A comparative study of genotoxicity endpoints for women exposed to different levels of indoor radon concentrations.

BACKGROUND AND PURPOSE: Radon and its radioactive progenies are the most important source of ionizing radiation of natural origin, being classified as a Group 1 carcinogen. The aim of this study is to investigate the genotoxic effects of a wide range of indoor radon concentrations, as well as the kinetics of the process of repairing DNA-induced lesions by a challenging dose of gamma irradiation. MATERIAL AND METHODS: Female subjects residing in the Baita-Stei radon priority area were selected as the exposed group. The reference group was comprised of women from the same county (Bihor), but located in an area with an average indoor radon concentration typical of the county from which they were taken. Radon concentration values of 300 Bq/m3 and 148 Bq/m3, respectively, were chosen as a threshold in order to capture the impact of radon exposure between the groups. The alkaline comet assay was used in order to measure the DNA damage, as well as the repair kinetics at 2 and 24 h after 2 Gy challenging doses of gamma irradiation using peripheral blood lymphocytes. From the serum of the subjects, the oxidative damage by 8-hydroxydeoxyguanosine as well as the PARP induction was evaluated. The chromosomal aberrations were evaluated using the Cytokinesis Block MicroNucleus Assay. RESULTS: A statistically significant increase was observed in terms of DNA-induced lesions assessed by comet assay for the exposed group compared to the reference group. A positive correlation was obtained between DNA damage and the annual effective dose, respectively with the radon progenies concentrations. A statistically significant difference was also observed for the frequency of the micronuclei between the exposed - reference groups. Significantly faster repair kinetics of DNA-induced lesions was recorded for the first 2 h after gamma irradiation in the reference group compared to the exposed group. Using the threshold of 300 Bq/m3 for radon concentration, faster kinetics of DNA damage repair for people exposed to low radon concentrations, compared to those exposed to higher concentrations for the second phase of DNA repair kinetics was observed. CONCLUSION: An increased radiosensitivity of lymphocytes, as well as slower repair kinetics, may be associated with exposure to higher indoor radon concentrations.

The Future of Stem Cells and Their Derivates in the Treatment of Glaucoma. A Critical Point of View.

This review focuses on the clinical translation of preclinical studies, especially those that have used stem cells in the treatment of glaucoma, with an emphasis on optic nerve regeneration. The studies referred to in the review aim to treat optic nerve atrophy, while cell therapies targeting other sites in the eye, such as the trabecular meshwork, have not been addressed. Such complex and varied pathophysiological mechanisms that lead to glaucoma may explain the fact that although stem cells have a high capacity of neuronal regeneration, the treatments performed did not have the expected results and the promise offered by animal studies was not achieved. By analyzing the facts associated with failure, important lessons are to be learned: the type of stem cells that are used, the route of administration, the selection of patients eligible for these treatments, additional therapies that support stem cells transplantation and their mode of action, methods of avoiding the host's immune response. Many of these problems could be solved using exosomes (EV), but also miRNA, which allows more targeted approaches with minimal side effects.

Multilayered Porous Titanium-Based 3rd Generation Biomaterial Designed for Endosseous Implants.

This work proposes a novel complex multi-layered material consisting of porous titanium as a substrate and a complex coating consisting of a chitosan film engulfing microsphere loaded with growth factors such as BMP2 (bone morphogenic protein 2) and IGF1 (insulin-like growth factor-1). The microspheres were obtained through deposition of dual layers of calcium cross linked pectin-chitosan/pectin polyelectrolyte onto a BSA (bovine serum albumin) gel core. The multilayer was conceived to behave like a 3rd generation biomaterial, by slow delivery of viable growth factors around implants, and to assist the healing of implantation wound and the development of new vital bone. The biologic effect of the delivery of growth factors was studied in vitro, on MSC-CD1 mesenchymal stem cells, and in vivo, on CD1 mice. Proliferation and differentiation of cells were accelerated by growth factors, especially IGF1 for proliferation and BMP2 for differentiation. In vivo tests analyzed histologically and by MicroCT show a more structured tissue around BMP2 samples. The present concept will give the best clinical results if both growth factors are delivered together by a coating film that contains a double population of microcarriers.

The expression of copper transporters associated with the ototoxicity induced by platinum-based chemotherapeutic agents.

