The inhibitory effect of zinc on cadmium-induced cell apoptosis and reactive oxygen species (ROS) production in cell cultures

Szuster‐Ciesielska, Agnieszka; Stachura, Anna; Słotwińska, Maria; Kamińska, Teresa; Śnieżko, R.; Paduch, Roman; Abramczyk, Dariusz; Filar, J; Kandefer‐Szerszeń, Martyna

doi:10.1016/s0300-483x(00)00144-x

Cited by 211 publications

(107 citation statements)

References 41 publications

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“…Several reports have shown that cadmium induces apoptosis in various tissues and cells, both in vivo and in vitro (Hamada et al, 1997). E.g., cadmium-induced apoptosis was reported in rat testes (Xu et al, 1996), mouse liver (Habeebu et al, 1998), rat lung epithelial cells (Hart et al, 1999), CL-3 human lung carcinoma cells (Chuang et al, 2000), HeLa human cervix carcinoma cells (Szuster-Ciesielska et al, 2000) and Rat-1 fibroblast cells (Kim et al, 2000). Copper, for its part, can induce an upregulation of apoptosis and related genes in zebrafish (Luzio et al, 2013) or induces the apoptotic cell death in the copepod Tigriopus japonicus (Rhee et al, 2013).…”

Section: Discussionmentioning

confidence: 99%

In vitro effect of cadmium and copper on separated blood leukocytes of Dicentrarchus labrax

Vazzana¹,

Celi²,

Tramati³

et al. 2014

Ecotoxicology and Environmental Safety

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a b s t r a c tThe immunotoxic effects of heavy metals on blood leukocytes of sea bass (Dicentrarchus labrax) were examined. The cells, separated by a discontinuous Percoll-gradients, were exposed in vitro to various sublethal concentrations of cadmium and copper (10 À 7 M, 10 À 5 M, and 10 À 3 M) and their immunotoxic effect was then evaluated by measuring neutral red uptake, MTT assay, DNA fragmentation and Hsp70 gene expression. First of all, we demonstrated that the cells treated in vitro could incorporate Cd and Cu. A relationship between heavy metal exposure and dose-time-dependent alterations in responses of leukocytes from blood was found for both metals, but copper was more immunotoxic than cadmium in all assays performed. A significant reduction in the cells' ability to uptake neutral red and viability by MTT assay was recorded, indicating that both cadmium and copper could change the membrane permeability, inducing cellular apoptosis when the concentration of metals reached 10 À 3 M. The apoptotic effect may also explain the high level of cytotoxicity found when the leukocytes were exposed to higher concentration of metals. These results demonstrated that toxic effect of copper and cadmium affect on the mechanisms of cellmediated immunity reducing the immune defences of the organism.

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Section: Discussionmentioning

confidence: 99%

In vitro effect of cadmium and copper on separated blood leukocytes of Dicentrarchus labrax

Vazzana¹,

Celi²,

Tramati³

et al. 2014

Ecotoxicology and Environmental Safety

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“…There is an increasing body of evidence that the toxicity of Cd may be associated with the production of reactive oxygen species (ROS) [24][25][26]. Although detailed studies in the past two decades have demonstrated that metals like cadmium possess the ability to affect the activation of various signaling pathways and to produce reactive radicals resulting in DNA damage and lipid and protein oxidation, no direct evidence for the generation of free radicals by Cd in vivo has been reported.…”

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confidence: 99%

Cadmium generates reactive oxygen- and carbon-centered radical species in rats: Insights from in vivo spin-trapping studies

Liu

Qian

Guo

et al. 2008

Free Radical Biology and Medicine

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Cadmium (Cd) is a known industrial and environmental pollutant. In the present work, an in vivo spintrapping technique was used in conjunction with electron spin resonance (ESR) spectroscopy to investigate free radical generation in rats following administration of cadmium chloride (CdCl 2 , 40 µmol/kg) and the spin trapping agent α-(4-pyridyl-1-oxide)-N-tert-butylnitrone (POBN, 1 g/kg). In Cd-treated rats, POBN radical adducts were formed in the liver, were excreted into the bile, and exhibited an ESR spectrum consistent with a carbon-centered radical species probably derived from endogenous lipids. Isotope substitution of dimethyl sulfoxide [(CH 3 ) 2 SO] with 13 C demonstrated methyl radical formation (POBN/* 13 CH 3 ). This adduct indicated the production of hydroxyl radical, which reacted with [( 13 CH 3 ) 2 SO] to form * 13 CH 3 , which then reacted with POBN to form POBN/ * 13 CH 3 . Depletion of hepatic glutathione by diethyl maleate significantly increased free radical production, whereas inactivation of Kupffer cells by gadolinium chloride and chelation of iron by desferal inhibited it. Treatment with the xanthine oxidase inhibitor allopurinol, the catalase inhibitor aminobenzotriazole, or the cytochrome P450 inhibitor 3-amino-1,2,4-triazole had no effect. This is the first study to show Cd generation of reactive oxygen and carbon-centered radical species by involvement of both iron mediation through iron-catalyzed reactions and activation of Kupffer cells, the resident liver macrophages.

