Effects of gestational administration of nickel on postnatal development in Swiss albino mice

Saini, Shivi; Nair, Neena; Saini,

doi:10.1177/0960327114527627

Cited by 5 publications

(2 citation statements)

References 28 publications

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“…Taking into consideration that a regular reaty‐to‐eat sushi box contains 200–300 g of sushi and that sushi is not the only food product containing nickel, frequent sushi consumption might result in exceeding the established safety levels. Because orally administered nickel is hazardous for fetal development, including skeletal development, fetal weight or even mortality, pregnant women should be discouraged from sushi consumption. Although the nori contained high levels of Ni, relatively small amounts of nori in the final product suggest that nori was not the main source of nickel contamination in the sushi samples.…”

Section: Resultsmentioning

confidence: 99%

Heavy metal contamination, microbiological spoilage and biogenic amine content in sushi available on the Polish market

et al. 2017

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Sushi is not the source of high levels of biogenic amines even with high microbiological loads. Nevertheless, the high microbiological loads at the end of the shelf-life indicate that some processors might have problems with the distribution chain or implement a poor hygienic regime. Moreover as a result of possible risk associated with heavy metal contamination, the present study highlights the need to establish new regulations regarding the contamination of nori and sushi. © 2017 Society of Chemical Industry.

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Section: Resultsmentioning

confidence: 99%

Heavy metal contamination, microbiological spoilage and biogenic amine content in sushi available on the Polish market

et al. 2017

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“…Effects of nickel on the postnatal development of Swiss albino mice exposed during the three gestation periods were examined (Saini et al., 2014a). Nickel chloride hexahydrate was administered to pregnant females by gavage (46, 92, or 185 mg Ni/kg bw) during GD 0–5 (pre‐implantation period), GD 6–13 (organogenetic period) or GD 14–18 days (fetal period).…”

Section: Assessmentmentioning

confidence: 99%

Update of the risk assessment of nickel in food and drinking water

Schrenk¹,

Bignami²,

Bodin³

et al. 2020

EFS2

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The European Commission asked EFSA to update its previous Opinion on nickel in food and drinking water, taking into account new occurrence data, the updated benchmark dose (BMD) Guidance and newly available scientific information. More than 47,000 analytical results on the occurrence of nickel were used for calculating chronic and acute dietary exposure. An increased incidence of postimplantation loss in rats was identified as the critical effect for the risk characterisation of chronic oral exposure and a BMDL 10 of 1.3 mg Ni/kg body weight (bw) per day was selected as the reference point for the establishment of a tolerable daily intake (TDI) of 13 lg/kg bw. Eczematous flare-up reactions in the skin elicited in nickel-sensitised humans, a condition known as systemic contact dermatitis, was identified as the critical effect for the risk characterisation of acute oral exposure. A BMDL could not be derived, and therefore, the lowest-observed-adverse-effect-level of 4.3 lg Ni/kg bw was selected as the reference point. The margin of exposure (MOE) approach was applied and an MOE of 30 or higher was considered as being indicative of a low health concern. The mean lower bound (LB)/upper bound (UB) chronic dietary exposure was below or at the level of the TDI. The 95th percentile LB/UB chronic dietary exposure was below the TDI in adolescents and in all adult age groups, but generally exceeded the TDI in toddlers and in other children, as well as in infants in some surveys. This may raise a health concern in these young age groups. The MOE values for the mean UB acute dietary exposure and for the 95th percentile UB raises a health concern for nickel-sensitised individuals. The MOE values for an acute scenario regarding consumption of a glass of water on an empty stomach do not raise a health concern.

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The C57BL/6J mice offspring originated from a parental generation exposed to tannery effluents shows object recognition deficits

et al. 2016

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The main aim of the present paper is to assess whether the parental generation exposure to such discharges could cause object recognition deficits in their offspring. Male and female C57Bl/6J mice were put to mate after they were exposed to 7.5% and 15% tannery effluents or water (control group), for 60 days. The male mice were withdrawn from the boxes after 15 days and the female mice remained exposed to the treatment during the gestation and lactation periods. The offspring were subjected to the object recognition test after weaning in order to assess possible cognition losses. The results of the analysis of the novel object recognition index found in the testing session (performed 1 h after the training session) applied to offspring from different experimental groups appeared to be statistically different. The novel object recognition index of the offspring from female mice exposed to tannery effluents (7.5% and 15% groups) was lower than that of the control group, and it demonstrated object recognition deficit in the studied offspring. The present study is the first to report evidences that parental exposure to effluent of tannery (father and mother) can cause object recognition deficit in the offspring, which is related to problems in the central nervous system.

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Effects of gestational administration of nickel on postnatal development in Swiss albino mice

Cited by 5 publications

References 28 publications

Heavy metal contamination, microbiological spoilage and biogenic amine content in sushi available on the Polish market

Heavy metal contamination, microbiological spoilage and biogenic amine content in sushi available on the Polish market

Update of the risk assessment of nickel in food and drinking water

The C57BL/6J mice offspring originated from a parental generation exposed to tannery effluents shows object recognition deficits

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