BACKGROUND: Antitumor agents based on platinum have gained a well-established place in the treatment of several forms of cancer. Their efficiency is hampered by serious toxic effects against healthy tissues as well. Ototoxicity is a serious side effect leading to hearing impairment and represents an important issue affecting the patients' quality of life. The currently used platinum chemotherapeutics exert different toxicity towards cochlear cells. The aim of our study was to answer some questions regarding the differential uptake and cellular pharmacodynamics of Cisplatin (CDDP), Carboplatin (CBDCA) and Oxaliplatin (L-OHP) in the HEI-OC1 cochlear cell line. METHODS: We studied the expression of copper transporters CTR1, ATP7A and ATP7B which are presumably involved in the uptake, cellular transport and efflux of platinum compounds by immunofluorescence microscopy and flow-cytometry. The cellular uptake of the compounds was evaluated through the determination of intracellular platinum concentration by atomic absorption spectroscopy. The effects of the treatment of HEI-OC1 cells with platinum compounds were also evaluated: cytotoxicity with the Cell Titer Blue viability test, formation of reactive oxygen species with 2',7' -dichlorofluorescein diacetate, genotoxicity with the comet assay and apoptosis with the cleaved PARP ELISA test. RESULTS: CTR1, ATP7A and ATP7B were all expressed by HEI-OC1 cells. The treatment with the platinum compounds led to a modulation of their expression, manifested in a differential platinum uptake. Treatment with Cisplatin led to the highest intracellular concentration of platinum compared to Oxaliplatin and Carboplatin at the same dose. Treatment with CuSO4 reduced platinum uptake of all the compounds, significantly in the case of Cisplatin and Carboplatin. CDDP was the most cytotoxic against HEI-OC1 cells, with an IC50 = 65.79  µM, compared to 611.7 µM for L-OHP and 882.9 µM for CBDCA, at the same molar concentration. The production of ROS was the most intense after CDDP, followed by L-OHP and CBDCA. In the comet assay, at the 100 µM concentration, L-OHP and CBDCA induced DNA adducts while CDDP induced adducts as well as DNA strand breaks. CBDCA and L-OHP lead to a significant increase of cleaved PARP at 24h (p < 0.001), suggesting an important apoptotic process induced by these compounds at the used concentrations. CONCLUSIONS: The results obtained in the current study suggest that the modulation of copper transporters locally may represent a new strategy against platinum drugs ototoxicity.

Low-dose radiations derived from cone-beam CT induce transient DNA damage and persistent inflammatory reactions in stem cells from deciduous teeth.

OBJECTIVES: Cone-beam CT (CBCT), a radiographic tool for diagnosis, treatment, and follow-up in dental practice, was introduced also in pediatric radiology, especially orthodontics. Such patients subjected to repetitive X-rays examinations may receive substantial levels of radiation doses. Ionizing radiation (IR), a recognized carcinogenic factor causing DNA double-strand breaks (DSBs) could be harmful to undifferentiated cells such as dental pulp stem cells (DPSCs) since inaccurately repaired or unrepaired DSBs may lead to malignant transformation. The H2AX and MRE11 proteins generated following DSBs formation and pro-inflammatory cytokines (CKs) secreted after irradiation are relevant candidates to monitor the cellular responses induced by CBCT. METHODS: DPSCs were extracted from human exfoliated deciduous teeth and their phenotype was assessed by immunocytochemistry and flow-cytometry. Cells were exposed to IR doses: 5.4-107.7 mGy, corresponding to 0.5-8 consecutive skull exposures, respectively. H2AX and MRE11 were detected in whole cells, while IL-1α, IL-6, IL-8, TNFα in supernatants, using enzyme-linked immunosorbent assay (ELISA) at different time points after exposure. RESULTS: The phosphorylation level of H2AX in DPSCs increased considerably at 0.5 h after exposure (p < 0.001 for 3, 5, 8 skull exposures and p < 0.05 for 1 skull exposure, respectively). MRE11 response could only be detected for the highest IR dose (p < 0.001) in the same interval. CKs secretion increased upon CBCT exposure according to doses and time. CONCLUSIONS: The DPSCs exposure to CBCT induces transient DNA damage and persistent inflammatory reaction in DPSCs drawing the attention on the potential risks of IR exposures and on the importance of dose monitoring in pediatric population.

Targeting MAPK (p38, ERK, JNK) and inflammatory CK (GDF-15, GM-CSF) in UVB-Activated Human Skin Cells with Vitis vinifera Seed Extract.

