On the mechanism of nickel absorption in the rat jejunum

Foulkes, E. C.; McMullen, Diane M.

doi:10.1016/0300-483x(86)90170-8

Cited by 38 publications

(16 citation statements)

References 8 publications

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“…In the rat, nickel uptake deviates from a firstorder process at Ni'+ concentrations <O. 1 mM (23,24) in the perfusate (23,24), whereas the present study indicates that nickel uptake in humans did not deviate from first-order kinetics following ingestion of water containing Ni2+ at concentrations up to 0.6 m M (which was, of course, substantially diluted postingestion by the gastrointestinal juices). The absorption rate constant for nickel in humans was not significantly different at dosages of 12, 18, or 50 pg of nickel/kg body wt.…”

Section: Discussioncontrasting

confidence: 65%

Nickel Absorption and Kinetics in Human Volunteers

Hopfer²,

Kr³

et al. 1989

Experimental Biology and Medicine

124

109

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Mathematical modeling of the kinetics of nickel absorption, distribution, and elimination was performed in healthy human volunteers who ingested NiSO, drinking water (Experiment 1) or added to food (Experiment 2). Nickel was analyzed by electrothermal atomic absorption spectrophotometry in serum, urine, and feces collected during 2 days before and 4 days after a specified NiS0, dose (12 pg of nickel/kg, n = 4; 18 pg of nickel/kg, n = 4; or 50 pg of nickel/kg, n = 1). In Experiment 1, each of the subjects fasted 12 hr before and 3 hr after drinking one of the specified NiSO, doses dissolved in water; in Experiment 2, the respective subjects fasted 12 hr before consuming a standard American breakfast that contained the identical dose of NiS0, added to scrambled eggs. Kinetic analyses, using a compartmental model, provided excellent goodness-of-fit for paired data sets from all subjects. Absorbed nickel averaged 27 2

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Section: Discussioncontrasting

confidence: 65%

Nickel Absorption and Kinetics in Human Volunteers

Hopfer²,

Kr³

et al. 1989

Experimental Biology and Medicine

124

109

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“…Soluble nickel, for example nickel carbonyl is fat soluble and can freely cross cell membranes, most probably by diffusion or through calcium channels. Some authors in fact [248] suggested absorption of nickel by transmembrane diffusion, whilst others proposed absorption of Ni(II) via Ca(II) channels [249]. treatment of cultured HeLa cells induced a 1.5-fold increase in 8-hydroxy-2'-deoxyguanosine (8-OH-dG) compared with a control.…”

