Micronuclei-induction and its correlation to cell survival in HeLa cells treated with different doses of adriamycin

Jagetia, Ganesh Chandra; Nayak, Vijayashree

doi:10.1016/s0304-3835(96)04470-9

Cited by 24 publications

(16 citation statements)

References 18 publications

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“…The frequency of MNBNC increased with time, and a peak was observed at 30 h post-treatment which may be due to the APE-induced cell cycle delay. A similar effect has been reported earlier in HeLa cells [8]. The micronuclei frequency will be highest immediately after first cell division, which seems to be the reason of maximum frequency of micronuclei at 30 h post treatment and decline with subsequent cell division.…”

Section: Discussionsupporting

confidence: 88%

“…The cytotoxic effect of APE increased with time up to 6h post-treatment and remained almost unaltered thereafter as evident by cell viability and clonogenic assays. An identical effect was observed earlier when HeLa cells were treated with doxorubicin, acyclovir, azidothymidine or extract of Tinospora cordifolia [8,21,35,36]. The cytotoxic effect of APE increased with increasing concentrations and an IC 50 concentration was found to be 25µg/ml.…”

Section: Discussionsupporting

confidence: 80%

“…Similarly, other antineoplastic agents like, doxorubicin, vinblastine, taxol and teniposide (VM-26) have been reported to induce cytotoxicity in V79 cells [11,[39][40][41][42]. Treatment of HeLa, MCF-7, HL 60, or KB cells to alcoholic extract of the stem bark of Alstonia scholaris or echitamine chloride have been reported to induce cytotoxicity earlier [8,20,43,44]. The cytotoxic effect of APE is reflected in proliferation indecies (PI), where a concentration dependent reduction in PI was observed at all post-treatment times in cells treated with various concentrations of APE.…”

Section: Discussionmentioning

confidence: 99%

“…This is probably the first report describing the APE-induced DNA damage in HeLa cells. Similarly, doxorubicin, extract of Tinospora cordifolia, acyclovir and azidothymidine have been reported to increase the frequency of micronuclei in a concentration-dependent manner in HeLa cells earlier [8][9][10]35]. The treatment of V79 cells with doxorubicin has been found to increase the micronuclei frequency in concentration dependent manner [11].…”

Section: Discussionmentioning

confidence: 99%

“…Cisplatin has also been reported to induce micronuclei in 9L tumor cells [7]. Similarly, adriamycin, acyclovir or methanolic extract of Tinospora cordifolia were reported to induce micronuclei in HeLa and V79; cells [8][9][10][11]. The use of natural products, especially plants may be beneficial in cancer treatment as more than 80% of the world population still depend on plants and natural products for healthcare [12,13].…”

Section: Introductionmentioning

confidence: 99%

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Determination of Antineoplastic Activity of Rohituka, Aphanamixis Polystachya (Wall) RN Parker in Hela Cells: Correlation with Clonogenicity and DNA Damage

Jagetia

Venkatesha

2016

IJCAM

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The antineoplastic activity of chloroform stem bark extract of rohituka, Aphanamixis polystachya (APE) used traditionally to treat spleen and liver tumors was evaluated in cultured HeLa cells by clonogenic and micronucleus assays. Treatment of HeLa cells with 0, 5, 10, 25, 50, 75 or 100µg/ml APE for different times caused a concentration-dependent reduction in the cell survival up to 6 h post-treatment (p<0.005) followed by a non-significant decline in the cells treated with APE for 24 h. Therefore, 6h treatment time was considered as an optimum time for APE exposure and further studies were carried out using this treatment time. Exposure of HeLa cells to different concentrations of APE resulted in a concentration-dependent decline in the cell viability and 100µg/ ml APE resulted in 72% cell death when compared with the non-drug treated control group. These results were further confirmed by clonogenic assay where, APE treatment caused a concentration-dependent decline in the clonogenicity of HeLa cells, and the surviving fraction of cells was reduced to 0.22 after treatment with 100µg/ml APE, the highest concentration screened. The inhibitory concentration (IC50) of APE was found to be 25µg/ml. The APE-induced DNA damage was estimated by micronucleus assay, where the treatment of HeLa cells with various concentrations of APE resulted in a concentration-dependent rise in the frequency of micronuclei in binucleate HeLa cells (MNBNCs) at 20, 30, and 40 h post-treatment. This increase in MNBNCs was significantly higher than the baseline frequency of MNBNCs. APE treatment also increased the frequency of HeLa cells bearing more than one micronucleus (MN) indicating higher degree of DNA damage. The frequency of MNBNC increased with scoring time and a maximum elevation in the MNBNC frequency was observed at 30 h posttreatment. The MNBNC induction and clonogenicity of HeLa cells was inversely related indicating that increased MNBNC formation resulted in a corresponding reduction in the cell survival. The cell proliferation indices (PI) declined with increasing concentration of APE that increased with screening time. Our study demonstrates that APE is able to kill HeLa cells effectively and this cell killing effect of APE may be due its ability to induce DNA damage.