Ultraviolet B radiation (UVB) activates mitogen-activated protein kinases (MAPK): p38, extracellular signal regulated (ERK), and c-Jun N-terminal (JNK) kinases in human skin cells. Human keratinocytes (KC) exposed to UVB secrete several cytokines (CK), among which the growth differentiation factor-15 (GDF-15) is augmented in inflammatory and aging processes and the granulocyte macrophage-colony stimulating factor (GM-CSF) is involved in cell proliferation, differentiation, and survival, and both CK have implications in skin carcinogenesis. We assessed p38, ERK, JNK, GDF-15, and GM-CSF in UVB-exposed skin cells and a red grape (Vitis vinifera) seed extract's (GSE) capacities to regulate these pathways in UVB-exposed KC. Two concentrations of the GSE extract were selected: GSE1 (37.5 µgEqGA/mL) and GSE2 (75 µgEqGA/mL) and a UVB dose (100 mJ/cm2) within the physiological range. Molecules were assessed with ELISA, semiquantitative results being confirmed by Western blot. UVB triggered the signaling molecules' phosphorylation and the concentrations of CK. All molecules but GM-CSF increased early, at 2 h, from UVB exposure while GM-CSF increased later (at 8 h). MAPK and GDF-15 were regulated by GSE1; GM-CSF, by the higher concentration, GSE2. The amplitude and kinetics of the responses were diverse according to time point, molecules, and the extract's concentration. GSE exerted beneficial effects on MAPK and CK triggered by UVB in human skin cells: reduction of phosphorylation of the assessed signaling molecules and anti-inflammatory effects. Targeting MAPK and specific inflammatory mediators such as GDF-15 and GM-CSF with GSE in UVB-induced skin cells represents a novel and a promising starting point for future photoprotection strategies.

SChitosan-capped gold nanoparticles impair radioresistant glioblastoma stem-like cells.

PURPOSE: Glioblastoma is a rapidly evolving lethal disease mainly due to its highly chemo- and radioresistant glioblastoma stem cells (GSCs). Herein, we tested if chitosan-capped gold nanoparticles (Chit-GNPs) may overcome the limitations of drug concentrations by increased cell internalization in GSCs and if such GNPs could enhance the response to irradiation. METHODS: Chitosan was used for Chit-GNP synthesis as a reducing and stabilizing agent. Chit-GNPs were characterized by spectroscopy, dark field, transmission electron microscopy and zeta potential measurements. Patient-derived GSCs and human osteoblasts were treated with increasing concentrations of nanoparticles and irradiated. The uptake and cytotoxicity of Chit-GNPs were compared to that of uncoated GNPs. RESULTS: The positively-charged, 26 nm-sized, spherical Chit-GNPs, showed a huge intracellular accumulation into the cytosol, lysosomes and near the nucleus, whereas no uncoated GNPs were internalized within GSCs. Surprisingly, Chit-GNPs were highly cytotoxic for GSCs irrespective of cell irradiation, that failed to add an additional benefit when combined with Chit-GNPs/GNPs. Moreover, Chit-GNPs were selectively cytotoxic for GSCs and did not affect the normal cells, despite an increased nanoparticle internalization. CONCLUSIONS: The important Chit-GNP internalization and their selective cytotoxicity for GSCs make this compound a potential novel anticancer agent and a promising backbone for drug delivery in glioblastoma.

G.I.S. Surveillance of Chronic Non-occupational Exposure to Heavy Metals as Oncogenic Risk.

INTRODUCTION: The potential oncogenic effect of some heavy metals in people occupationally and non-occupationally exposed to such heavy metals is already well demonstrated. This study seeks to clarify the potential role of these heavy metals in the living environment, in this case in non-occupational multifactorial aetiology of malignancies in the inhabitants of areas with increased prevalent environmental levels of heavy metals. METHODS: Using a multidisciplinary approach throughout a complex epidemiological study, we investigated the potential oncogenic role of non-occupational environmental exposure to some heavy metals [chrome (Cr), nickel (Ni), copper (Cu), zinc (Zn), cadmium (Cd), lead (Pb) and arsenic (As)-in soil, drinking water, and food, as significant components of the environment] in populations living in areas with different environmental levels (high vs. low) of the above-mentioned heavy metals. The exposures were evaluated by identifying the exposed populations, the critical elements of the ecosystems, and as according to the means of identifying the types of exposure. The results were interpreted both epidemiologically (causal inference, statistical significance, mathematical modelling) and by using a GIS approach, which enabled indirect surveillance of oncogenic risks in each population. RESULTS: The exposure to the investigated heavy metals provides significant risk factors of cancer in exposed populations, in both urban and rural areas [ χ2 test (p < 0.05)]. The GIS approach enables indirect surveillance of oncogenic risk in populations. CONCLUSIONS: The role of non-occupational environmental exposure to some heavy metals in daily life is among the more significant oncogenic risk factors in exposed populations. The statistically significant associations between environmental exposure to such heavy metals and frequency of neoplasia in exposed populations become obvious when demonstrated on maps using the GIS system. Environmental surveillance of heavy metals pollution using GIS should be identified as an important element of surveillance, early detection, and control of neoplastic risks in populations, at the level of a single locality, but even on a wider geographical scale.

