Copper metabolism in the LEC rat: Involvement of induction of metallothionein and disposition of zinc and iron

Sakata, Naoki; Sugawara, Chieko; Katakura, Michihiro; Takahashi, Hidetoshi; Mori, Makoto

doi:10.1007/bf01923342

Cited by 50 publications

(36 citation statements)

References 16 publications

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“…This increase of metal ions in brain observed on clioquinol treatment might either be attributed to an inefficiency of the chelator with weak affinities for Zn (K 1 ϭ 7.0) and for Cu (K 1 ϭ 8.9) (38) or even more likely, due to a facilitated uptake in brain of clioquinol-Cu complexes, similarly to Cu-nitrilotriacetic acid (Cu-NTA)-treated mice (39).…”

Section: Discussionmentioning

confidence: 99%

Dietary Cu stabilizes brain superoxide dismutase 1 activity and reduces amyloid Aβ production in APP23 transgenic mice

Bayer

Schäfer

Simons

et al. 2003

Proc. Natl. Acad. Sci. U.S.A.

318

255

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The Cu-binding ␤-amyloid precursor protein (APP), and the amyloid A␤ peptide have been proposed to play a role in physiological metal regulation. There is accumulating evidence of an unbalanced Cu homeostasis with a causative or diagnostic link to Alzheimer's disease. Whereas elevated Cu levels are observed in APP knockout mice, APP overexpression results in reduced Cu in transgenic mouse brain. Moreover, Cu induces a decrease in A␤ levels in APP-transfected cells in vitro. To investigate the influence of bioavailable Cu, transgenic APP23 mice received an oral treatment with Cu-supplemented sucrose-sweetened drinking water (1). Chronic APP overexpression per se reduced superoxide dismutase 1 activity in transgenic mouse brain, which could be restored to normal levels after Cu treatment (2). A significant increase of brain Cu indicated its bioavailability on Cu treatment in APP23 mice, whereas Cu levels remained unaffected in littermate controls (3). Cu treatment lowered endogenous CNS A␤ before a detectable reduction of amyloid plaques. Thus, APP23 mice reveal APP-induced alterations linked to Cu homeostasis, which can be reversed by addition of dietary Cu.

show abstract

Section: Discussionmentioning

confidence: 99%

Dietary Cu stabilizes brain superoxide dismutase 1 activity and reduces amyloid Aβ production in APP23 transgenic mice

Bayer

Schäfer

Simons

et al. 2003

Proc. Natl. Acad. Sci. U.S.A.

318

255

View full text Add to dashboard Cite

show abstract

“…This strain, associated with spontaneous hepatitis (12,13). exhibits excessive hepatic copper accumulation and lower copper level and ceruloplasmin oxidase activity in serum (14)(15)(16)(17)(18)(19). Because of the similarities of its clinical and biochemical characteristics to the hepatic-type Wilson's disease, the LEC rat is regarded as one of potential animal models of Wilson's disease (18).…”

mentioning

confidence: 99%

“…Because of the similarities of its clinical and biochemical characteristics to the hepatic-type Wilson's disease, the LEC rat is regarded as one of potential animal models of Wilson's disease (18). However, data are limited regarding biliary copper excretion in LEC rats (16,17). T o further explain the pathogenesis of excessive copper accumulation in the liver of LEC rats, we determined the changes in biliary coppcr excretion as well as serum and hepatic copper contents in LEC rats before and after the onset of spontaneous hepatitis.…”

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confidence: 99%

Impaired Hepatic Copper Homeostasis in Long-Evans Cinnamon Rats: Reduced Biliary Excretion of Copper

Suzuki

Aoki

1994

Pediatr Res

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“…27,[36][37][38][39] Dietary curcumin does not increase the Cu level in LEC rat liver, 40) so that curcumin per se may not aggravate hepatitis. Curcumin does, however, inhibit activator protein 1 activity that promotes gene transcription of metallothionein, 34,41) implicating that the decreased degradation of free radicals due to downregulation of metallothionein might diminish the anti-tumorigenesis effect by curcumin in these rats.…”

Section: Discussionmentioning

confidence: 99%

Concomitant Oral Ingestion of Germanium-132 and Curcumin Increased Mortality Rate by Aggravating Hepatic Dysfunction in Long-Evans Cinnamon Rats

Sunagawa

Shingaki

Oonishi

et al. 2006

JOURNAL OF HEALTH SCIENCE

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To determine the effect of concomitant oral ingestion of germanium-132 (Ge-132) and curcumin on the onsets of hepatitis and hepatic cancer in Long-Evans Cinnamon (LEC) rats, 40 rats were administered sterile water (NT), corn oil (Vehicle), Ge-132 (Ge), curcumin (Cur), or Ge-132 plus curcumin (GeCur) for 50 weeks. Plasma enzyme levels of asparate aminotransferase (AST), alanine aminotransferase (ALT), γ-glutamyltrasferase (γGTP), and lactate dehydrogenase (LDH) were measured at Pre (6 weeks), Early (18-26 weeks), Late (30-38 weeks) and End (42-50 weeks) stages. Liver damage was assessed by the Histology Activity Index (HAI). In the group of Ge, LDH was significantly decreased at the End stage. In the group of Cur, LDH was remarkably decreased in the Early stage, whereas AST and LDH were significantly decreased in the End stage. In the GeCur group, AST, ALT, and γGTP were significantly increased in the Early stage, whereas LDH was significantly decreased in the End stage. The onset rate of icterus and the mortality rate were significantly increased in the GeCur groups (vs. Vehicle group, p < 0.01). There was no statistically significant difference in HAI among the groups. Thus, concomitant oral ingestion of Ge-132 and curcumin may aggravate hepatic dysfunction, thereby increasing the mortality rate in LEC rats.

show abstract

Copper metabolism in the LEC rat: Involvement of induction of metallothionein and disposition of zinc and iron

Cited by 50 publications

References 16 publications

Dietary Cu stabilizes brain superoxide dismutase 1 activity and reduces amyloid Aβ production in APP23 transgenic mice

Dietary Cu stabilizes brain superoxide dismutase 1 activity and reduces amyloid Aβ production in APP23 transgenic mice

Impaired Hepatic Copper Homeostasis in Long-Evans Cinnamon Rats: Reduced Biliary Excretion of Copper

Concomitant Oral Ingestion of Germanium-132 and Curcumin Increased Mortality Rate by Aggravating Hepatic Dysfunction in Long-Evans Cinnamon Rats

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