Cadmium accumulation in liver and kidney of mice exposed to the same weekly cadmium dose continuously or once a week

Lind, Ylva; Engman, Joakim; Jorhem, Lars; Glynn, Anders

doi:10.1016/s0278-6915(97)00068-9

Cited by 37 publications

(27 citation statements)

References 14 publications

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“…The induction of GRP78 mRNA was associated with accumulation of GRP78 protein (Figure 1d). Similarly, induction of GRP78 (and GRP94) was also observed in response to maximum, non-toxic concentrations of (CH 3 COO) 2 Figure 1a and b).…”

Section: Resultsmentioning

confidence: 59%

“…Induction of ER stress by CdCl 2 was attenuated in these transfectants when the levels of GRP78 was examined ( Figure 3e). In these clones, the apoptogenic effect of CdCl 2 …”

Section: Resultsmentioning

confidence: 99%

“…1,2 In particular, the highest concentrations of cadmium are observed in the kidney, the main target of the cadmium-related toxicity. 3,4 In the kidney, accumulation of cadmium occurs mainly in the proximal tubules and other nephron segments are affected only at later stages of intoxication.…”

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confidence: 99%

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Atypical, bidirectional regulation of cadmium-induced apoptosis via distinct signaling of unfolded protein response

et al. 2007

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Cadmium is a widely distributed nephrotoxic metal that causes renal tubular injury. In this report, we investigated involvement of endoplasmic reticulum (ER) stress and individual unfolded protein responses in cadmium-initiated apoptosis of tubular epithelial cells. Cadmium chloride (CdCl 2 ) induced expression of endogenous ER stress markers, GRP78, GRP94 and CHOP in vitro and in vivo, and subsequently caused cytological changes typical of apoptosis. Attenuation of ER stress by transfection with ER chaperone GRP78 or ORP150 suppressed CdCl 2 -triggered apoptosis. In response to CdCl 2 , phosphorylation of RNAdependent protein kinase-like ER kinase (PERK) and eukaryotic translation initiation factor 2a (eIF2a) was observed. Enhanced phosphorylation of eIF2a attenuated, whereas inhibition of eIF2a exacerbated CdCl 2 -induced apoptosis. Activating transcription factor 6 (ATF6) was also activated by CdCl 2 and blockade of this process suppressed induction of CHOP and thereby improved cell survival. CdCl 2 also triggered activation of the inositol-requiring ER-to-nucleus signal kinase 1 (IRE1)-X-box-binding protein 1 (XBP1) pathway and inhibition of XBP1 attenuated apoptosis independent of GRP78 and CHOP. c-Jun N-terminal kinase (JNK), another molecule downstream of IRE1, was also phosphorylated by CdCl 2 and its inhibition attenuated apoptosis. These results evidenced bidirectional regulation of apoptosis in cadmium-exposed cells. The ATF6 and IRE1 pathways cooperatively caused apoptosis via induction of CHOP, activation of XBP1 and phosphorylation of JNK, and the PERK-eIF2a pathway counteracted the proapoptotic processes.

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Section: Resultsmentioning

confidence: 59%

“…Induction of ER stress by CdCl 2 was attenuated in these transfectants when the levels of GRP78 was examined ( Figure 3e). In these clones, the apoptogenic effect of CdCl 2 …”

Section: Resultsmentioning

confidence: 99%

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Atypical, bidirectional regulation of cadmium-induced apoptosis via distinct signaling of unfolded protein response

et al. 2007

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“…In our study, liver, by virtue of its mass (154.5 ± 43.7 g), accounted for up to 5.8% of the ingested dose of Cd, but concentrations remained low. The distribution of Cd in mainly kidney or mainly liver is the result of complex interactions between parameters such as the treatment dose size (low doses vs. high doses; Ando et al 1998), dosing regime (single dose vs. chronic exposure; Lind et al 1997), type of contamination (administration of Cd-MT vs. CdCl2; Groten et al 1991).…”

