Physiological and Pharmacological Effects of Zinc on Immune Responsea

Cunningham‐Rundles, Susanna; Bockman, Richard S.; Lin, Andrew N.; Giardina, Patricia-Jane; Hilgartner, M W; Caldwell-Brown, D; Carter, D. M.

doi:10.1111/j.1749-6632.1990.tb00139.x

Cited by 62 publications

(25 citation statements)

References 32 publications

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“…Normal zinc levels have been reported previously (Rea et al, 1984;CunninghamRundles et al, 1990). This important immune regulator was found to cause rapid thymic atrophy and extensive loss of T lymphocyte function when deficient (Cunningham-Rundles et al, 1990). Several studies had reported low zinc levels in multitransfused b-thalassemia major patients (Kajanachumpol et al, 1997;Arcasoy et al, 2001;Consolini et al, 2001); this deficiency is usually a result of intensive iron chelating therapy (Bartakke et al, 2005).…”

Section: Discussionmentioning

confidence: 96%

Investigation of the distribution of lymphocyte subsets and zinc levels in multitransfused β‐thalassemia major patients

Al-Awadhi

AlFadhli

Al-Khaldi

et al. 2010

Int J Lab Hematology

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Homozygous beta-thalassemia is a common genetic disorder in the Arabian Peninsula and an important cause of morbidity in Kuwait. The anemia is so severe that chronic blood transfusions, and the resulting iron overload, cause a shift in immunoregulatory balances and a deficiency in zinc. It was reported that individual immunological profile of CD8+ T-lymphocytes may have a modifying effect on the severity of iron overload in HFE homozygous hemochromatosis patients, with low numbers being negatively correlated with the total amount of body iron stores. This has not been tested in thalassemia major patients. This study was designed to utilize flow cytometric immunophenotyping to characterize effects of regular blood transfusion, and high serum ferritin levels because of irregular use of iron chelation therapy on T lymphocytes (CD2, CD3, CD4 and CD8), B lymphocytes (CD19) and natural killer cells (CD56) and zinc levels in the blood of patients with thalassemia major (n = 49) and healthy normal controls (n = 60) in Kuwait. None of the patients had active infections. T-cell markers' percentage levels were comparable between patients and controls (P > 0.05), while B cell marker (CD19) was significantly higher in patients (P = 0.007). Patients had lower percentage levels of CD56 cells (P = 0.007) and normal serum zinc. All patients had high serum ferritin levels with no significant correlation to CD8+ T lymphocytes (P > 0.05). High iron stores did not have an effect on T lymphocytes' profile, with normal zinc levels perhaps related to non compliance with chelation therapy. The high B cell marker may be indicative of stimulation of antibody producing cells as a result of regular blood transfusions.

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Section: Discussionmentioning

confidence: 96%

Investigation of the distribution of lymphocyte subsets and zinc levels in multitransfused β‐thalassemia major patients

Al-Awadhi

AlFadhli

Al-Khaldi

et al. 2010

Int J Lab Hematology

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“…More recently, we found that acute ethanol-induced hepatocyte cell death mediated through the Fas (CD95/Apo-1)/Fas ligand pathway was significantly inhibited by zinc pretreatment (Lambert et al, 2003). In addition, zinc is well known to be protective in cells of the macrophage-monocyte lineage, although the mechanism is still not clear (Brown and Carter, 1990). Therefore, although we observed a correlation between the protective effect of zinc against TNF-␣ production and the inhibition of acute alcohol-induced increases in endotoxin absorption at the level of the intestine, we cannot rule out direct protection of Kupffer cells by zinc.…”

Section: Discussionmentioning

confidence: 99%

Prevention of Alterations in Intestinal Permeability Is Involved in Zinc Inhibition of Acute Ethanol-Induced Liver Damage in Mice

Lambert

Zhou

Wang³

et al. 2003

The Journal of Pharmacology and Experimental Therapeutics

133

114

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Acute ethanol exposure causes liver injury in experimental animals, and accumulating evidence suggests that a major responsible factor for the pathogenesis is endotoxemia, which results from bacterial endotoxin leakage from the small intestine due to increased intestinal permeability under alcohol challenge. The purpose of this study was to examine whether zinc pretreatment would inhibit acute ethanolinduced liver injury through prevention of intestinal permeability changes. Male 129 Sv PC J mice were treated with three intragastric doses of ZnSO 4 at 5 mg of zinc ion per kg each dosing prior to acute ethanol challenge with a single oral dose of 6 g/kg ethanol. The zinc treatment did not alter the elevation of serum concentrations of alcohol. The acute ethanol exposure caused an elevation in serum alanine aminotransferase levels as well as fatty liver and hepatic degenerative necrotic foci as determined by biochemical assay and histochemical analysis, respectively. A significant increase in liver tumor necrosis factor-␣ (TNF-␣) levels was detected by enzyme-linked immunosorbent assay. These pathological effects correlated well with increases in serum endotoxin levels. Importantly, acute ethanol treatment caused significant damage to the small intestine as determined by morphological analysis of intestinal sections and permeability assay. These alcohol-induced hepatic pathological changes and TNF-␣ elevation were significantly inhibited in the zinc-pretreated animals. The inhibitory action of zinc on alcohol-induced liver damage and activation of inflammation was associated with zinc suppression of alcoholinduced intestinal permeability changes. These results thus demonstrate that zinc prevention of increased intestinal permeability is importantly involved in the inhibition of acute ethanol-induced liver damage in mice.

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“…Moreover, several studies report that Cd can block calcium channels in several cell types (Nelson, 1986;Hinkle et al, 1987). We found that Zn, added simultaneously to Cd, prevented the inhibition of thymidine uptake in stimulated lymphocytes; however, zinc is known to be a lymphocyte mitogen ( Cunningham-Rundles et al, 1990) and its e#ect may be di#erent and independent from that of Cd.…”

Section: Discussionmentioning

confidence: 84%

Effects of cadmium on lymphocyte proliferation and macrophage activation in catfish,Ictalurus melas

Albergoni

Viola

1995

Fish & Shellfish Immunology

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Physiological and Pharmacological Effects of Zinc on Immune Responsea

Cited by 62 publications

References 32 publications

Investigation of the distribution of lymphocyte subsets and zinc levels in multitransfused β‐thalassemia major patients

Investigation of the distribution of lymphocyte subsets and zinc levels in multitransfused β‐thalassemia major patients

Prevention of Alterations in Intestinal Permeability Is Involved in Zinc Inhibition of Acute Ethanol-Induced Liver Damage in Mice

Effects of cadmium on lymphocyte proliferation and macrophage activation in catfish,Ictalurus melas

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