Growth and inhibition of zinc anode dendrites in Zn-air batteries:Model and experiment

Zinc(Zn)-air batteries are widely used in secondary battery research owing to their high theoretical energy density,good electrochemical reversibility,stable discharge performance,and low cost of the anode active material Zn.However,the Zn anode also leads to many challenges,including dendrite growth,deformation,and hydrogen precipitation self-corrosion.In this context,Zn dendrite growth has a greater impact on the cycle lives.In this dissertation,a dendrite growth model for a Zn-air battery was established based on electrochemical phase field theory,and the effects of the charging time,anisotropy strength,and electrolyte temperature on the morphology and growth height of Zn dendrites were studied.A series of experiments was designed with different gradient influencing factors in subsequent experiments to verify the theoretical simulations,including elevated electrolyte temperatures,flowing electrolytes,and pulsed charging.The simulation results show that the growth of Zn dendrites is controlled mainly by diffusion and mass transfer processes,whereas the electrolyte temperature,flow rate,and interfacial energy anisotropy intensity are the main factors.The experimental results show that an optimal electrolyte temperature of 343.15 K,an optimal electrolyte flow rate of 40 ml·min^(-1),and an effective pulse charging mode.

Treatment of metastatic colorectal carcinomas by systemic inhibition of vascular endothelial growth factor signaling in mice

AIM： Tumor angiogenesis has been shown to be promoted by vascular endothelial growth factor （VEGF） via stimulating endothelial cell proliferation, migration, and survival. Blockade of VEGF signaling by different means has been demonstrated to result in reduced tumor growth and suppression of tumor angiogenesis in distinct tumor entities. Here, we tested a recombinant adenovirus, AdsFItl-3, that encodes an antagonistically acting fragment of the VEGF receptor 1 （Fit-l）, for systemic antitumor effects in pre-established subcutaneous CRC tumors in mice.METHODS： Murine colorectal carcinoma cells （CT26） were inoculated subcutaneously into Balb/c mice for in vivo studies. Tumor size and survival were determined. 293 cell line was used for propagation of the adenoviral vectors. Human lung cancer line A549 and human umbilical vein endothelial cells were transfected for in vitro experiments.RESULTS： Infection of tumor cells with AdsFlt1-3 resulted in protein secretion into cell supernatant, demonstrating correct vector function. As expected, the secreted sFlt1-3 protein had no direct effect on CT26 tumor cell proliferation in vitro, but endothelial cell function was inhibited by about 46% as compared to the AdLacZ control in a tube formation assay. When AdsFlt1-3 （5×10^9 PFU/animal） was applied to tumor bearing mice, we found a tumor inhibition by 72% at d 12 after treatment initiation, in spite of these antitumoral effects, the survival time was not improved. According to reduced intratumoral microvessel density in AdsFlt1-3-treated mice, the antitumor mechanism can be attributed to angiostatic vector effects. We did not detect increased systemic VEGF levels after AdsFlt1-3 treatment and liver toxicity was low as judged by serum alanine aminotransferase determination.CONCLUSION： In this study we confirmed the value of a systemic administration of AdsFItl-3 to block VEGF signaling as antitumor therapy in an experimental metastatic colorectal carcinoma model in mice.

Transactivation of the TIEG1 confers growth inhibition of transforming growth factor-β-susceptible hepatocellular carcinoma cells