Comparative in vitro study regarding the biocompatibility of titanium-base composites infiltrated with hydroxyapatite or silicatitanate.

BACKGROUND: The development of novel biomaterials able to control cell activities and direct their fate is warranted for engineering functional bone tissues. Adding bioactive materials can improve new bone formation and better osseointegration. Three types of titanium (Ti) implants were tested for in vitro biocompatibility in this comparative study: Ti6Al7Nb implants with 25% total porosity used as controls, implants infiltrated using a sol-gel method with hydroxyapatite (Ti HA) and silicatitanate (Ti SiO2). The behavior of human osteoblasts was observed in terms of adhesion, cell growth and differentiation. RESULTS: The two coating methods have provided different morphological and chemical properties (SEM and EDX analysis). Cell attachment in the first hour was slower on the Ti HA scaffolds when compared to Ti SiO2 and porous uncoated Ti implants. The Alamar blue test and the assessment of total protein content uncovered a peak of metabolic activity at day 8-9 with an advantage for Ti SiO2 implants. Osteoblast differentiation and de novo mineralization, evaluated by osteopontin (OP) expression (ELISA and immnocytochemistry), alkaline phosphatase (ALP) activity, calcium deposition (alizarin red), collagen synthesis (SIRCOL test and immnocytochemical staining) and osteocalcin (OC) expression, highlighted the higher osteoconductive ability of Ti HA implants. Higher soluble collagen levels were found for cells cultured in simple osteogenic differentiation medium on control Ti and Ti SiO2 implants. Osteocalcin (OC), a marker of terminal osteoblastic differentiation, was most strongly expressed in osteoblasts cultivated on Ti SiO2 implants. CONCLUSIONS: The behavior of osteoblasts depends on the type of implant and culture conditions. Ti SiO2 scaffolds sustain osteoblast adhesion and promote differentiation with increased collagen and non-collagenic proteins (OP and OC) production. Ti HA implants have a lower ability to induce cell adhesion and proliferation but an increased capacity to induce early mineralization. Addition of growth factors BMP-2 and TGFß1 in differentiation medium did not improve the mineralization process. Both types of infiltrates have their advantages and limitations, which can be exploited depending on local conditions of bone lesions that have to be repaired. These limitations can also be offset through methods of functionalization with biomolecules involved in osteogenesis.

Oxaliplatin induces different cellular and molecular chemoresistance patterns in colorectal cancer cell lines of identical origins.

BACKGROUND: Cancer cells frequently adopt cellular and molecular alterations and acquire resistance to cytostatic drugs. Chemotherapy with oxaliplatin is among the leading treatments for colorectal cancer with a response rate of 50%, inducing intrastrand cross-links on the DNA. Despite of this drug's efficiency, resistance develops in nearly all metastatic patients. Chemoresistance being of crucial importance for the drug's clinical efficiency this study aimed to contribute to the identification and description of some cellular and molecular alterations induced by prolonged oxaliplatin therapy. Resistance to oxaliplatin was induced in Colo320 (Colo320R) and HT-29 (HT-29R) colorectal adenocarcinoma cell lines by exposing the cells to increasing concentrations of the drug. Alterations in morphology, cytotoxicity, DNA cross-links formation and gene expression profiles were assessed in the parental and resistant variants with microscopy, MTT, alkaline comet and pangenomic microarray assays, respectively. RESULTS: Morphology analysis revealed epithelial-to-mesenchymal transition in the resistant vs parental cells suggesting alterations of the cells' adhesion complexes, through which they acquire increased invasiveness and adherence. Cytotoxicity measurements demonstrated resistance to oxaliplatin in both cell lines; Colo320 being more sensitive than HT-29 to this drug (P < 0.001). The treatment with oxaliplatin caused major DNA cross-links in both parental cell lines; in Colo320R small amounts of DNA cross-links were still detectable, while in HT-29R not. We identified 441 differentially expressed genes in Colo320R and 613 in HT-29R as compared to their parental counterparts (at least 1.5 -fold up- or down- regulation, p < 0.05). More disrupted functions and pathways were detected in HT-29R cell line than in Colo320R, involving genes responsible for apoptosis inhibition, cellular proliferation and epithelial-to-mesenchymal transition. Several upstream regulators were detected as activated in HT-29R cell line, but not in Colo320R. CONCLUSIONS: Our findings revealed a more resistant phenotype in HT-29R as compared to Colo320R and different cellular and molecular chemoresistance patterns induced by prolonged treatment with oxaliplatin in cell lines with identical origins (colorectal adenocarcinomas).

