DNA damage induced by paclitaxel and DNA repair capability of peripheral blood lymphocytes as evaluated by the alkaline comet assay

Branham, Marı́a Teresita; Nadin, Silvina B.; Vargas–Roig, Laura M.; Ciocca, Daniel R.

doi:10.1016/j.mrgentox.2004.01.013

Cited by 59 publications

(37 citation statements)

References 22 publications

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“…It has been reported that paclitaxel can induce DNA singlestrand breaks (30)(31)(32). Our data indicate that paclitaxel may induce oxidative DNA damage by generating increased levels of H 2 O 2 and NO.…”

Section: Discussionsupporting

confidence: 58%

Resistance to Paclitaxel Is Proportional to Cellular Total Antioxidant Capacity

et al. 2005

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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, G 2 -M arrest, and cells with fragmented nuclei. Antioxidants pyruvate and selenium, the NO synthase inhibitor N W -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-G 1 cells. In contrast, the glutamylcysteine synthase inhibitor buthionine sulfoximine (BSO) and the superoxide dismutase (SOD) inhibitor 2-methoxyestradiol (2-ME) increased the sub-G 1 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 (As 2 O 3 ), 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. (Cancer Res 2005; 65(18): 8455-60)

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Section: Discussionsupporting

confidence: 58%

Resistance to Paclitaxel Is Proportional to Cellular Total Antioxidant Capacity

et al. 2005

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“…Interestingly, the results obtained (Table 3) show that all essential oils (S1-S18) selectively affect the survival of human melanoma cancer cells. In fact, as the positive control doxorubicin, a commonly used chemotherapeutic agents (Branham et al, 2004;Padjas et al, 2005), the samples were able to inhibit the growth of A375, M14, and A2058 cells at non toxic concentration in normal cells (data not shown). But samples S6, S13 and S18 exhibited the major effects, in particular the essential oil S13 had a high inhibitory activity, with the IC 50 values of 8.2, 12.1 and 11.7 lg/mL in M14, A375 and A2058 cells, respectively.…”

Section: Resultsmentioning

confidence: 95%

Chemical composition and anticancer activity of essential oils of Mediterranean sage (Salvia officinalis L.) grown in different environmental conditions

Russo

Formisano

Rigano

et al. 2013

Food and Chemical Toxicology

191

101

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“…A visual score based on extend of migration was used: 0, very low migration; 1, 5-10 % of migrated DNA; 2, 11-30 % of migrated DNA; 3, 31-60 % of migrated DNA; 4, 61-95 % of migrated DNA; and 5, >95 % of migrated DNA (Anderson et al 1994). To facilitate the management of the data, an average of DNA migration was calculated as [(% of cells with score 1)× 1+(% of cells with score 2)x2+(% of cells with score 3)×3+ (% of cells with score 4)×4+(% of cells with score 5)×5]/100 (Branham et al 2004). As a positive control, we used cells treated with 60 μM of hydrogen peroxide for 1 h.…”

Section: Alkaline Comet Assaymentioning

confidence: 99%

Effects of temozolomide (TMZ) on the expression and interaction of heat shock proteins (HSPs) and DNA repair proteins in human malignant glioma cells

Castro

Cayado-Gutiérrez

Zoppino

et al. 2015

Cell Stress and Chaperones

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We previously reported the association of HSPA1A and HSPB1 with high-grade astrocytomas, suggesting that these proteins might be involved in disease outcome and response to treatment. With the aim to better understand the resistance/susceptibility processes associated to temozolomide (TMZ) treatment, the current study was performed in three human malignant glioma cell lines by focusing on several levels: (a) apoptotic index and senescence, (b) DNA damage, and (c) interaction of HSPB1 with players of the DNA damage response. Three human glioma cell lines, Gli36, U87, and DBTRG, were treated with TMZ evaluating cell viability and survival, apoptosis, senescence, and comets (comet assay). The expression of HSPA (HSPA1A and HSPA8), HSPB1, O 6 -methylguanine-DNA methyltransferase (MGMT), MLH1, and MSH2 was determined by immunocytochemistry, immunofluorescence, and Western blot. Immunoprecipitation was used to analyze protein interaction. The cell lines exhibited differences in viability, apoptosis, and senescence after TMZ administration. We then focused on Gli36 cells (relatively unstudied) which showed very low recovery capacity following TMZ treatment, and this was related to high DNA damage levels; however, the cells maintained their viability. In these cells, MGMT, MSH2, HSPA, and HSPB1 levels increased significantly after TMZ administration. In addition, MSH2 and HSPB1 proteins appeared co-localized by confocal microscopy. This colocalization increased after TMZ treatment, and in immunoprecipitation analysis, MSH2 and HSPB1 appeared interacting. In contrast, HSPB1 did not interact with MGMT. We show in glioma cells the biological effects of TMZ and how this drug affects the expression levels of heat shock proteins (HSPs), MGMT, MSH2, and MLH1. In Gli36 cells, the results suggest that interactions between HSPB1 and MSH2, including co-nuclear localization, may be important in determining cell sensitivity to TMZ.

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DNA damage induced by paclitaxel and DNA repair capability of peripheral blood lymphocytes as evaluated by the alkaline comet assay

Cited by 59 publications

References 22 publications

Resistance to Paclitaxel Is Proportional to Cellular Total Antioxidant Capacity

Resistance to Paclitaxel Is Proportional to Cellular Total Antioxidant Capacity

Chemical composition and anticancer activity of essential oils of Mediterranean sage (Salvia officinalis L.) grown in different environmental conditions

Effects of temozolomide (TMZ) on the expression and interaction of heat shock proteins (HSPs) and DNA repair proteins in human malignant glioma cells

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