AIM:To investigate the role of transforming growth factor(TGF)-β-inducible early gene 1(TIEG1) in TGF-β-induced growth inhibition in hepatocellular carcinoma(HCC) cells.METHODS:Human hepatocyte and HCC cell lines with varied susceptibilities to TGF-β1 were tested by methylthiazoletetrazolium(MTT) assay.The expression changes of Smad2,Smad3,Smad4,Smad7,TIEG1 and TIEG2 gene following treatment with TGF-β1 in a TGF-β-sensitive hepatocyte cell line(MIHA),a TGF-β-sensitive hepatoma cell line(Hep3B) and two TGF-β-insensitive hepatoma cell lines(HepG2 and Bel7404) were examined.SiRNA targeting TIEG1 was transfected into Hep3B cells and the sensitivity of cells to TGF-β1 was examined.Overexpression of TIEG1 was induced by lentiviral-mediated transduction in TGF-β1-resistant hepatoma cell lines(Bel7404 and HepG2).MTT assay and 4',6-Diamidino-2-phenylindole staining were used to identify cell viability and apoptosis,respectively.The expression level of stathmin was measured by reverse transcriptase polymerase chain reaction and Western-blotting analysis,and stathmin promoter activity by TIEG1 was monitored by a luciferase reporter gene system.RESULTS:TIEG1 was significantly upregulated by TGF-β1 in the TGF-β1-sensitive HCC cell line,Hep3B,but not in the resistant cell lines.The suppression of TIEG1 by siRNAs decreased the sensitivity of Hep3B cells to TGF-β1,whereas the overexpression of TIEG1 mediated growth inhibition and apoptosis in TGF-β1-resistant HCC cell lines,which resembled those of TGF-β1-sensitive HCC cells treated with TGF-β1.Our data further suggested that stathmin was a direct target of TIEG1,as stathmin was signif icantly downregulated by TIEG1 overexpression,and stathmin promoter activity was inhibited by TIEG1 in a dose-dependent manner.CONCLUSION:Our data suggest that transactivation of TIEG1 conferred growth inhibition of TGF-β-susceptible human HCC cells.

Growth Inhibition, Induction of Apoptosis by Green Tea Constituent (-)-Epigallocatechin-3-gallate in Cultured Rabbit Lens Epithelial Cells

Purpose: To evaluate effect of green tea extract (-)-Epigallocatechin-3-gallate (EGCG) in cultured rabbit lens epithelial cells in order to pave a new way to postcapsular opacity (PCO) prevention.Methods: Cell survival rate was measured by 3-(4, 5-dimethylthiazol-2-yl)-2, 5-diphenyl tetrazolium bromide (MTT) coloimetric assay. Cell apoptosis was detected by electron microscopy, Hochest 33258 stain and flow cytometer. DNA fragment was detected using agarose gel electrophoresis.Result: Proliferation of the cultured rabbit lens epithelia cells was inhibited by EGCG in a dose and time dependent manner. Morphologic study showed that the cells became shrunk, round shaped with their nuclei condensed and broken. Apoptotic bodies were also seen under electron microscope and in Hochest 33258 stain assay 24 hours after EGCG was added to the medium. DNA ladders were shown in agarose gel eletrophoresis. In flow cytometry assay, apoptosis peak was also evident.Conclusion: Green Tea Constituent(-)

Inhibition of the growth and development of mosquito larvae of Culex quinquefasciatus(Diptera:Culicidae) treated with extract from leaves of Pseudocalymma alliaceum(Bignonaceae)

Objective:To determine larvicidal activity of the essential oil,hydrolat and botanical extracts derived from leaves ol Pseudocalymma alliaceum an mosquito larvae of Culex quinquefasciatus.Methods:Groups of twenty lanae were used in the larvicidal assays.The mortality,relative growth rate,the larval and pupal duration and viability was estimated.The essential oil was analyzed by solid phase microextraction using gas chromatography coupled to mass spectrometry.Results:Essential oil at 800 ppm showed larvicidal activity at 24 h with lethal values of LC_(50) and LC_(90) of 267.33 and 493.63 ppm.The hvdrolat at 20% and 10% on 2nd stage larvae showed 100%effectiveness after 24 h.The aqueous extract at 10% had a relative growth index of 0.58.while the ethanolic and methanolic extract obtained values of 0.76 and 0.70 and control reached 0.99.Larvae treated with 10% of methanol,ethanol and aqueous extract showed a reduction in larval duration of 5.00,2.20 and 4.35 days;ethanol extract at 1% provoke decrease of 2.40 days in the development and exhibited an increment of 3.30 days when treated with 0.01%.Aqueous,ethanol and methanol extracts at 10%reduced in 6.15,3.42 and 5.57 days pupal development.The main compounds were diallyl disulfide(50.05%),diallyl sulfide(11.77%) and disulfide di-2-propenyl(10.37%).Conclusions:The study demonstrated for the first time,the larvicidal activity of the essential oil and hydrolat of Pseudocalymma alliaceum:aqueous,ethanol and methanol extracts inhibited the normal growth and development of mosquito larvae,prolonging and delaying larval and pupal duration.

