Arsenic-cadmium interaction in rats

Dı́az-Barriga, Fernando; Llamas, Edmundo; Mejia, Jose; Carrizales, Leticia; Santoyo, Martha; Vega-Vega, Lourdes; Yáñez, Leticia

doi:10.1016/0300-483x(90)90135-4

Cited by 28 publications

(14 citation statements)

References 31 publications

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“…Cells (1 × 10 4 /cm 2 ) were plated in 25-cm 2 culture flasks in triplicate. Viable cells at 5,8,10,12,15, and 17 days after initial plating were counted by trypan blue exclusion on a hemocytometer. Culture medium was changed every 3 days.…”

Section: Chemicalsmentioning

confidence: 99%

“…Additionally, the activity of a metal in any given tissue is dependent on its speciation and metabolism (6). To further complicate the picture, metals have been shown to interact at multiple levels and, most likely, modify one another's cytotoxicity and/or carcinogenic potential (8)(9)(10)(11). As a result, we are still a long way from a fundamental understanding of the actions of metals or metal mixtures at the cellular level, particularly as they relate to toxic end points.…”

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confidence: 99%

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Characterization of gene expression changes associated with MNNG, arsenic, or metal mixture treatment in human keratinocytes: application of cDNA microarray technology.

Bae

Hanneman

Yang

et al. 2002

Environ Health Perspect

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Section: Chemicalsmentioning

confidence: 99%

mentioning

confidence: 99%

Characterization of gene expression changes associated with MNNG, arsenic, or metal mixture treatment in human keratinocytes: application of cDNA microarray technology.

Bae

Hanneman

Yang

et al. 2002

Environ Health Perspect

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“…A recent study has shown that chronic exposures to mixture combinations of As plus Cd in mice produced more renal injury than either single element alone, and metallothionein-I/II null mice were especially susceptible to combined element toxicity [7]. Another interaction study demonstrated that combined As and Cd exposures produced higher levels of lipid peroxidation in the kidneys and livers of rats than either element administered alone [8]. It is apparent from these few studies that concurrent exposures to a mixture of elements can alter the severity or type of biological response normally produced by one on an individual basis and hence further analysis is required for understanding the mechanisms of combined element interactions.…”

Section: Introductionmentioning

confidence: 96%

A comparison of 60, 70, and 90 kDa stress protein expression in normal rat NRK‐52 and human HK‐2 kidney cell lines following in vitro exposure to arsenite and cadmium alone or in combination

Madden

Akkerman

Fowler

2002

J Biochem & Molecular Tox

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Arsenite and cadmium are two potent nephrotoxicants and common Superfund site elements. These elements are included among the stress protein inducers, but information regarding relationships between toxicity produced by combinations of these agents to the stress protein response is lacking. In this study, the immortalized cell lines normal rat kidney NRK-52E and human kidney HK-2 were exposed in vitro to arsenite (As(3+)), cadmium (Cd(2+)), or to equimolar As(3+) plus Cd(2+) mixture combinations for 3 and 5 h over a concentration range of 0.1-100 microM. After a 12-h recovery period, cultured cells were then evaluated for expression of the 60, 70, and 90 kDa major stress protein families. Results indicated that expression of stress proteins varied depending on the species of kidney cells exposed, the exposure concentrations, and the length of exposure to each element on an individual basis and for combined mixtures. For the HK-2 kidney cell line, increased levels of the 70 kDa stress protein was observed for single and combined element exposures whereas there was no change or a decrease of stress proteins 60 and 90 kDa. Increased 70 kDa expression was observed for 10-microM doses of single elements and for a lower dose of 1 microM of the As plus Cd mixture at 3- and 5-h exposures. NRK-52 kidney cells exposed to equivalent doses of As(3+) and Cd(2+) alone or in combination showed increased levels of all stress proteins 60, 70, and 90 kDa. This increase was seen for 10 microM of the As plus Cd mixture at 3 h whereas for single element exposures, increased stress protein levels were generally observed for the 100-microM doses. At 5 h- exposure, 60 and 90 kDa levels increased for 10 microM of Cd(2+) and 60 kDa levels increased for 1 microM of As(3+). However, exposures to 10 microM of the As plus Cd mixture decreased 60 kDa protein expression to control levels at 5 h. For both kidney cell lines, there was a decrease in the stress protein expression levels for all three stress protein families for 100-microM doses of the mixture combination for 3- and 5-h exposures. These data indicate a dose- and combination-related correlation between depression of the stress protein response and the onset of overt cellular toxicity and/or cell death. The threshold for these changes was cell line specific.

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“…Previously, we have shown that the mixture of As+ Cd is more toxic than either arsenic or cadmium alone (4,5). However, in testes of rats treated with As+ Cd, a 37% increase in glutathione (GSH) content was related to protection against cadmium-induced morphologic changes (4).…”

Section: Introductionmentioning

confidence: 98%

“…However, in testes of rats treated with As+ Cd, a 37% increase in glutathione (GSH) content was related to protection against cadmium-induced morphologic changes (4). Furthermore, in heart tissue of rats treated with As + Cd, an increase in arsenic content was related to an increase in GSH (5).…”

Section: Introductionmentioning

confidence: 99%

Arsenic Increased Lipid Peroxidation in Rat Tissues by a Mechanism Independent of Glutathione Levels

Ramos¹,

Carrizales²,

Yáñez³

et al. 1995

Environmental Health Perspectives

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The role of lipid peroxidation in the mechanism of arsenic toxicity was investigated in female rats pretreated with N-acetylcysteine (NAC, a glutathione [GSHI inducer) or with buthionine sulfoximine (BSO, a GSH depletor). Rats were challenged with sodium arsenite, and sacrificed 1 hr after this treatment. Results showed that arsenic decreased GSH levels and increased lipid peroxidation in liver, kidney, and heart, with a larger effect at 18.2 mg/kg than at 14.8 mg/kg for lipid peroxidation induction. In the liver of rats treated with arsenic, pretreatment with NAC increased the levels of GSH and decreased lipid peroxidation. In kidney and heart, NAC pretreatment protected the tissues against arsenic-induced depletion of GSH levels,but the same degree of protection was not found for lipid peroxidation induction. In its turn, BSO had an additive effect with arsenic in lowering the levels of GSH in the liver and kidney, but an inverse correlation between GSH levels and lipid peroxidation was found only in liver. Arsenic content in tissues of rats pretreated with NAC was lower than in rats treated only with arsenic. In rats with depleted levels of GSH (BSO-pretreated rats), a shift in arsenic tissue distribution was found, with higher levels in skin and lower levels in kidney. A clear tendency for a positive correlation between arsenic concentration and lipid peroxidation levels was found in liver, kidney, and heart. -Environ Health Perspect 103(Suppl 1): 85-88 (1995)

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Arsenic-cadmium interaction in rats

Cited by 28 publications

References 31 publications

Characterization of gene expression changes associated with MNNG, arsenic, or metal mixture treatment in human keratinocytes: application of cDNA microarray technology.

Characterization of gene expression changes associated with MNNG, arsenic, or metal mixture treatment in human keratinocytes: application of cDNA microarray technology.

A comparison of 60, 70, and 90 kDa stress protein expression in normal rat NRK‐52 and human HK‐2 kidney cell lines following in vitro exposure to arsenite and cadmium alone or in combination

Arsenic Increased Lipid Peroxidation in Rat Tissues by a Mechanism Independent of Glutathione Levels

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