Copper inhibits selenite-induced cytotoxicity in human colonic carcinoma cells (HT29)

R. L. Davis, J. E. Spallholz, B. C. Pence

Research output: Contribution to journalArticle

Abstract

We (RLD, JES) have recently demonstrated in a cell free model that seleuite, in the presence of glutathione (GSH), catalyzed the generation of reactive oxygen species (ROS) as measured by lucigenin-dependent chemiluminescence. Generation of ROS was inhibited by zinc, aurintricarboxylic acid and copper (Cu). Cu was the strongest inhibitor. ROS have also been shown to induce apoptosis and cytotoxicity. These findings prompted us to study the ability of Cu to inhibit selenite-induced toxicity in the human colonic carcinoma cell line, HT29. When HT29 cells were treated with both Cu and selenite for 24, 48, or 96 hr, Cu (0.1-5.0 μg Cu/ml as CuSO4) inhibited selenite (1.0 and 5.0 μg Se/ml)-induced cytotoxicity as measured by trypan blue exclusion. When cells were treated for 48 hr, then reseeded in unsupplemented medium and incubated for an additional 96 hr, untreated control cells, cells treated with Cu alone, and cells treated with Cu and selenite, were able to proliferate significantly better than cells treated with selenite alone. This further demonstrated the protective properties of Cu against selenite-induced toxicity. This protection may be related to GSH, in that GSH levels declined to the same level for Cu alone and Cu plus selenite, as with selenite alone, all resulting in a 40% depletion of GSH. These data indicate a potential role for antioxidant elements in preventing selenite toxicity.

Original languageEnglish
JournalFASEB Journal
Volume11
Issue number3
StatePublished - 1 Dec 1997

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Selenious Acid
HT29 Cells
selenites
Cytotoxicity
carcinoma
cytotoxicity
Copper
copper
Cells
Carcinoma
cells
Toxicity
reactive oxygen species
Reactive Oxygen Species
toxicity
Aurintricarboxylic Acid
Chemiluminescence
Trypan Blue
copper sulfate
chemiluminescence

Cite this

@article{55de539fd45c4deeb7077fe76ce60a05,
title = "Copper inhibits selenite-induced cytotoxicity in human colonic carcinoma cells (HT29)",
abstract = "We (RLD, JES) have recently demonstrated in a cell free model that seleuite, in the presence of glutathione (GSH), catalyzed the generation of reactive oxygen species (ROS) as measured by lucigenin-dependent chemiluminescence. Generation of ROS was inhibited by zinc, aurintricarboxylic acid and copper (Cu). Cu was the strongest inhibitor. ROS have also been shown to induce apoptosis and cytotoxicity. These findings prompted us to study the ability of Cu to inhibit selenite-induced toxicity in the human colonic carcinoma cell line, HT29. When HT29 cells were treated with both Cu and selenite for 24, 48, or 96 hr, Cu (0.1-5.0 μg Cu/ml as CuSO4) inhibited selenite (1.0 and 5.0 μg Se/ml)-induced cytotoxicity as measured by trypan blue exclusion. When cells were treated for 48 hr, then reseeded in unsupplemented medium and incubated for an additional 96 hr, untreated control cells, cells treated with Cu alone, and cells treated with Cu and selenite, were able to proliferate significantly better than cells treated with selenite alone. This further demonstrated the protective properties of Cu against selenite-induced toxicity. This protection may be related to GSH, in that GSH levels declined to the same level for Cu alone and Cu plus selenite, as with selenite alone, all resulting in a 40{\%} depletion of GSH. These data indicate a potential role for antioxidant elements in preventing selenite toxicity.",
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Copper inhibits selenite-induced cytotoxicity in human colonic carcinoma cells (HT29). / Davis, R. L.; Spallholz, J. E.; Pence, B. C.

In: FASEB Journal, Vol. 11, No. 3, 01.12.1997.

Research output: Contribution to journalArticle

TY - JOUR

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AU - Davis, R. L.

AU - Spallholz, J. E.

AU - Pence, B. C.

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AB - We (RLD, JES) have recently demonstrated in a cell free model that seleuite, in the presence of glutathione (GSH), catalyzed the generation of reactive oxygen species (ROS) as measured by lucigenin-dependent chemiluminescence. Generation of ROS was inhibited by zinc, aurintricarboxylic acid and copper (Cu). Cu was the strongest inhibitor. ROS have also been shown to induce apoptosis and cytotoxicity. These findings prompted us to study the ability of Cu to inhibit selenite-induced toxicity in the human colonic carcinoma cell line, HT29. When HT29 cells were treated with both Cu and selenite for 24, 48, or 96 hr, Cu (0.1-5.0 μg Cu/ml as CuSO4) inhibited selenite (1.0 and 5.0 μg Se/ml)-induced cytotoxicity as measured by trypan blue exclusion. When cells were treated for 48 hr, then reseeded in unsupplemented medium and incubated for an additional 96 hr, untreated control cells, cells treated with Cu alone, and cells treated with Cu and selenite, were able to proliferate significantly better than cells treated with selenite alone. This further demonstrated the protective properties of Cu against selenite-induced toxicity. This protection may be related to GSH, in that GSH levels declined to the same level for Cu alone and Cu plus selenite, as with selenite alone, all resulting in a 40% depletion of GSH. These data indicate a potential role for antioxidant elements in preventing selenite toxicity.

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