Effect of Vitamin K1 on Cell Growth Inhibition and Apoptosis on the U937 Cell Line

This experiment was conducted in order to verify the role of Vitamin K1 as a cell growth inhibitor on the U937 cell line. This experiment was performed in two parts—one with a lesser concentration of Vitamin K1, and the other with a range of concentrations from low-to-high. Through the remaining number of U937 cells, as well as cell areas, it was concluded that the presence of Vitamin K1 reduces the number of cancer cells. It was also concluded that as Vitamin K1 concentration increases, so does the frequency and effects of apoptosis.

Inhibition of Chlamydospore Germination and Mycelial Growth of Trichoderma spp. by Chemical Fungicides

For exploring the influences of application and residue of chemical fungi- cides on chlamydospore preparations of Trichoderma spp., the effects of seven chemical fungicides on chlamydospore germination and mycelia growth of two bio- control fungi T. harzianum 610 and T. Iongibrachiatum 758 were studied. Carben- dazim, tebuconazole and difenoconazole showed strong toxicities, thiram and car- bexin showed moderate toxicities, and metalaxyl showed Mycelia growth of the two strains was more sensitive to most tested fungicides than those of chlamydospore germination. Chlamydospore germination of 610 was more sensitive to tested fungicides than those of 758, and mycelia growth of 758 was more sensitive to most tested fungi- cides than those of 610. Among the seven fungicides, 98% carbendazim had the strongest effects （ECru values were 1.64 and 0.05μpg/ml）, and 70% pentachloroni- trobenzene had the weakest effects （EC50 values were 1.64 and 0,05 μg/ml） for chlamydospore germination and mycelia growth of 610. As for 758, 98% carbendaz- im had the strongest inhibitory effects and 95% metalaxyl had the weakest inhibitory for chlamydospore germination of 756 （EC50 values were 0.62 and 1 108.61 μg/ml respectively）, whereas 96.2% tebuconazole showed the strongest inhibitory effects for mycelia growth of 758 （EC= value was 0.32μg/ml）, and 95% metalaxyl was the weakest （EC= value was 1 206.29 μg/ml）. According to the applied concentration of different fungicides in practice, we concluded that chlamydospore preparations of 610 and 758 could not be combined with carbendazim, tebuconazole, thiram and carboxin for controlling plant diseases, and the pesticide residues to the biocontrol effects should be kept in mind. Chlamydospore preparations of 610 and 758 can be and difenoconazole for controlling plant dis- eases, 758 chlamydospore preparations and germinated chlamydospore of 610 can be combined with metalaxyl for controlling plant diseases, and pesticide residue risk was not serious.

Inhibitory effect of arsenic trioxide on angiogenesis and expression of vascular endothelial growth factor in gastric cancer

