Physiological properties of copper and zinc

Albergoni, V.

doi:10.1007/978-94-011-3963-2_2

Cited by 3 publications

(2 citation statements)

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“…We also observed that hepatic Zn concentration decreases with treatment period. This decrease may be explained by induction of MT at the intestinal level that could bind both Cu and Zn, so reducing their absorption (Albergoni 1998). In fact, even intestinal Cu concentration, after a decrease, returned to control values by the end of the second week of treatment, while hepatic Cu concentration decreased; however, this difference is not statistically significant.…”

Section: Discussioncontrasting

confidence: 48%

Metallothionein and antioxidant enzymes in Long-Evans Cinnamon rats treated with zinc

Medici

Santon

Sturniolo

et al. 2002

Archives of Toxicology

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The Long-Evans Cinnamon (LEC) rat is a mutant animal model for Wilson's disease. It is known that an abnormal accumulation of Cu and Fe in the liver and low concentrations of both ceruloplasmin and Cu in the serum occur in these rats. The accumulation of Cu is explained by the defective expression of the Cu-transporting P-type ATPase gene, homologous to the gene for Wilson's disease (ATP7B). The aim of this work was to clarify the action mechanism of Zn, and to verify the role that this metal plays in LEC rats in short-term treatment experiments (1 and 2 weeks) on concentrations of Cu, Zn, Fe, metallothionein (MT), 8-hydroxy-2'-deoxyguanosine (oh(8)dG) and on the activity of antioxidant enzymes. It is well known that Zn induces MT and has the ability to prevent redox-active metals, Cu and Fe, binding to and causing oxidative damage at active sites of Zn metalloenzymes and nonspecific binding sites on proteins. Zn administration reduces Cu and Fe transport from mucosal to serosal intestinal sides through competitive mechanisms. Our findings show that treatment with zinc acetate increases tissue Zn and MT contents and decreases Cu and Fe concentrations in the liver and kidneys, even if hepatic Zn and MT concentrations decrease with treatment period. Induction of MT synthesis by Zn contributes to the reduction in free radicals produced by Cu and Fe. We also observed that the superoxide dismutase (SOD)activity in liver decreases with treatment duration in association with the Cu and Fe liver decrease. However, the SOD activity in kidney increases in untreated rats at 2 weeks relative to those untreated for 1 week.

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Section: Discussioncontrasting

confidence: 48%

Metallothionein and antioxidant enzymes in Long-Evans Cinnamon rats treated with zinc

Medici

Santon

Sturniolo

et al. 2002

Archives of Toxicology

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“…A decrease in the serum zinc concentration is well documented after systemic inflammation or infection as part of the acute-phase response [30, 31]. During the acute-phase or stress response, zinc is redistributed to specific organs and cellular compartments, especially the liver, leading to a decrease in the serum zinc concentration [32]. CRP is an acute phase protein that is elevated with infection/inflammation.…”

Section: Discussionmentioning

confidence: 99%

Association of serum zinc with markers of liver injury in very heavy drinking alcohol-dependent patients

Vatsalya

Kong

Cave

et al. 2018

The Journal of Nutritional Biochemistry

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Zinc deficiency is a frequent complication of alcohol abuse for multiple reasons including poor intake, increased excretion, internal redistribution and altered transporters. Zinc deficiency has been postulated to play a role in the development/progression of alcoholic liver disease (ALD). This study aimed to relate serum zinc levels with alcohol intake, serum albumin concentration and markers of inflammation and liver injury. One hundred and eight male and female very heavy drinking (≥10 drinks/day) individuals without clinical evidence of ALD were grouped by serum zinc concentration: normal-zinc group (zinc level≥71 μg/dl) included 67 patients, and low-zinc group (zinc level<71 μg/dl) included 41 patients. Data were collected on demographics, drinking history in last 90 days (heavy drinking days, HDD90 and total drinks, TD90), lifetime drinking history (LTDH) and clinical/ laboratory assessments. Our data show that in a very well-characterized, chronically heavy-drinking population without clinical evidence of liver disease, about 40% of subjects had low serum zinc levels. Frequency of heavy drinking days (HDD90) was significantly higher in the low-zinc group. Total drinks in past 90 days, LTDH and HDD90 showed significant associations with low zinc levels. The group with the low serum zinc had a higher aspartate aminotransferase/alanine aminotransferase ratio (good marker of alcoholic liver disease). Those in the low-zinc group had the lower albumin levels, a marker of hepatic synthetic function, and the highest C-reactive protein level, a biomarker of inflammation.

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