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Section: Discussionsupporting

confidence: 88%

Section: Discussionsupporting

confidence: 80%

Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Determination of Antineoplastic Activity of Rohituka, Aphanamixis Polystachya (Wall) RN Parker in Hela Cells: Correlation with Clonogenicity and DNA Damage

Jagetia

Venkatesha

2016

IJCAM

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Naringin, a grapefruit flavanone, protects V79 cells against the bleomycin‐induced genotoxicity and decline in survival

Jagetia

Jha

2006

J of Applied Toxicology

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The effect of naringin, a grapefruit flavonone was studied on bleomycin-induced genomic damage and alteration in the survival of cultured V79 cells. Exposure of V79 cells to bleomycin induced a concentration dependent elevation in the frequency of binucleate cells bearing micronuclei (MNBNC) and a maximum number of MNBNCs were observed in the cells treated with 50 microg ml(-1) bleomycin, the highest concentration evaluated. This genotoxic effect of bleomycin was reflected in the cell survival, where a concentration dependent decline was observed in the cells treated with different concentrations of bleomycin. Treatment of cells with 1 mm naringin before exposure to different concentrations of bleomycin arrested the bleomycin-induced decline in the cell survival accompanied by a significant reduction in the frequency of micronuclei when compared with bleomycin treatment alone. The cell survival and micronuclei induction were found to be inversely correlated. The repair kinetics of DNA damage induced by bleomycin was evaluated by exposing the cells to 10 microg ml(-1) bleomycin using single cell gel electrophoresis. Treatment of V79 cells with bleomycin resulted in a continuous increase in DNA damage up to 6 h post-bleomycin treatment as evident by migration of more DNA into the tails (% tail DNA) of the comets and a subsequent increase in olive tail moment (OTM), an index of DNA damage. Treatment of V79 cells with 1 mm naringin reduced bleomycin-induced DNA damage and accelerated DNA repair as indicated by a reduction in % tail DNA and OTM with increasing assessment time. A maximum reduction in the DNA damage was observed at 6 h post-bleomycin treatment, where it was 5 times lower than bleomycin alone. Our study, which was conducted on the basis of antioxidant, free radical scavenging and metal chelating properties of naringin demonstrates that naringin reduced the genotoxic effects of bleomycin and consequently increased the cell survival and therefore may act as a chemoprotective agent in clinical situations.

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Effect of Terminalia arjuna extract on adriamycin‐induced DNA damage

Reddy¹,

Seshadri²,

Reddy³

et al. 2008

Phytotherapy Research

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The effect of a bark extract of Terminalia arjuna (TAE) was studied on the alteration of adriamycin (ADR)-induced micronuclei formation in cultured human peripheral blood lymphocytes. Exposure of lymphocytes to ADR resulted in a dose-dependent increase in the micronuclei formation indicating DNA damage. Pretreatment of lymphocytes with TAE before ADR treatment resulted in a significant decline in micronuclei formation. Increasing doses of ADR caused a dose-dependent increase in the frequency of lymphocytes bearing one, two and multiple micronuclei. Prior exposure of lymphocytes to 15 microg/mL of TAE significantly reduced the frequency of lymphocytes bearing one, two and multiple micronuclei when compared with ADR-treated control. TAE-inhibited the induction of (*)OH (hydroxyl), O2(*-) (superoxide), DPPH (1,1-diphenyl-2-picrylhydrazyl), ABTS(*+) (2,2-azino-bis-3-ethyl benzothiazoline-6-sulphonic acid) radicals in a dose-dependent manner. These results demonstrate that TAE protects DNA against ADR-induced damage.

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Micronuclei-induction and its correlation to cell survival in HeLa cells treated with different doses of adriamycin

Cited by 24 publications

References 18 publications

Determination of Antineoplastic Activity of Rohituka, Aphanamixis Polystachya (Wall) RN Parker in Hela Cells: Correlation with Clonogenicity and DNA Damage

Determination of Antineoplastic Activity of Rohituka, Aphanamixis Polystachya (Wall) RN Parker in Hela Cells: Correlation with Clonogenicity and DNA Damage

Naringin, a grapefruit flavanone, protects V79 cells against the bleomycin‐induced genotoxicity and decline in survival

Effect of Terminalia arjuna extract on adriamycin‐induced DNA damage

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