Grape seed extract as photochemopreventive agent against UVB-induced skin cancer.

BACKGROUND: In the recent years, the use of natural antioxidants as photochemoprotective agents against skin damages produced by ultraviolet radiation gained considerable attention. Our goal was to show that the hydroethanolic extract obtained from red grape seeds, Burgund Mare (BM) variety could have a protective effect on keratinocytes exposed to UVB radiation. MATERIALS AND METHODS: HaCaT keratinocytes were treated with BM extract 30 min. before UVB exposure. The effect was evaluated by assessing cell viability with MTT; the generation of lipid peroxides with malondialdehide (MDA) assay; DNA damage using comet assay; the quantification of DNA photolesions by ELISA and apoptosis by immunocytochemistry with AnnexinV. RESULTS: After irradiation with UVB, HaCaT cells pretreated with BM showed: increased cell viability compared to those exposed to UVB only; significantly lower lipid peroxides level; the lesion scores and DNA photolesions were significantly lower and a significant reduction of the cells undergoing apoptosis. CONCLUSIONS: These results recommend the use of the BM extract as photochemoprotective agent as such or in combination with sunscreens and/or other natural products with similar or complementary properties.

Assessment of cytotoxicity, apoptosis and DNA damages in Colo320 colorectal cancer cells selected for oxaliplatin resistance.

Despite the notable efficacy of oxaliplatin in the treatment of colorectal cancers, the metastatic tumours ultimately become resistant to the drug. This study investigated whether the oxaliplatin-resistant cells display different behaviour to this drug versus the sensitive cells and if this difference may be further exploited into the clinical treatments improvement. In order to establish a stable cell line resistant to oxaliplatin, a human colorectal cancer cell line (Colo320) was exposed to increasing doses of the drug up to the clinically relevant plasma concentration. Four cell groups with different levels of chemoresistance were subjected to additional doses of oxaliplatin, and their cytotoxicity, apoptosis and DNA damage production were assessed. Cells selected for resistance to oxaliplatin reacted differently to the application of additional doses of the drug, displaying lower toxicity and cellular death and fewer DNA cross-links formation, in accordance with the extent of the oxaliplatin pretreatments. As the cross-links formation by oxaliplatin being the main cause for cytotoxicity of this drug and a correlation between cytotoxicity and clinical outcome being shown repeatedly, we consider that the evaluation of oxaliplatin-induced cytotoxicity, apoptosis and DNA damage could be a valuable tool to assess the tumour cells sensitivity and thus to predict the response to chemotherapy.

Expression of VEGF, VEGFR, EGFR, COX-2 and MVD in cervical carcinoma, in relation with the response to radio-chemotherapy.

