Copper induces Cu-ATPase ATP7A mRNA in a fish cell line, SAF1

Minghetti, Matteo; Leaver, Michael J.; Taggart, John B.; Casadei, Elisa; Auslander, Meirav; Tom, Moshe; George, Stephen

doi:10.1016/j.cbpc.2011.03.010

Cited by 14 publications

(11 citation statements)

References 38 publications

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“…When copper elevated, ATP7A left the TGN and facilitated copper excretion. Copper also induced the mRNA expression and might regulate the transcription of ATP7A in a fish cell line [20]. In our study the increased ATP7A expression was in accordance with the concentrations of free copper,which suggested that the elevated expression of ATP7A may be induced by the increased copper in the brain on the early phages of PA treatment.…”

Section: Discussionsupporting

confidence: 73%

Penicillamine Increases Free Copper and Enhances Oxidative Stress in the Brain of Toxic Milk Mice

Chen

Lin

et al. 2012

PLoS ONE

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Wilson disease (WD) is characterized by the accumulation of copper arising from a mutation in the ATP7B gene. Penicillamine (PA) makes 10–50% of the patients with neurologic symptoms neurologically worse at the early stage of administration. The aim of this study was to determine how the copper metabolism changes and whether the change impairs the brain of toxic milk (tx) mice, an animal model of WD, during the PA administration. The free copper and protein-bound copper concentrations in the serum, cortex and basal ganglia of tx mice with PA administration for 3 days, 10 days and 14 days, respectively, were investigated. The expression of copper transporters, ATP7A and CTR1,was analyzed by real-time quantitative PCR, immunofluorescence and Western blot. Then SOD, MDA and GSH/GSSG were detected to determine whether the oxidative stress changed correspondingly. The results revealed the elevated free copper concentrations in the serum and brain, and declined protein-bound copper concentrations in the brain of tx mice during PA administration. Meanwhile, transiently increased expression of ATP7A and CTR1 was observed generally in the brain parenchyma by immunofluorescence, real-time quantitative PCR and Western blot. Additionally, ATP7A and CTR1 were observed to locate mainly at Golgi apparatus and cellular membrane respectively. Intense staining of ATP7A in the choroid plexus was found in tx mice on the 3rd and 10th day of PA treatment, but rare staining of ATP7A and CTR1 in the blood-brain barrier (BBB). Decreased GSH/GSSG and increased MDA concentrations were also viewed in the cortex and basal ganglia. Our results suggested the elevated free copper concentrations in the brain might lead to the enhanced oxidative stress during PA administration. The increased free copper in the brain might come from the copper mobilized from brain parenchyma cells but not from the serum according to the ATP7A and CTR1 expression analysis.

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Section: Discussionsupporting

confidence: 73%

Penicillamine Increases Free Copper and Enhances Oxidative Stress in the Brain of Toxic Milk Mice

Chen

Lin

et al. 2012

PLoS ONE

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“…Interestingly, metallothionein, at either gene or protein level, has been found to be increased in fish specimens after heavy metal exposure in vivo (Garcia-Santos et al, 2011;Ghedira et al, 2010;Monteiro et al, 2013). In vitro, the seabream SAF-1 cells showed up-regulated mta transcription when exposed for 24 h to Cd, Hg or Pb, but not to As (Morcillo et al, 2015) and to Cu, Zn and Cd (Minghetti et al, 2011). However, no other study has evaluated the mta expression in fish leucocytes after exposure to heavy metals.…”

Section: Discussionmentioning

confidence: 93%

Toxicological in vitro effects of heavy metals on gilthead seabream (Sparus aurata L.) head–kidney leucocytes

Morcillo

Cordero

Meseguer

et al. 2015

Toxicology in Vitro

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“…Scientists also track macromolecular and cellular damages. In animal cells, the mitochondria are very often analyzed, showing destabilization and function modification due to oxidative stress resulting from toxic metals [16,46]. This destabilization has direct consequences on cellular respiration (see Section 7).…”

Section: Redox Homeostasis Disturbancementioning

confidence: 99%

“…This destabilization has direct consequences on cellular respiration (see Section 7). At the cellular level, lipid peroxidation and lysosomal activity can be affected by metal toxicity [16,46]. These effects have been reviewed in Mytilus spp.…”

Section: Redox Homeostasis Disturbancementioning

confidence: 99%

New Insights into Cellular Impacts of Metals in Aquatic Animals

et al. 2020

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Toxic metals remain a current important threat to aquatic ecosystems, despite regulatory efforts to reduce their release. Several toxic metals already appear in the list of priority substances polluting surface waters, while concerns arise from the increasing use of technology-critical metals such as metallic nanoparticles, rare-earth, and platinum group metals. In aquatic environments, various chemical, biological and physical processes determine the impact of metals on the biota. This review provides insights into responses to toxic metals recently reported in freshwater and marine animals. The specific emphasis is on: (i) common cellular and molecular responses; (ii) stress proteins; (iii) redox homeostasis; (iv) cytoskeleton rearrangement; (v) metabolism reshuffle; (vi) free cellular energy and mitochondrial metabolism; and (vi) immunity. These endpoints are promising, notably in multi-biomarker approaches to identify precise cellular toxicity pathways and anticipate the impact of environmental metal pollution.

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Copper induces Cu-ATPase ATP7A mRNA in a fish cell line, SAF1

Abstract: Copper transporting ATPase, ATP7A, is an ATP dependent copper pump present in all vertebrates, critical for the maintenance of intracellular and whole body copper homeostasis. Effects of copper treatment on

Cited by 14 publications

References 38 publications

Penicillamine Increases Free Copper and Enhances Oxidative Stress in the Brain of Toxic Milk Mice

Penicillamine Increases Free Copper and Enhances Oxidative Stress in the Brain of Toxic Milk Mice

Toxicological in vitro effects of heavy metals on gilthead seabream (Sparus aurata L.) head–kidney leucocytes

New Insights into Cellular Impacts of Metals in Aquatic Animals

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