AIM: To investigate the inhibitory effect of As2O3 on angiogenesis of tumor and expression of vascular endothelial growth factor (VEGF) in tumor cells in vivo and in vitro. METHODS: The solid tumor model was formed in nude mice with the gastric cancer cell line SGC-7901. The animals were randomly divided into three groups. As2O3 was injected into the arsenic-treated groups (2.5 mg/kg and 5 mg/kg) and the same volume of saline solution was injected into the control group. Microvessel density (MVD) and expression of VEGF were detected with immunofluorescence laser confocal technology. Further expression of VEGF protein and VEGF mRNA was measured with Western bloting and fluorescence quantitative RT- PCR in SGC-7901 cells treated with As2O3. RESULTS: In nude mice, after treatment with 5 mg/kg and 2.5 mg/kg As2O3 respectively, about 50% and 30% tumor growth inhibition were observed correspondingly (P < 0.05, P < 0.05). Decrease in MVD appeared in As2O3-treated tumors compared with control group (P < 0.001, P < 0.001). MVD in tumors was significantly lower in 5 mg/kg group than in 2.5 mg/kg group (P < 0.01). The fluorescence intensity levels of VEGF in tumor cells were significantly lowered in the arsenic-treated groups (P < 0.01, P < 0.01). The fluorescence intensity level of VEGF in 5 mg/kg group was lower than that in 2.5 mg/ kg group (P < 0.01). In vitro, the expression of VEGF protein decreased in dose- and time-dependent manner after the treatment with As2O3, but in VEGF mRNA no significant difference was found between the control group and the treated groups. CONCLUSION: As2O3 can inhibit solid tumor growth by inhibiting the formation of new blood vessels. One of the mechanisms is that As2O3 can inhibit VEGF protein expression.

Effect of arsenic trioxide on vascular endothelial cell proliferation and expression of vascular endothelial growth factor receptors Flt-1 and KDR in gastric cancer in nude mice

AIM： To investigate the effect of arsenic trioxide （As2O3） on expression of vascular endothelial growth factor receptor-1 （VEGFR-1, Flt-1） and VEGFR-2 （KDR） in human gastric tumor cells and proliferation of vascular endothelial cells.METHODS： The solid tumor model was formed in nude mice with the gastric cancer cell line SGC-7901. The animals were treated with As2O3. Microvessel density （MVD） and expression of Flt-1 and KDR were detected by immunofluorescence laser confocal microscopy. SGC-7901 cells were treated respectively by exogenous recombinant human VEGF165 or VEGF165 ＋ As2O3. Cell viability was measured by MTT assay. Cell viability of ECV304 cells was measured by MTT assay, and cell cycle and apoptosis were analyzed using flow cytometry.RESULTS： The tumor growth inhibition was 30.33% and 50.85%, respectively, in mice treated with As2O3 2.5 and 5 mg/kg. MVD was significantly lower in arsenic-treated mice than in the control group. The fluorescence intensity levels of Flt-1 and KDR were significantly less in the arsenic-treated mice than in the control group. VEGF165 may accelerate growth of SGC7901 cells, but As2O3 may disturb the stimulating effect of VEGF165. ECV304 cell growth was suppressed by 76.51%, 71.09% and 61.49% after 48 h treatment with As2O3 at 0.5, 2.5 and 5 μmol/L, respectively. Early apoptosis in the As2O3- treated mice was 2.88-5.1 times higher than that in the controls, and late apoptosis was 1.17-1.67 times higher than that in the controls.CONCLUSION： Our results showed that As2O3 delays tumor growth, inhibits MVD, down-regulates Flt-1 and KDR expression, and disturbs the stimulating effect of VEGF165 on the growth of SGC7901 cells. These results suggest that As2O3 might delay growth of gastric tumors through inhibiting the paracrine and autocrine pathways of VEGF/VEGFRs.