INTRODUCTION: Despite the improvement in the treatment results due to modern irradiation techniques and to the association of chemo-radiotherapy, cervical cancer remains an unsolved problem of oncology both due to the increased rate of local failures and of the distant metastasis. Efforts to implement new therapeutic strategies in order to obtain better results in patients with cervical cancer appear justified. Neovascularization is an important step in the tumor progression and the therapeutic targeting of the tumor blood vessels appears to be a good strategy to follow in the anti-cancer treatment. Thus, even in an incipient phase of the clinical research process, the combination between the anti-angiogenic aimed therapies and the current radio-chemotherapy seems to represent a new, feasible and promising approach. The aim of the present study was to determine the prognostic and/or predictive value of some biological markers of tumor angiogenesis and of their implication in increasing the efficacy of current treatments for this cancer. MATERIALS AND METHODS: So far, 54 women were included in a prospective trial: 44 having an advanced cervical carcinoma and 10 healthy women, as controls. A tumor biopsy and a blood sample were obtained from each patient before the start of therapy. The density of microvascularization was assessed using CD34 monoclonal antibody (hot spot technique), the expression of angiogenic factors VEGFR, EGFR and COX-2 were determined in tumor biopsies by specific immunohistochemistry techniques, using primary antibodies anti-EGFR, anti-VEGF and anti-COX-2 respectively. The quantitative polymerase chain reaction (Real Time PCR) was employed for assessing the expression level of the genes involved. Serum VEGF was determined by quantitative ELISA technique. RESULTS: Among the studied clinical and molecular factors, we found to be predictive for the type of response the following factors: tumor size at diagnosis (p=0.01), VEGFR2 expression (p=0.02) and a tendency to significance for patients' age (p=0.06). From the large panel of studied markers it was observed correlation between MVD expression with stromal COX-2 (p=0.01) and a tendency with epithelial COX-2 (p=0.06). Stromal COX-2 has higher correlation with VEGFR2 (p=0.01) and MVD (p=0.01) and also has a lower correlation with tumor size (p=0.08). CONCLUSIONS: Univariate analysis demonstrates that the response to radio-chemotherapy in cervical cancer is related to a set of clinical and molecular factors as: the tumor size, the expression of VEGFR2 as mRNA level and the patients' age. Unfortunately, the multivariate analysis by logistic model selects only VEGFR2 expression for prediction of tumor response. The interrelations between the different biomarkers demonstrate the complexity of the tumor progression process and the necessity of further studies to identify new therapeutic targets.

Effects of 60Co gamma-rays on human osteoprogenitor cells.

BACKGROUND: Radiation therapy is one of the most efficient treatments of neoplastic diseases used worldwide. However, patients who undergo radiotherapy may develop side effects that can be life threatening because tissue complications caused by radiation-induced stem cell depletion may result in structural and functional alterations of the surrounding matrix. This treatment also damages the osteogenic activity of human bone marrow by suppressing osteoblasts, leading to post-irradiation sequelae. Even if widely used in oncology, there is still little information on the fate and potential therapeutic efficacy of electromagnetic rays. MATERIAL AND METHODS: We addressed this question using both human mesenchymal stem cells and osteoblasts. Monoclonal antibody characterization identified specific surface markers for stem cells (SSEA-4, CD29, CD105, Oct 3, Nanog and SOX2) and osteoblasts (Osteopontin and Osteonectin). The technique of anti-alkaline phosphatase FITC-staining demonstrated the presence of this specific ectoenzyme. Cells were cultured in complex osteogenic medium (DMEM, 15% fetal calf serum, non-essential amino acids, L-glutamine, dexametazone, ascorbic acid, insulin, TGF-beta, BMP-2 and beta-glycero-phosphate) after being irradiated at 0.5 Gy, 1 Gy, 2 Gy and 4 Gy using a Theratron 1000 60Co source. The viability of irradiated cells was assessed using Trypan Blue staining. The comparison between cell lineages after culture in osteogenic media regarding phenotypical characterization and the intensity of the mineralization process included histology stainings (Alizarin Red S, Alcian Blue and von Kossa), and the MTT-based proliferation assay. RESULTS: After irradiation, the proliferation and differentiation of osteoprogenitor cells is dose-dependent. CONCLUSIONS: This study is one among the first papers investigating the biophysics of low-dose gamma-irradiation on stem cell culture, focusing on the potential applications in radiation oncology and various palliative treatments.

The CellScan technology for in vitro studies on novel platinum complexes with organoarsenic ligands.

The present paper examines one of the multiple uses of the CellScan technique, its utilization in the biological evaluation of novel compounds, in order to improve the methods concerning the prediction of their anti-proliferative effects and application as anti-cancer drugs. The CellScan is a laser scanning static cytometer, enabling repetitive spectroscopic measurements in intact living cells. The detection of cell viability and apoptosis is possible, based on the transformations that occur in the cytoplasm matrix of tumour cells influenced by cytotoxic compounds. The measurement of fluorescence changes, due to this phenomenon, is possible with the CellScan system. The potential of this technology to detect the in vitro effects of the inhibitory molecules on tumour cells was demonstrated, making this method a valuable tool for chemosensitivity tests. We synthesized and fully characterised three novel platinum complexes of tertiary arsine ligands: trans-[PtI2(2-iPrOC6H4AsPh2)2] (), trans-[PtCl2(2-MeOC6H4AsPh2)2] () and cis-[PtCl2(2-HOC6H4AsPh2)2] (). The three compounds are biologically active against tumour cells and their cytotoxicity is comparable with standard drugs. Measurements using the CellScan technology correlate well with the results provided by other bioassay methods.