Effect of various concentrations of acyclovir on cell survival and micronuclei induction on cultured HeLa cells

Jagetia, Ganesh Chandra; Aruna, R

doi:10.1016/s1383-5718(99)00159-x

Cited by 15 publications

(15 citation statements)

References 23 publications

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“…A similar relationship has been reported for HeLa cells after treatment with various doses of acyclovir and azidothymidine [9]. However, a linear quadratic relationship has also been reported for HeLa cells treated with doxorubicin or Tinospora cordifolia [8,9] and also for V79 cells treated with various doses of taxol, vindesine or teniposide or doxorubicin [11,[39][40][41][42]. In contrast, Bush & McMillan [48] did not find any relationship between micronuclei induction and cell survival.…”

Section: Discussionsupporting

confidence: 62%

“…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: 62%

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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“…4). Acyclovir is clastogenic in somatic cells as revealed by the formation of micronuclei in vitro or in vivo mouse (Shobukhov and Luruchenko, 1988;Thust, 1996;Jagetia and Aruna, 1999), or chromosomal damage in humans (Tucker, 1982). Thus, induced sperm abnormalities might be due to mutagenicity of Acyclovir in germ cells (Wyrobek et al, 1983;Narayana et al, 2002bNarayana et al, , 2005b, or interference with DNA synthesis during mitotic stage of spermatogenesis or interference with chromosome structure, although this aspect of the toxicity has to be investigated further.…”

Section: Discussionmentioning

confidence: 99%

“…Acyclovir acts via inhibiting viral DNA replication much more effectively than cellular DNA replication indicating that mild host cell damage could be possible (Schaeffer et al, 1978;Elion, 1986;Dollery, 1999). Acyclovir appeared to be nonmutagenic in Ame's test (Tucker, 1982); however, exposure to HeLa cells resulted in complete inhibition of cell division but without any appreciable changes in the cell number (Jagetia and Aruna, 1999). On the other hand, Acyclovir induced the formation of micronuclei indicating its ability to destruct the chromosome structure (Jagetia and Aruna, 1999).…”

Section: Introductionmentioning

confidence: 91%

A purine nucleoside analogue-acyclovir [9-(2-hydroxyethoxymethyl)-9h-guanine] reversibly impairs testicular functions in mouse

Narayana

2008

J. Toxicol. Sci.

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-The present study was designed to investigate testicular effects of Acyclovir [9-(2-hydroxyethoxymethyl)-9H−guanine] in mouse. Swiss albino male mice (N=6/group/dose/sample time) were treated (i. p.) every day with 4, 16, 32, and 48 mg/kg body weight of Acyclovir for 15 d. The testis was examined for histopathological changes and the seminiferous tubular diameter (STD) and epithelial height (SE) were measured. The sperm count, sperm motility and sperm morphology assay in caudae epididymes, and intra-testicular levels lactate dehydrogenase (LDH) and testosterone were estimated on 7 d, In conclusion, Acyclovir is cytotoxic to germ cells inducing the cellular destruction, and reducing the sperm count and motility, and increasing sperm abnormalities. Further, Acyclovir also caused cellular destruction thus releasing LDH from the cells, and affecting the Leydig cell function. All adverse effects of Acycovir are reversible by 70 d, except the sperm count and LDH level, which appear to be affected over an extended period of time at a higher dose-level.

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Chitosan Oligosaccharide inhibits203HgCl2-induced genotoxicity in mice: Micronuclei occurrence and chromosomal aberration

et al. 2005

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The purpose of this study was to investigate the safety of chitosan oligosaccharide and the effects of chitosan oligosaccharide on mercury induced genotoxicity in mice using the micronuclei and chromosome aberration. The micronuclei test was performed by microscopic examination (x1,000, stained using a May-Grunwald solution) after administering 0.01, 0.1, and 1% (10 mg/mL) chitosan oligosaccharide for 7, 60, and 180 days ad libitum in mice. Total micronuclei of 1,000 polychromatic erythrocytes were recorded for each group. There was no difference between the untreated and experimental groups. The intake periods and concentrations of chitosan oligosaccharide did not affect the occurrence of micronuclei in bone marrow cells (P>0.05). The chromosomal aberration test was performed by microscopic examination (x1,000, stained using a 4% Giemsa solution) after administering the same concentration of chitosan oligosaccharide to mice, in F1, F2, F3 generations and parents. The frequency of chromosomal aberrations was defined as [Ydr = (D+R)/total number of counted lymphocytes]. Similar to the micronuclei test, there was no difference between the untreated and treated groups. These results showed that the intake periods and concentrations of chitosan oligosaccharide did not affect chromosomal aberrations in bone marrow cells (P>0.05). To investigate the effect of chitosan oligosaccharide on mercury-induced chromosome aberration, mice in each condition were supplied with 203HgCl2 and chitosan oligosaccharide ad libitum. Chitosan oligosaccharide significantly inhibited 203HgCl2-induced chromosome aberration in mice. Based on the results of this study, it may be concluded that the chitosan oligosaccharide is a nontoxic material that could be used as a suppressor of heavy metal-induced genotoxicity.

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Effect of various concentrations of acyclovir on cell survival and micronuclei induction on cultured HeLa cells

Cited by 15 publications

References 23 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

A purine nucleoside analogue-acyclovir [9-(2-hydroxyethoxymethyl)-9h-guanine] reversibly impairs testicular functions in mouse

Chitosan Oligosaccharide inhibits203HgCl2-induced genotoxicity in mice: Micronuclei occurrence and chromosomal aberration

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