Effect of chronic exposure to excess dietary copper and dietary selenium supplementation on liver specimens from rats

Aburto, Enrique; Cribb, Alastair E.; Fuentealba, I. C.

doi:10.2460/ajvr.2001.62.1423

Cited by 9 publications

(4 citation statements)

References 26 publications

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“…Additional available data from experimental animal studies report consistent findings, including increased hepatic copper concentrations, and hepatic and renal toxicity following repeated oral intake at high dose levels of copper, with higher sensitivity of the rat compared with the mouse (Haywood, 1980; Fuentealba, 2000 #437; Haywood and Loughran, 1985; Haywood et al., 1985; Fuentealba et al., 1989, 2000; Aburto et al., 2001), as cited in Scientific Committee on Health and Environmental Risks (2008) and Taylor et al. (2020, supplementary information table).…”

Section: Assessmentmentioning

confidence: 78%

Re‐evaluation of the existing health‐based guidance values for copper and exposure assessment from all sources

More¹,

Bampidis²,

Benford³

et al. 2023

EFS2

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Copper is an essential micronutrient and also a regulated product used in organic and in conventional farming pest management. Both deficiency and excessive exposure to copper can have adverse health effects. In this Scientific Opinion, the EFSA 2021 harmonised approach for establishing health‐based guidance values (HBGVs) for substances that are regulated products and also nutrients was used to resolve the divergent existing HBGVs for copper. The tightly regulated homeostasis prevents toxicity manifestation in the short term, but the development of chronic copper toxicity is dependent on copper homeostasis and its tissue retention. Evidence from Wilson disease suggests that hepatic retention is indicative of potential future and possibly sudden onset of copper toxicity under conditions of continuous intake. Hence, emphasis was placed on copper retention as an early marker of potential adverse effects. The relationships between (a) chronic copper exposure and its retention in the body, particularly the liver, and (b) hepatic copper concentrations and evidence of toxicity were examined. The Scientific Committee (SC) concludes that no retention of copper is expected to occur with intake of 5 mg/day and established an Acceptable Daily Intake (ADI) of 0.07 mg/kg bw. A refined dietary exposure assessment was performed, assessing contribution from dietary and non‐dietary sources. Background copper levels are a significant source of copper. The contribution of copper from its use as plant protection product (PPP), food and feed additives or fertilisers is negligible. The use of copper in fertilisers or PPPs contributes to copper accumulation in soil. Infant formula and follow‐on formula are important contributors to dietary exposure of copper in infants and toddlers. Contribution from non‐oral sources is negligible. Dietary exposure to total copper does not exceed the HBGV in adolescents, adults, elderly and the very elderly. Neither hepatic copper retention nor adverse effects are expected to occur from the estimated copper exposure in children due to higher nutrient requirements related to growth.

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Section: Assessmentmentioning

confidence: 78%

Re‐evaluation of the existing health‐based guidance values for copper and exposure assessment from all sources

More¹,

Bampidis²,

Benford³

et al. 2023

EFS2

View full text Add to dashboard Cite

show abstract

“…Ideally, more samples for both ICP-MS and XFM analysis, and the separation of ICP-MS tissues into cortical and medullary sections for analysis to better match the observations from XFM, would resolve these issues. In the absence of more samples, we argue that the evidence of a relationship, largely unexplored, between Se and Cu in selenitetreated cells and rats that is already present in the literature, [50][51][52][53][54][55][56][57][58] our own observations of a spatial relationship between Se and Cu in selenite-treated cells 59 and the very strong correlation between Se and Cu observed in the 5 ppm Se kidney sections themselves, makes this spatial relationship worth reporting and investigating.…”

Section: Gpx1 But Not Sod1 Is Increased In 5 Ppm Se Kidney Tissuesmentioning

confidence: 94%

“…By contrast, dietary Se supplementation (2 ppm Se as sodium selenite) did not prevent liver damage in rats concurrently exposed to long term Cu(II) (as CuSO 4 ) supplementation. 54 The antagonism of Se and Cu has been observed in primary human keratinocytes, where CuSO 4 protected the cells against selenite toxicity. 55 Other studies suggest that an extracellular interaction of Cu and Se is responsible for the protective effects of Cu against Se toxicity.…”