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“…Cadmium inhibits L-type calcium channels (present in smooth muscle cells), reacts with thiol groups, may displace zinc from important metabolic enzymes, and is associated with the generation of oxygenderived free radicals. 16,17 These and other factors are likely to contribute to the relative concentration of cadmium in the medial layer of the aortic wall.We calculated that the average cadmium concentration in the medial layer was 7 mol/L. This is identical to the concentration of cadmium calculated to be in the lungs of patients with moderate to severe emphysema.…”

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confidence: 99%

Cadmium Accumulation in Aortas of Smokers

Abu‐Hayyeh

Sian

Jones

et al. 2001

ATVB

111

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Abstract-Abdominal aortic aneurysm is a smoking-related disorder. Cadmium, inhaled from cigarettes, may accumulate in the aorta and facilitate weakening of the aorta through adverse effects on smooth muscle cell metabolism. Cadmium was measured by atomic absorption spectrometry in infrarenal aortas from 13 patients with abdominal aortic aneurysm and from 17 age-and sex-matched patients with normal-diameter abdominal aorta. Total cadmium content was associated with smoking, assessed as pack-years (rϭ0.54, Pϭ0.004), but was similar in aneurysmal and undilated aortas. The cadmium content (meanϮSE) was higher in the media (3.25Ϯ0.53 ng/mg dry wt, 7Ϯ1.2 mol/L) than in the intima or adventitia (1.14Ϯ0.24 and 1.87Ϯ0.38 ng/mg dry wt, respectively; ANOVA, PϽ0.005). There was a strong correlation between medial cadmium content and pack-years of smoking (rϭ0.87, PϽ0.001). In aortic smooth muscle cells cultured on fibrillar collagen, cadmium inhibited DNA synthesis and collagen synthesis and diminished cell numbers (IC 50 2 mol/L, 6 mol/L, and 6 mol/L, respectively), but higher concentrations of cadmium were required for upregulation of metallothionein (EC 50 23 mol/L). The cadmium content of the aorta increases in direct proportion to the pack-years of cigarettes smoked, with selective accumulation in the medial layer. However, the cadmium content of aneurysmal aortas was not higher than that of nondilated aortas for patients with matched smoking history. In smokers, the level of cadmium accumulation is probably sufficient to impair the viability of cultured smooth muscle cells. Similar mechanisms could underlie the development of degenerative aortic disease in smokers. Key Words: aortas Ⅲ aneurysm Ⅲ smoking Ⅲ muscle smooth Ⅲ collagen C admium is one of the many toxic components of inhaled tobacco smoke. The amount of cadmium inhaled from each pack of 20 cigarettes is Ϸ16 g. 1 Cadmium has a long elimination time (estimated at 10 to 30 years), providing the possibility for the accumulation of substantial amounts of cadmium during the lifetime of a smoker. There are reports that cadmium alters the metabolism of cultured human aortic smooth muscle cells and the processing of collagen. 2,3 Cadmium also blocks calcium channels and inhibits ATPases and other ion transport systems.Smoking is the most consistent risk factor for the development and expansion of abdominal aortic aneurysms (AAAs). 4,5 The histological features of AAA include atherosclerosis, loss of medial smooth muscle (with evidence of apoptosis), and loss of elastin (with remodeling of the connective tissue). Therefore, we wished to investigate the hypothesis that cadmium, from cigarettes, accumulates in the infrarenal abdominal aorta, thus stimulating aneurysmal dilatation. To test this hypothesis, we compared the concentration of cadmium in infrarenal aortas from patients with and without AAAs.After finding that the highest concentration of cadmium was in the medial layer of the aorta, we investigated whether similar concentrations of cadmium altered the metabol...

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The inhibitory effect of zinc on cadmium-induced cell apoptosis and reactive oxygen species (ROS) production in cell cultures

Cited by 211 publications

References 41 publications

In vitro effect of cadmium and copper on separated blood leukocytes of Dicentrarchus labrax

In vitro effect of cadmium and copper on separated blood leukocytes of Dicentrarchus labrax

Cadmium generates reactive oxygen- and carbon-centered radical species in rats: Insights from in vivo spin-trapping studies

Cadmium Accumulation in Aortas of Smokers

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