Cadmium‐Induced Enteropathy in Domestic Cocks: A Biochemical and Histological Study after Subchronic Exposure

Berzina, Nadezhda; Markovs, Jurijs; Isajevs, Sergejs; Apsite, M. R.; Смирнова, Г. В.

doi:10.1111/j.1742-7843.2007.00072.x

Cited by 24 publications

(12 citation statements)

References 32 publications

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“…In this study, between 20 and 40 days of contamination, the metal appeared to be unable to efficiently penetrate the intestinal epithelium to reach liver but was still accumulated in muscle. This can be relevant with previous studies that have shown that Cd uptake triggers an inflammatory and secretory response in the small intestines of chickens (Berzina et al 2007). Moreover, Cd dietary contamination with enriched food can impair the efficiency of the metal to penetrate the intestinal epithelium of fish species (Pierron et al 2008).…”

Section: Bioaccumulationmentioning

confidence: 50%

Impact of cadmium on aquatic bird Cairina moschata

et al. 2009

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The impact on palmiped Cairina moschata of two levels of dietary cadmium (Cd) contamination (C1: 1 mg kg(-1) and C10: 10 mg kg(-1)) was investigated on liver gene expression by real-time PCR. Genes involved in mitochondrial metabolism, in antioxidant defences, detoxification and in DNA damage repair were studied. Metallothionein (MT) protein levels and Cd bioaccumulation were also investigated in liver, kidneys and muscle. Male ducks were subjected to three periods of exposure: 10, 20 and 40 days. Cd was mainly bioaccumulated in kidneys first and in liver. The concentrations in liver and kidneys appeared to reach a stable level at 20 days of contamination even if the concentrations in muscle still increased. Cd triggered the enhancement of mitochondrial metabolism, the establishment of antioxidant defences (superoxide dismutase Mn and Cu/Zn; catalase) and of DNA repair from 20 days of contamination. Discrepancies were observed in liver between MT protein levels and MT gene up-regulation. MT gene expression appeared to be a late hour biomarker.

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Section: Bioaccumulationmentioning

confidence: 50%

Impact of cadmium on aquatic bird Cairina moschata

et al. 2009

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“…This toxic metal is known to have various adverse effects on organisms, such as lesions in the kidney or intestinal tissues, induction of reactive oxygen species, DNA damage, impact on hepatic enzymes activities and lipid peroxidation (Mayack et al 1981;Jordan et al 1990;Wang et al 2004;Erdogan et al 2005;Berzina et al 2007). Moreover, Cd impairment on lipid metabolism has also been demonstrated on fish and mammalian species (Pierron et al 2007;Larregle et al 2008).…”

Section: Introductionmentioning

confidence: 95%

Effect of dietary cadmium on lipid metabolism and storage of aquatic bird Cairina moschata

et al. 2009

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In environment, birds often fast in connection with breeding, migration or drastic climatic conditions and need to mobilize lipid reserves during these periods. The impairment of lipid metabolism by cadmium (Cd; 1 mg kg(-1) added in diet) was investigated on palmiped Cairina moschata. Expression levels of genes involved in lipid metabolism, mitochondrial metabolism and detoxification were investigated in liver and muscle of ducks. Lipid content in muscle and liver were analysed and plasma triglycerides were quantified. After 20 days, ducks exposed to Cd displayed a lower body weight and lower lipid content in liver than controls. In muscle, the increase of lipid content was only significant for control ducks but not for exposed ducks. Exposed ducks appeared unable to sufficiently transport and store lipids into peripheral tissues. Cd impairs lipid metabolism by several ways. First, Cd triggered the down-regulation of fatty acids synthesis in liver even if the NADPH production and the mitochondrial metabolism are enhanced, suggesting a stronger energy needs. Secondly, the associated decrease of plasma triglycerides and lipoprotein lipase activity with Cd are consistent with impairment of lipids storage in peripheral tissues.

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“…Damage to intestinal epithelium integrity, including increased paracellular permeability, altered cell viability and inflammatory response, have been reported following exposure to Cd (Duizer et al 1999;Boveri et al 2004;Berzina et al 2007). Cd also favors the production of oxygen species leading to oxidative stress (Wang et al 2004), and induces stress proteins such as MT-IIa, a metal-binding protein, and the heat shock protein HSP70 (Reeves and Rossow 1996;Kiang and Tsokos 1998;Blais et al 1999).…”

Section: Introductionmentioning

confidence: 97%

Resistance to cadmium as a function of Caco-2 cell differentiation: role of reactive oxygen species in cadmium- but not zinc-induced adaptation mechanisms

2009

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Cadmium (Cd) is a highly toxic metal that enters the food chain. Following oral ingestion, the intestinal epithelium is the first biological barrier crossed by Cd and is also an important target tissue. In the present study, the human intestinal Caco-2 cell line was used to evaluate the impact of a low level of exposure on both undifferentiated and differentiated intestinal cells. As revealed by the LC(50) values estimated with the 3-[4,5-dimethyl-2-thiazol-2-yl]-2,5-diphenyltetrazolium bromide (MTT) assay, mature Caco-2 cells were more resistant to Cd. However, following a 24-h exposure to non-cytotoxic levels of Cd (10 microM) or zinc (Zn, 100 microM), threefold increases were obtained in the LC(50) values of 7-day-old cells, whereas increased resistance in 21-day-old cells was observed exclusively with Zn. Induction of MT-IIa and HSP70 mRNAs was higher in undifferentiated cells and an increase in cellular glutathione (GSH) content was observed exclusively in these cell cultures. However, the results obtained with cycloheximide used for inhibiting protein synthesis and with L-buthionine sulfoximine (BSO), which inhibits GSH synthesis, revealed that protein synthesis is not a prerequisite to the development of resistance. The presence of 100 mM 3-amino-1,2,4-triazole (3AT), a catalase inhibitor, prevented Cd-induced but not Zn-induced resistance, as well as sensitized cells to Cd toxicity. These results show for the first time differences in constitutive and acquired resistance to Cd as a function of enterocytic differentiation status and suggest the involvement of different mechanisms for Cd- and Zn-induced adaptation in the intestinal cells. Redox signals may trigger Cd-induced adaptation mechanisms but pro-oxidant conditions would eliminate proliferative intestinal cells capability to develop resistance. This would be critical for Cd- but not Zn-induced mechanisms of resistance since Cd but not Zn may cause oxidative stress.

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Cadmium‐Induced Enteropathy in Domestic Cocks: A Biochemical and Histological Study after Subchronic Exposure

Cited by 24 publications

References 32 publications

Impact of cadmium on aquatic bird Cairina moschata

Impact of cadmium on aquatic bird Cairina moschata

Effect of dietary cadmium on lipid metabolism and storage of aquatic bird Cairina moschata

Resistance to cadmium as a function of Caco-2 cell differentiation: role of reactive oxygen species in cadmium- but not zinc-induced adaptation mechanisms

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