Section: Gpx1 But Not Sod1 Is Increased In 5 Ppm Se Kidney Tissuesmentioning

confidence: 99%

XAS and XFM studies of selenium and copper speciation and distribution in the kidneys of selenite-supplemented rats

et al. 2014

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Dietary selenium has been implicated in the prevention of cancer and other diseases, but its safety and efficacy is dependent on the supplemented form and its metabolites. In this study, X-ray absorption spectroscopy (XAS) and X-ray fluorescence microscopy (XFM) have been used to investigate the speciation and distribution of Se and Cu in vivo. In kidneys isolated from rats fed a diet containing 5 ppm Se as selenite for 3 weeks, Se levels increased 5-fold. XFM revealed a strong correlation between the distribution of Se and the distribution of Cu in the kidney, a phenomenon that has previously been observed in cell culture (Weekley et al., JBIC, J. Biol. Inorg. Chem., 2014, DOI: 10.1007/s00775-014-1113-x). However, X-ray absorption spectra suggest that most of the Se in the kidney is found as Se-Se species, rather than Cu-bound, and that most of the Cu is bound to S and N, presumably to amino acid residues in proteins. Furthermore, SOD1 expression did not change in response to the high Se diet. We cannot rule out the possibility of some Cu-Se bonding in the tissues, but our results suggest mechanisms other than the formation of Cu-Se species and SOD1 upregulation are responsible for the highly correlated distributions of Se and Cu in the kidneys of rats fed high selenite diets.

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“…Among natural antioxidants in poultry feed, selenium and copper are needed in trace amounts. Overload intake of these trace elements leads to several disorders and toxicity mainly caused by synthesis of reactive oxygen species (ROS) in vivo (Aburto et al, 2001). Therefore, an optimal balance between selenium and copper in food and organism is essential for normal antioxidant status and health of poultry.…”

Section: Introductionmentioning

confidence: 99%

Effects of High but Non-Toxic Dietary Intake of Selenium and Copper on Indices of the Antioxidant Defence System and on Accumulation of Trace Elements in Chicks

Apsite¹,

Bērziņa²,

N.³

2012

Proceedings of the Latvian Academy of Sciences. Section B. Natural, Exact, and Applied Sciences

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Lohman Brown chickens with age from the 1stto 35thday received the food with high doses ofselenium (Se1 mg/kg), copper (Cu100 mg/kg), or both elements (Se1 + Cu100). Live weight increaseof all three experimental chicken groups was by 9.3, 12.9 and 8.1%, respectively, in comparisonwith the control. The concentration of selenium in the blood of the Se1 group chickenswas by 45.5, in liver by 63.4 and in kidney by 19.7% higher that in organs of control group chickens.Selenium accumulation in organs of Se1 group chickens was highly correlated with increaseof glutathionperoxidase activity in blood (r = 0.90) and in liver (r = 0.85) and with decrease of glutathioneconcentration in liver. In Cu100 group chickens, copper concentration increased by 11.7in blood, in liver by 23.7, and in kidney by 19.9%. Together with more intensive excretion of glutathionefrom hepatocytes, copper concentration in bile increased by 17.7% compared to that incontrol group chickens. Also wing feathers participated in the regulation of copper homeostaticbalance, as copper concentration in feathers increased by 66.7%. The concentration of malondialdehidein liver of chickens from all groups was similar (43.5-45.2 μmol·g-1wet wt.), indicatingthat overload of selenium and copper did not cause profuse production of oxyradicals in the organism.Increased accumulation of selenium and copper in chickens influenced biochemical regulationof iron, zinc and cadmium deposition in liver, kidney, tibia and feather, changing therelations between Se and Fe, Se and Cd, Cu and Fe, Cu and Zn, and Cu and Cd concentrations.The analysis indicates increased tolerance of chicken to loads of selenium (1 mg/kg) and copper(100 mg/kg) doses

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Effect of chronic exposure to excess dietary copper and dietary selenium supplementation on liver specimens from rats

Abstract: Long-term exposure to excess dietary Cu caused mild hepatic lesions in Fischer 344 rats. Dietary Se supplementation did not prevent hepatic damage in rats with Cu toxicosis.

Cited by 9 publications

References 26 publications

Re‐evaluation of the existing health‐based guidance values for copper and exposure assessment from all sources

Re‐evaluation of the existing health‐based guidance values for copper and exposure assessment from all sources

XAS and XFM studies of selenium and copper speciation and distribution in the kidneys of selenite-supplemented rats

Effects of High but Non-Toxic Dietary Intake of Selenium and Copper on Indices of the Antioxidant Defence System and on Accumulation of Trace Elements in Chicks

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