Growth inhibition of high-intensity focused ultrasound on hepatic cancer in vivo

AIM： To investigate the damaging effect of high-intensity focused ultrasound （HIFU） on cancer cells and the inhibitory effect on tumor growth. METHODS： Hurine H22 hepatic cancer cells were treated with HIFU at the same intensity for different lengths of time and at different intensities for the same length oftime in vitro, the dead cancer cells were determined by trypan blue staining. Two groups of cancer cells treated with HIFU at the lowest and highest intensity were inoculated into mice. Tumor masses were removed and weighed after 2 wk, tumor growth in each group was confirmed pathologically.RESULTS： The death rate of cancer cells treated with HIFU at 1 000 W/cm^2 for 0.5, 1, 2, 4, 8, and 12 s was 3.11±1.21%, 13.37±2.56%, 38.84±3.68%, 47.22±5.76%,87.55±7.32%, and 94.33±8.11%, respectively. A positive relationship between the death rates of cancer cells and the length of HIFU treatment time was found （r = 0.96,P〈0.01）. The death rate of cancer cells treated with HIFU at the intensity of 100, 200, 400, 600, 800, and 1 000 W/cm^2 for 8 s was 26.31±3.26%, 31.00±3.87%, 41.97±5.86%,72.23±8.12%, 94.90±8.67%, and 99.30±9.18%, respectively. A positive relationship between the death rates of cancer cells and the intensities of HIFU treatment was confirmed （r= 0.98, P〈0.01）. The cancer cells treated with HIFU at 1 000 W/cm^2 for 8 s were inoculated intomice ed into. The tumor inhibitory rate was 90.35% compared to the control （P〈0.01）. In the experimental group inoculated with the cancer cells treated with HIFU at 1 000 W/cm^2 for 0.5 s, the tumor inhibitory rate was 22.9% （P〈0.01）. By pathological examination, tumor growth was confirmed in 8 out of 14 mice （57.14%, 8/14） inoculated with the cancer cells treated with HIFU at 1 000 W/cm^2 for 8 s, which was significantly lower than that in the control （100%, 15/15, P〈O.05）.CONCLUSION： HIFU is effective on killing or damage of H22 hepatic cancer cells in vitro and on inhibiting tumor growth in mice ex vivo.

Inhibition of human gastric carcinoma cell growth by atofluding derivative N_3-o-toluyl-fluorouracil

AIM： To evaluate the growth inhibition efficacy of atofluding derivative N3-o-toluyl-fluorouracil （TFU） on human gastric carcinoma cell lines SGC-7901 and MKN-45. METHODS： Cell growth inhibition by TFU was measured by MTT and clonogenic assays without or with liver microsomal enzymes. Xenografts of cancer cells in nude mice were employed to study the anti-proliferative effects of TFU in vivo. RESULTS： TFU inhibited the growth of SGC-7901 and MKN-45 cells. However, the inhibitory effects of TFU on cell growth were not significant. The inhibition rates were enhanced in the presence of liver microsomal enzymes, ranging 4.73%-48.57% in SGC-7901 cells and 9.0%-62.02% in MKN-45 cells. In v/vo, TFU delayed the growth of SGC-7901 and MKN-45 cells in nude mice. The inhibition rates were 40.49%, 63.24%, and 75.98% in SGC-7901 cells and 40.76%, 61.41%, and 82.07% in MKN-45 cells when the oral doses were 25, 50, and 100 mg/kg, respectively. TFU treatment was generally well tolerated by mice with less than 20% reduction in body weight. CONCLUSION： TFU inhibits the growth of human gastric carcinoma cells. The inhibition rates are increased in the presence of liver microsomal enzymes. The efficacy of TFU may be associated with the sustaining release of 5-fluorouracil （5-FU） mediated by the enzymes.

Treatment of gastrointestinal neuroendocrine tumors with inhibitors of growth factor receptors and their signaling pathways: Recent advances and future perspectives

The limited efficacy of conventional cytotoxic treatment regimes for advanced gastrointestinal neuroendocrine cancers emphasizes the need for novel and more effective medical treatment options. Recent findings on the specific biological features of this family of neoplasms has led to the development of new targeted therapies, which take into account the high vascularization and abundant expression of specific growth factors and cognate tyrosine kinase receptors. This review will briefly summarize the status and future perspectives of antiangiogenic, mTOR- or growth factor receptor-based pharmacological approaches for the innovative treatment of gastrointestinal neuroendocrine tumors. In view of the multitude of novel targeted approaches, the rationale for innovative combination therapies, i.e. combining growth factor (receptor)-targeting agents with chemo- or biotherapeutics or with other novel anticancer drugs such as HDAC or proteasome inhibitors will be taken into account.

