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  1. NTU Scholars
  2. 醫學院
  3. 醫學系
Please use this identifier to cite or link to this item: https://scholars.lib.ntu.edu.tw/handle/123456789/544261
Title: Resistance to paclitaxel is proportional to cellular total antioxidant capacity
Authors: Ramanathan B.
Jan K.-Y.
Chen C.-H.
Hour T.-C.
HONG-JENG YU 
YEONG-SHIAU PU 
Issue Date: 2005
Journal Volume: 65
Journal Issue: 18
Start page/Pages: 8455-8460
Source: Cancer Research
Abstract: 
Paclitaxel, one of the most commonly prescribed chemotherapeutic agents, is active against a wide spectrum of human cancer. The mechanism of its cytotoxicity, however, remains controversial. Our results indicate that paclitaxel treatment increases levels of superoxide, hydrogen peroxide, nitric oxide (NO), oxidative DNA adducts, G2-M arrest, and cells with fragmented nuclei. Antioxidants pyruvate and selenium, the NO synthase inhibitor Nω-nitro-L-arginine methyl ester, and the NO scavenger manganese (III) 2-(4-carboxyphenyl)-4,4,5,5-tetramethyl-imidazoline-1-oxyl-3- oxide all decreased paclitaxel-mediated DNA damage and sub-G1 cells. In contrast, the glutamylcysteine synthase inhibitor buthionine sulfoximine (BSO) and the superoxide dismutase (SOD) inhibitor 2-methoxyestradiol (2-ME) increased the sub-G1 fraction in paclitaxel-treated cells. These results suggest that reactive oxygen and nitrogen species are involved in paclitaxel cytotoxicity. This notion is further supported with the observation that concentrations of paclitaxel required to inhibit cell growth by 50% correlate with total antioxidant capacity. Moreover, agents such as arsenic trioxide (As2O3), BSO, 2-ME, PD98059, U0126 [mitogen-activated protein/extracellular signal-regulated kinase inhibitors], and LY294002 (phosphatidylinositol 3-kinase/Akt inhibitor), all of which decrease clonogenic survival, also decrease the total antioxidant capacity of paclitaxel-treated cells, regardless whether they are paclitaxel sensitive or paclitaxel resistant. These results suggest that paclitaxel chemosensitivity may be predicted by taking total antioxidant capacity measurements from clinical tumor samples. This, in turn, may then improve treatment outcomes by selecting out potentially responsive patients. ?2005 American Association for Cancer Research.
URI: https://www.scopus.com/inward/record.uri?eid=2-s2.0-24944486664&doi=10.1158%2f0008-5472.CAN-05-1162&partnerID=40&md5=f7a2bc7e32e220ef671ca45d186e1add
https://scholars.lib.ntu.edu.tw/handle/123456789/544261
ISSN: 0008-5472
DOI: 10.1158/0008-5472.CAN-05-1162
SDG/Keyword: 1,4 diamino 1,4 bis(2 aminophenylthio) 2,3 dicyanobutadiene; 2 (2 amino 3 methoxyphenyl)chromone; 2 (4 carboxyphenyl) 4,4,5,5 tetramethylimidazoline 1 oxyl 3 oxide; 2 morpholino 8 phenylchromone; arsenic trioxide; hydrogen peroxide; mitogen activated protein kinase inhibitor; n(g) nitroarginine methyl ester; nitric oxide; nitrogen; paclitaxel; phosphatidylinositol 3 kinase inhibitor; pyruvic acid; reactive oxygen metabolite; selenium; superoxide; antioxidant activity; article; cell cycle G1 phase; cell cycle G2 phase; cell growth; controlled study; cytotoxicity; DNA adduct; DNA damage; human; human cell; mitosis; priority journal; Antineoplastic Agents, Phytogenic; Antioxidants; Breast Neoplasms; Cell Division; Cell Growth Processes; Cell Nucleus; Drug Resistance, Neoplasm; G2 Phase; Humans; Nitric Oxide; Paclitaxel; Reactive Oxygen Species
[SDGs]SDG3
Appears in Collections:醫學系

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臺大位居世界頂尖大學之列,為永久珍藏及向國際展現本校豐碩的研究成果及學術能量,圖書館整合機構典藏(NTUR)與學術庫(AH)不同功能平台,成為臺大學術典藏NTU scholars。期能整合研究能量、促進交流合作、保存學術產出、推廣研究成果。

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