Lipopolysaccharide induced protection against sulfur mustard cytotoxicity in RAW264.7 cells through generation of TNF-α
-
- Allon Nahum
- Department of Pharmacology, Israel Institute for Biological Research
-
- Chapman Shira
- Department of Pharmacology, Israel Institute for Biological Research
-
- Shalem Yoav
- Department of Pharmacology, Israel Institute for Biological Research
-
- Brandeis Rachel
- Department of Pharmacology, Israel Institute for Biological Research
-
- Weissman Ben Avi
- Department of Pharmacology, Israel Institute for Biological Research
-
- Amir Adina
- Department of Pharmacology, Israel Institute for Biological Research
書誌事項
- タイトル別名
-
- Lipopolysaccharide induced protection against sulfur mustard cytotoxicity in RAW264.7 cells through generation of TNF-.ALPHA.
- Lipopolysaccharide induced protection against sulfur mustard cytotoxicity in RAW264 7 cells through generation of TNF a
この論文をさがす
抄録
Sulfur mustard (HD), a very potent alkylating agent and lipopolysacchride (LPS), are both well characterized inflammatory factors. We have found that concomitant exposure of murine macrophage cells (RAW264.7) to LPS and HD induced protection against HD induced cytotoxicity. Both HD and LPS induce release of inflammatory markers in RAW264.7 cells. However, there are marked differences in the repertoire of inflammatory factors released by the two toxins: While exposure to HD, induced a dose-dependant death of these cells, no significant change in survival rate was observed following LPS (1-100 ng/ml) exposure. Additionally, LPS elicited a robust nitric oxide (NO) and TNF-α secretion whereas HD was practically ineffective. Both toxins increased PGE2 secretion in a concentration dependent manner. Treatment of HD-exposed RAW264.7 cells with anti-inflammatory drugs such as dexamethazone (5 μM), voltaren (diclofenac) (8 μM) or doxycycline (5 μM), decreased the release of cytokines but had no effect on cell viability. Simultaneous application of LPS (100 ng/ml) and HD (20-100 μM) resulted in an amelioration of HD cytotoxicity. Adding the NO generator S-nitrosoglutathione (GSNO) or inhibiting NO production using L-NG-monomethyl Arginine, had no effect on cell viability. Moreover, addition of PGE2 (20 ng/ml) failed to induce any changes in cell viability under basal or HD-induced toxicity. In contrast, TNF-α (20 ng/ml) provided remarkable protection against HD-induced cell death. These findings strongly suggest that LPS exerts its protective action against HD toxicity through the generation of TNF-α and may provide better understanding of the mechanism of cytoprotection.
収録刊行物
-
- The Journal of Toxicological Sciences
-
The Journal of Toxicological Sciences 35 (3), 345-355, 2010
一般社団法人 日本毒性学会
- Tweet
詳細情報 詳細情報について
-
- CRID
- 1390001204903043968
-
- NII論文ID
- 10026469694
-
- NII書誌ID
- AN00002808
-
- ISSN
- 18803989
- 03881350
-
- NDL書誌ID
- 10731728
-
- 本文言語コード
- en
-
- データソース種別
-
- JaLC
- NDL
- Crossref
- CiNii Articles
-
- 抄録ライセンスフラグ
- 使用不可