Screening of the Growth-Inhibitory Effects of 168 Plant Species against Lettuce Seedlings

The methanol extracts of 168 plant species from 68 families were evaluated for their inhibitory activity against lettuce seedling elongation. Among the plant species tested, 12 species had EC50 values for radicle growth inhibition ranging from 0.01 to 5.00 mg fresh weight equivalent mL-1. Enterolobium contortisiliquum, a traditionally used herbal medicine, exhibited the strongest inhibitory activity (estimated EC50: 0.28 fresh weight equivalent mL-1). Among the 12 species, Pachysandra terminalis, Tamarindus indica, and Albizia guachapele required investigation, because only little has been reported about their chemical constituents to date. The data in the present study would be useful in finding new lead compounds for natural herbicides.

Growth Inhibition of Breast Cancer in Rat by AAV Mediated Angiostatin Gene

Objective： To observe growth inhibition effect of adeno-associated viral vectors （AAV） mediated angiostatin （ANG） gene on implanted breast cancer in rat and its mechanism. Methods： Gene transfer technique was used to transfer AAV-ANG to the tumor. Growth curves were drawn to observe the growth of breast cancer implanted in rat, and immunohistochemical method was used to detect the effects of angiostatin on microvesel density （MVD） of breast cancer implanted in rat. Results： Angiostatin inhibited the growth of breast cancer implanted in rat and decreased the microvessel density of tumor. Conclusion： Expression of an angiostatin transgene can suppress the growth of breast cancer implanted in rat through the inhibition of the growth of microvessels, surggesting that angiostatin gene transfer technique may be effective against breast cancer.

Dual HER2 inhibition strategies in the management of treatment-refractory metastatic colorectal cancer:History and status

Human epidermal growth factor receptor 2(HER2) signaling pathway activation has been identified as a contributor to de novo or acquired resistance to epidermal growth factor receptor(EGFR) inhibitors in a small subset of patients with metastatic colorectal cancer(mCRC). Dual anti-HER2-targeted treatment exhibits strong antitumor activity in preclinical models of HER2-positive mCRC, supporting its testing in clinical trials. The HERACLES trial at four Italian academic cancer centers has confirmed the effectiveness of dual blockage of HER2 with trastuzumab plus lapatinib in patients with heavily pretreated HER2-positive mCRC, refractory to the anti-EGFR antibodies cetuximab or panitumumab. Here, we reviewed the preclinical studies exploring the role of HER2 signaling in the development of anti-EGFR therapy resistance and discussed the status of clinical trials assessing the activity of HER2 inhibitors in this setting.

Inhibition of invasiveness and expression of epidermal growth factor receptor in human colorectal carcinoma cells induced by retinoic acid

Human amniotic basement membrane (HABM) model and agarose drop explant method were used to in-vestigate the effects of retinoic acid(RA) on the invasive-ness alld adhesiveness to the basement membrane, and the migration of a highly invassive human colorectal cancer cell line CCL229. Results showed that 5 ×106 MRA markedly reduced the in vitro invasiveness and adhesiveness to the HABM, and the migration of the CCL229 cells. In addi-tion, to elucidate the relation between expression of epider-mal growth factor receptor (EGFR) and the invasiveness of the colorectal carcinoma cells, two well-differentiated, but with different invasiveness colorectal cancer cell lines were compared at mRNA level for expressioll of EGFR by using EGFR cDNA probe labeled with digoxigenin (DIG). Expression of EGFR was showll to be markedly higher in the highly invassive CCL229 cells than that in the low in- vasive CX-1 cells. Furthermore, expression of EGFR in RA treated CCL229 cells gradually decreased with time,the level being the lowest on day 6 of the RA treatment.