Section: Discussionmentioning

confidence: 99%

“…Dietary transfer, accumulation, kinetics and the effects of Cd have been widely studied in mammals (Chan et al 2004;Lind et al 1997;Matsuno et al 1991;Schilderman et al 1997), whereas little is still known about reptiles (snakes: Hopkins et al 2002;lizards: Mann et al 2007). In those studies, individual animals were contaminated with Cd via food, and distribution in the organs was investigated.…”

Section: Introductionmentioning

confidence: 99%

Cadmium toxicokinetics and bioaccumulation in turtles: trophic exposure of Trachemys scripta elegans

Guirlet

Das

2011

Ecotoxicology

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Ecotoxicological data in reptiles are mainly represented by field studies reporting the tissue burden of wild-captured individuals but much less is known regarding the processes of uptake, depuration, accumulation and the effects of inorganic contaminants in these species. In the present study, the accumulation, the path and the effects of exposure to cadmium (Cd) through diet intake were investigated in female red eared slider turtles, Trachemys scripta elegans. In the first phase of the experiment, turtles underwent an acclimatization period during which they were fed a control diet. In the second phase, the turtles were exposed to cadmium through a CdCl 2 supplementeddiet with increased environmentally relevant concentrations for a period of 13 weeks. Following this, the turtles went through a third phase, a recovery phase of 3 weeks, during which they were fed uncontaminated food. Blood and feces were collected during the three phases of the experiment. The turtles were euthanized at the end of the experiment and organ samples collected. The Cd-concentrations in blood remained stable over the course of the experiment while Cd-concentrations in feces increased with time and with the amount of Cd ingested. The proportional accumulation in liver and kidney together was comprised between 0.7 and 6.1% and they represented the main organs of accumulation. Cd accumulated in the organs in the following order of concentration: kidney [ liver [ pancreas [ muscle. In terms of burden in organs, the Cd-burden was the highest in liver followed by kidney and pancreas. The proportional accumulation decreased as Cd ingestion increased, suggesting that at a higher dose of Cd, assimilation decreased. Mineral content of the liver and pancreas became modified according to Cd level; increasing dietary Cd exposure increased concentrations of zinc and iron in liver and copper in pancreas in a dose-dependent manner. Accumulation of Cd had no effect on survival, food consumption, growth, weight or length suggesting no effect of the treatment on female turtle body condition.

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Cadmium distribution and toxicity in tissues of small rodents

Świergosz-Kowalewska

2001

Microscopy Res & Technique

110

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The aim of the present paper is to discuss the accumulation and distribution of cadmium (Cd) in the various tissues of animals, the interactions of cadmium with other elements, and the damage to tissues caused by this metal. Cadmium is not physiologically or biochemically essential to an organism. It is absorbed via the gastrointestinal tract and lungs and accumulated in various tissues, mainly the kidneys and liver. The distribution of cadmium between various tissues depends on many endogenous and exogenous factors. Cadmium is bound to a low-molecular-weight protein, metallothionein (MT), and to high-molecular-weight proteins. This metal has a great affinity to thiol groups. Cadmium binds also to O- and N-containing ligands. The distribution of cadmium between organs differs markedly depending on the chemical form of administered Cd and the duration of exposure. Acute exposure results in a different distribution pattern throughout the body than does chronic exposure. Long-term exposure to high doses of cadmium may cause biochemical and functional changes in some critical organs. Cadmium can influence the absorption and distribution of essential elements and can replace them in enzymes. Metallothionein and glutathione play important roles in the transport of metals and in detoxification processes. Reported findings are mainly the results of experiments on laboratory animals. The lack of data concerning the localization of cadmium in various tissues of wild species is noticeable and there is a great need for such data.

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Cadmium accumulation in liver and kidney of mice exposed to the same weekly cadmium dose continuously or once a week

Cited by 37 publications

References 14 publications

Atypical, bidirectional regulation of cadmium-induced apoptosis via distinct signaling of unfolded protein response

Atypical, bidirectional regulation of cadmium-induced apoptosis via distinct signaling of unfolded protein response

Cadmium toxicokinetics and bioaccumulation in turtles: trophic exposure of Trachemys scripta elegans

Cadmium distribution and toxicity in tissues of small rodents

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