSP73 was present in kidney, liver, and ovary whereas HSP72 was only found in kidney. In kidney of nickel-treated animals, HSP73 and the 96 kDa proteins were overexpressed whereas HSP72 was strongly down regulated. No such effect was observed in liver or ovary. Similarly, in nickel-treated cell lines, HSP72 was downregulated and GRP94 (96 kDa protein) was overexpressed. HSP73 expression appeared moderately increased in A549 cells but decreased in COS-7 cells. Because long-term caloric restriction was reported to reduce free radical generation in cells, the effect of 1 month food restriction (50%) was tested in rats as a possible way to lower oxidative damages induced by Ni. No significant effect on HSP expression was observed.

show abstract

“…Furthermore, the expressed histologic damage scores were lower, showing minimal tubular generation, necrosis, and infiltration by inflammatory cells that were induced by nickel treatment.The nephrotoxic effect of Ni is observed in a significant increase in the serum level of urea and creatinine, which may result in a decrease in reabsorption at renal epithelium and disruption of glomerular filtration rate. This increases the risk of renal failure (26). The measurements of creatinine, urea, and uric acid are considered a tool in the clinical diagnosis of renal dysfunction following acute and chronic oxidative kidney injury (27,28).…”

Section: Kidney Histopathological Changesmentioning

confidence: 99%

Vitamin C pretreatment protects from nickel-induced acute nephrotoxicity in mice

Kadi

Dahdouh

2016

Archives of Industrial Hygiene and Toxicology

View full text Add to dashboard Cite

Nickel is an abundant carcinogenic and nephrotoxic metal whose activity leads to renal impairment. Previous studies have shown a protective effect of simultaneous vitamin C administration on acute and chronic nickel toxicity. However, very little research relating to the effect of vitamin C pretreatment in preventing nickel-induced acute nephrotoxicity is available. Therefore, the present study aimed to determine the efficiency of vitamin C (VC) pretreatment in preventing acute renal toxicity of nickel. Mice were pretreated orally with vitamin C (16.6 mg kg -1 body weight, b.w.) for seven consecutive days, prior to intraperitoneal (i.p.) administration of nickel chloride at different doses (3, 5, and 10 mg Ni kg -1 b.w.) for an exposure period of 24 hours. Thereafter, animals were killed and kidney tissue and blood samples were taken for histological examination and biochemical marker analyses. Vitamin C pretreatment alone did not alter the levels of serum kidney markers (creatinine, urea, and uric acid). However, treatment with Ni alone showed a significant increase in the levels of serum creatinine, urea, and uric acid with marked necrotic epithelial cells and infiltration by inflammatory cells in kidney sections as compared to the control group. Pretreatment with vitamin C and treatment with Ni at all doses tested for 24 hours showed a significant decrease in the levels of serum creatinine, urea, and uric acid, as well as an improvement in histological changes compared to those previously seen in the group treated with Ni alone. It is concluded that vitamin C pretreatment effectively improved renal function and tissue damage caused by nickel.

show abstract

Chronic Nephrotoxicity of Soluble Nickel in Rots

Cited by 35 publications

References 12 publications

Scientific Opinion on the risks to public health related to the presence of nickel in food and drinking water

Scientific Opinion on the risks to public health related to the presence of nickel in food and drinking water

Effects of nickel poisoning on expression pattern of the 72/73 and 94 kDa stress proteins in rat organs and in the COS‐7, HepG2, and A549 cell lines

Vitamin C pretreatment protects from nickel-induced acute nephrotoxicity in mice

Contact Info

Product

Resources

About