Growth Inhibition and Apoptosis Induced by Retinoic Acid Combined with Interferon Alpha-2a on Transitional Cell Carcinoma of Bladder

Objective:To identify new favorable agents and develop novel approaches for the chemoprevention and treatment of superficial bladder cancer and investigate the effects of combination of retinoids and interferon α-2a on growth inhibition and apoptosis induction in bladder cancer cell lines. Methods:Four bladder cancer cell lines,grade 1 to 3,and two retinoids,all-trans-retinoic acid(ATRA),9-cis retinoic acid(9cRA),combined with interferon α-2a(INF),were used in the study.We compared the competence of these agents to inhibit growth,induce apoptosis,affect the expression of nuclear retinoid receptors,and modulate STAT1 protein. Results: Most of the bladder cancer cell lines were resistant to the effect of ATRA and 9cRA on growth inhibition and apoptosis induction,even at higher concentration(10 -5M).The effects of ATRA and 9c RA on cell growth and apoptosis were enhanced by INF α- 2a. Combination of ATRA and IFNα-2a induced RARβ and Stat 1 expression in three bladder cancer cell lines. Conclusion:The results demonstrated that INFα-2a synergize with the inhibitory effect of ATRA and 9c RA on the growth inhibition and apoptosis of bladder cancer cells in vitro,which suggested that it has a potential interest for the treatment of transitional cell carcinoma of bladder.

A dual role of selenium in the growth control of seedlings of Stylosanthes humilis

The growth of seedlings of Townsville sytlo (Stylosanthes humilis H.B.K.) is inhibited by aluminium (Al) ions, their elongation being re-covered with sodium selenate at 1.0 μM. Methyl viologen and hydrogen peroxide, reactive oxy-gen species (ROS)-generating compounds, also inhibited seedling elongation and again growth was relieved by selenate. Selenate, thus, seemed to be operating as a ROS quencher, since N-acetylcysteine (NAC), an antioxidant com-pound, also stimulated largely the growth of Al-inhibited seedlings. At a higher concentra-tion (0.1 mM), however, selenate inhibited seed-ling growth and elongation was recovered by NAC. Ethylene production by selenate plus NAC-treated seedlings was very higher and thus the gaseous hormone was not responsible for the seedling growth inhibition caused by sele-nate. Hence, it seems that at high levels sele-nate operates as a ROS-generating compound whose effects were counteracted by NAC. It can be deduced that, at low concentration, sele-nates behave as a ROS quencher and at high level as a ROS-promoting species.

Allelopathic Effects of Adonis vernalis L.: Root Growth Inhibition and Cytogenetic Alterations

A possible alternative to synthetic agricultural chemicals is through the use of allelopathy. Adonis species are rich sources of secondary metabolites. Such allelochemicals offer potential for the development of future pesticides. Allelochemicals influence plant growth and cause morphological alterations. This visible effect could be due to primary effects at cellular or molecular level. Changes in the mitotic activity and disturbances in different phases of mitotic division are accepted as indicators of cytotoxic influence. Mitotic abnormalities and induction of micronuclei in interphase cells are parameters used to determine genotoxicity. The purpose of the current study was to establish the possible allelopathic effect of Adonis vernalis L. water extracts through evaluation of root growth inhibition effect and cytogenetic alterations. Adonis vernalis L. growing wild in Bulgaria was used in the present study. Two types of water extracts were prepared: Hot and Cold Water Extract of A. vernalis (HWЕА and СWЕА). A 72-h root growth inhibition test was provided in order to determine the toxicity level of extracts. EC50 values were determined. For toxicity test, seeds of Triticum aestivum L. cv. GTW were used. Cytotoxic and genotoxic potential of water extracts (EC50) were evaluated using Allium cepa L.-test. The EC50 for HWEA and CWEA was determined 1.83 g/l and 0.78 g/l respectively. Significant influence on mitotic activity values and a marked decrease in percentage of telophase cells were observed after treatment with both extracts. Adonis extracts also induced different mitotic abnormalities in root-tip cells of Allium cepa L. The percent of interphase cells with micronuclei increased significantly only after treatment with HWEA. The results indicated growth inhibitory, cytotoxic and genotoxic effects of crude water extracts of A. vernalis L. These effects demonstrated the presence of water soluble allelochemicals in Adonis aerial parts.