IN VITRO CYTOTOXICITY ACTIVITY AND IN VIVO ORAL TOXICITY OF Euphorbia hirta

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Date
2014-08
Authors
PING, KWAN YUET
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Euphorbia hirta is an annual plant that has been widely used in traditional medicine to treat various diseases. In vitro cytotoxicity, genotoxicity properties and in vivo toxicological evaluation of E. hirta methanol extract were investigated in this study. Various pharmacognostical parameters evaluation was carried out as per World Health Organization (WHO) guidelines procedure for the standardization of E. hirta extract. The chemical constituent aspect of standardization involves quantification of the main chemical components in E. hirta. The GC-MS analysis was used for quantification of 1,3,4,5-tetrahydroxycyclohexanecarboxylic acid in the extract was rapid, accurate and linear. Six major peaks in the range of 600 - 1500 and 2800 - 3400 cm-1 were observed in the FTIR spectra. The concentrations of heavy metals determined in E. hirta extract were well below the permissible limit. In 2,2- Diphenyl-1-picylhydrazyl radical (DPPH) assay, the extract showed a general consistency on antioxidant activity above 50%, independent of the extraction time. The potential cytotoxicity effect of E. hirta was investigated using brine shrimp lethality assay and the cytotoxicity assay against cancer cells. The extract of E. hirta showed significant toxicity against brine shrimp with (Lethal Concentration) LC50 value of 620.38μg/mL (24 h). Comparison with positive control potassium dichromate signifies that cytotoxicity exhibited by the methanol extract have moderate activity. The 3-(4, 5-dimethyl thiazol-2yl)-2, 5-diphenyltetrazolium bromide (MTT) cytotoxicity assay showed that E. hirta inhibited MCF-7 cell xxxi viability with the (Inhibitory Concentration) IC50 values 25.26 μg/ml in a dose and time-dependent manner. Microscopic studies showed that E. hirta treated cells exhibited marked morphological features characteristic of apoptosis. E. hirta extract also had an ignorable influence on the lactate dehydrogenase (LDH) leakage and generating intracellular reactive oxygen species (ROS). Therefore, E. hirta might induce the cytotoxicity via a ROS-independent mechanism in MCF-7 cells. The Annexin V/Propidium Iodide flow cytometry study confirmed that E. hirta extract induced apoptosis in MCF-7 cells. E. hirta extract treatment also resulted in DNA fragmentation in MCF-7 cells. Moreover, E. hirta treatment resulted in the accumulation of cells at the S and G2/M phases as well as apoptosis. The caspase activity study revealed that E. hirta extract induced apoptosis through the caspase-3 independent pathway by the activation of caspase-2, 6, 8 and 9. To identify the cytotoxic compound, E. hirta extract was subjected to bioassay-guided fractionation. E. hirta hexane subfraction, namely EH Hex 4 demonstrated highest activity among all the fractions tested. Further Liquid Chromatography–Mass Spectrometry (LC-MS) analysis of EH Hex 4 led to identification of 3,3’,4’,5,7-Pentahydroxy-8-(5-oxo-2- pyrrolidinyl) flavone as the likely cytotoxic agent in E. hirta extract. The data obtained from this study revealed that E. hirta induced apoptotic cell death and suggests that E. hirta could be used as an apoptosis-inducing anti-cancer agent for breast cancer treatment with further detailed studies. The potential genotoxic effect of E. hirta was investigated using Allium cepa and comet assay. In A. cepa assay, the result showed that the methanol extract of E. hirta exerted significant genotoxic and mitodepressive effects at 1000 μg/mL. A dose-dependent increase of chromosome aberrations was also observed such as stickiness, c-mitosis, bridges and vagrant chromosomes. Micronucleated cells were also observed at interphase. In the comet xxxii assay, the treatment of 25 μg/mL of E. hirta extract for 72 h on MCF-7 cells caused an increase in DNA damage by approximately 48.16% compared to the unchallenged control which confirmed the genotoxic effect of E. hirta extract. The acute and subchronic oral toxicity of E. hirta was evaluated in Sprague Dawley rats. The extract at a single dose of 5000 mg/kg did not produce treatment related signs of toxicity or mortality in the animals tested during the 14-day observation period. Therefore, the (Lethal Dose) LD50 of this plant was estimated to be more than 5000 mg/kg. In the subchronic toxicity study, the administration of 50 mg/kg, 250 mg/kg, 1000 mg/kg/day of E. hirta extract per body weight revealed no significant difference in the body weight change, haematological and biochemical parameters, relative organ weights and gross findings compared to the control group. Macropathology and histopathology examination of all organs did not reveal morphological alteration. Analyses of these results with the information of signs, behaviour and health monitoring could lead to the conclusion that the long-term oral administration of E. hirta extract for 90 days does not cause toxicity. In conclusion, in vitro and in vivo toxicity results obtained in this study proved the importance of both methods to obtain comprehensive toxicological evaluation of natural product agents.
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IN VITRO CYTOTOXICITY ACTIVITY
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