Section: Nickel Homeostasis Essentiality and Toxicitymentioning

confidence: 98%

Metals, Toxicity and Oxidative Stress

Valko

Morris²,

Cronin

2005

CMC

4,225

2,664

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Metal-induced toxicity and carcinogenicity, with an emphasis on the generation and role of reactive oxygen and nitrogen species, is reviewed. Metal-mediated formation of free radicals causes various modifications to DNA bases, enhanced lipid peroxidation, and altered calcium and sulfhydryl homeostasis. Lipid peroxides, formed by the attack of radicals on polyunsaturated fatty acid residues of phospholipids, can further react with redox metals finally producing mutagenic and carcinogenic malondialdehyde, 4-hydroxynonenal and other exocyclic DNA adducts (etheno and/or propano adducts). Whilst iron (Fe), copper (Cu), chromium (Cr), vanadium (V) and cobalt (Co) undergo redox-cycling reactions, for a second group of metals, mercury (Hg), cadmium (Cd) and nickel (Ni), the primary route for their toxicity is depletion of glutathione and bonding to sulfhydryl groups of proteins. Arsenic (As) is thought to bind directly to critical thiols, however, other mechanisms, involving formation of hydrogen peroxide under physiological conditions, have been proposed. The unifying factor in determining toxicity and carcinogenicity for all these metals is the generation of reactive oxygen and nitrogen species. Common mechanisms involving the Fenton reaction, generation of the superoxide radical and the hydroxyl radical appear to be involved for iron, copper, chromium, vanadium and cobalt primarily associated with mitochondria, microsomes and peroxisomes. However, a recent discovery that the upper limit of "free pools" of copper is far less than a single atom per cell casts serious doubt on the in vivo role of copper in Fenton-like generation of free radicals. Nitric oxide (NO) seems to be involved in arsenite-induced DNA damage and pyrimidine excision inhibition. Various studies have confirmed that metals activate signalling pathways and the carcinogenic effect of metals has been related to activation of mainly redox-sensitive transcription factors, involving NF-kappaB, AP-1 and p53. Antioxidants (both enzymatic and non-enzymatic) provide protection against deleterious metal-mediated free radical attacks. Vitamin E and melatonin can prevent the majority of metal-mediated (iron, copper, cadmium) damage both in vitro systems and in metal-loaded animals. Toxicity studies involving chromium have shown that the protective effect of vitamin E against lipid peroxidation may be associated rather with the level of non-enzymatic antioxidants than the activity of enzymatic antioxidants. However, a very recent epidemiological study has shown that a daily intake of vitamin E of more than 400 IU increases the risk of death and should be avoided. While previous studies have proposed a deleterious pro-oxidant effect of vitamin C (ascorbate) in the presence of iron (or copper), recent results have shown that even in the presence of redox-active iron (or copper) and hydrogen peroxide, ascorbate acts as an antioxidant that prevents lipid peroxidation and does not promote protein oxidation in humans in vitro. Experimental results have also shown a link ...

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“…Sunderman and Oskarsson (1991) reported that in mammals, Ni is rapidly distributed to the kidneys, pituitary, lungs, skin, adrenals, ovaries, and testes. Foulkes and McMullen (1986) suggested that dissolved Ni is absorbed in the small intestine by a two-phase mechanism. The first phase involves passage of Ni 2+ across the mucosal membrane, which is a saturable process, followed by passive ©2002 NRC Canada transfer of Ni, perhaps as an amino acid or other low-molecular-weight complex, from the mucosal cells into the body, presumably through the bloodstream.…”

Section: Absorption and Excretionmentioning

confidence: 99%

Essentiality of nickel and homeostatic mechanisms for its regulation in terrestrial organisms

Phipps¹,

Tank²,

Wirtz³

et al. 2002

Environ. Rev.

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Nickel (Ni) is a naturally occurring element with many industrial uses, including in stainless steel, electroplating, pigments, and ceramics. Consequently, Ni may enter the environment from anthropogenic sources, resulting in locally elevated concentrations in soils. However, Ni is a minor essential element, and, therefore, biota have established systems that maintain Ni homeostasis. This paper discusses the role of Ni as an essential element and reviews storage, uptake, and transport systems used to maintain homeostasis within terrestrial biota. The bioaccumulation and distribution of metals in these organisms are also addressed. In all cases, information on Ni essentiality is very limited compared to other essential metals. However, the available data indicate that Ni behaves in a similar manner to other metals. Therefore, inferences specific to Ni may be made from an understanding of metal homeostasis in general. Nevertheless, it is evident that tissue and organ Ni concentrations and requirements vary considerably within and between species, and metal accumulation in various tissues within a single organism differs as well. High rates of Ni deposition around smelters indicate that Ni in acidic soils may reach concentrations that are toxic to plants and soil decomposers. However, with the exception of hyperaccumulator plants, Ni does not biomagnify in the terrestrial food web, suggesting that toxicity to higher trophic levels is unlikely.

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On the mechanism of nickel absorption in the rat jejunum

Cited by 38 publications

References 8 publications

Nickel Absorption and Kinetics in Human Volunteers

Nickel Absorption and Kinetics in Human Volunteers

Metals, Toxicity and Oxidative Stress

Essentiality of nickel and homeostatic mechanisms for its regulation in terrestrial organisms

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