Effects ofFusarium solani naphthazarin toxins on the cytology and ultrastructure of rough lemon seedlings

Two naphthazarin phytotoxins (dihydrofusarubin and isomarticin) produced byFusarium solani were used to determine their effects on the cytology of leaves of rough lemon (Citrus jambhiri Lush) seedlings maintained in a dilute solution of the toxins. Dihydrofusarubin alone or in combination with isomarticin (80:20, v/v) caused cell necrosis above the midveins and lateral veins, plasmolysis or collapse of spongy mesophyll cells, collapse of phloem, depletion of starch, swelling of chloroplasts and disruption of cellular organization. At the ultrastructural level, the toxins affected chloroplast membranes by causing swelling, breaks in outer membranes, granal stack disorganization and swelling of intergranal membranes. The interstromal lamellae appeared as vesicles and sometimes as peripheral reticulum, with an increase in plastoglobuli. The tonoplast was broken or vesiculated. The only membranes not affected by the toxins were those of the nucleus and the mitochondria. This study establishes that the initial toxin effects of these fungal phytotoxins are on organellar membranes, primarily those of the chloroplasts, plasmalemma and tonoplast.Florida Agricultural Experiment Station Journal Series No. R-00648. This paper reports the results of research only. Mention of a trademark, warranty, proprietary product, or vendor does not constitute a guarantee by the US Department of Agriculture and does not imply its approval to the exclusion of other products or vendors that may also be suitable.     

Biological effects of RTX toxins: the possible role of lipopolysaccharide

RTX toxins are a family of related exotoxins with hemolytic, leukotoxic and leukocyte-stimulating activities that are produced by a diverse array of Gram-negative bacteria.

Lipopolysaccharide might be required for the maximal production of some RTX toxins and might be a cofactor in some of the biological effects of RTX toxins.     

The effect of increasing concentrations ofFusarium toxins in the diets for piglets on histological parameters of the uterus

The effects of feeding diets containing 0.01, 0.06, 0.15, 0.22 and 0.42 mg zearalenone and 0.2, 0.8, 1.0, 1.9 and 3.9 mg deoxynivalenol per kg, coming fromFusarium toxin contaminated maize, on the uterus of 50 prepubertal piglets were investigated. The mean weight of the uteri of the animals which received the most contaminated diet was significantly increased at the time of slaughtering. The histological investigation showed no marked differences between the feeding groups. Histometrical parameters of the surface epithelium of the uterus and of the uterine glands were not altered by the treatment. Presented at the 25^th Mykotoxin Workshop in Giessen, Germany, May 19–21, 2003     

A survey of the natural occurrence ofFusarium toxins in wheat grown ina southwestern area of Germany

Wheat for feed use (84 samples) was collected after harvest from 79 farms in a southwestern part of Germany (Baden-Wuerttemberg). The 1987 crop year was characterized by heavy rainfall in the summer months. The internal mycoflora of wheat samples was primarily fusaria, and storage fungi were rarely present. TheFusarium toxins, zearalenone (ZON), - and -zearalenol (,-ZOL), deoxynivalenol (DON), 3-acetyldeoxynivalenol (3-AcDON), nivalenol (NIV), T-2 Toxin (T-2), HT-2 toxin (HT-2) and diacetoxyscirpenol (DAS) were analysed by gas chromatography with mass selective detection (detection limit: 1–3 µg/kg). Each of the samples contained at least one of theFusarium toxins examined except DAS. DON, ZON, 3-AcDON, NIV, T-2, HT-2 and -ZOL were detected in 96%, 80%, 59%, 26%, 26%, 7% and 5% of samples, with an average of 1632, 178, 7, 9, 82, 10 and 23 µg/kg, and a maximum of 20538, 8036, 18, 32, 249, 20 and 71 µg/kg, respectively. -ZOL (12 µg/kg) was found in one sample with -ZOL (71 µg/kg). One, two, three, four, five and sixFusarium toxins were detected in 6%, 27%, 37%, 23%, 4%, and 4% of total samples, respectively. The most frequent combination was that of ZON with DON and 3-AcDON, followed by the combinations ZON/DON and ZON/DON/3-AcDON/NIV in 22, 20, and 11% of total samples, respectively.Abbreviations 3-AcDON 3-Acetyldeoxynivalenol - DAS Diacetoxyscirpenol - DON Deoxynivalenol - HT-2 HT-2 toxin - NIV Nivalenol - T-2 T-2 toxin - -ZOL -Zearalenol - -ZOL -Zearalenol - ZON Zearalenone     

Estradiol and catecholestradiols as possible genotoxic carcinogens

Estradiol and other estrogens are not classified as genotoxic carcinogens, but rather as tumor promoters in the multistage process of carcinogenesis. This study is a reexamination of the carcinogenic status of estradiol and the catecholestradiols (2-OHE2 and 4-OHE2) with the recently developed bacterial assays for genotoxic carcinogens, the Chromotest. The bacterial kits revealed estradiol and catecholestradiols as biphasic and potential genotoxic carcinogens with the following SOS inducing potency values: E2 43,265 (SD 8,300); 2-OHE2 30,153 (SD 2,500), and 4-OHE2 68,939 (SD 4,500). The differences between these values are statistically highly significant (p less than 0.0005). These results were confirmed by studies on Escherichia coli, which showed an increase in cell number and a stimulation of DNA content in the presence of the estrogens. It is therefore concluded that estradiol and the catecholestradiols are possible genotoxic carcinogens which probably act as tumor inducers rather than tumor promoters.     

Investigations of the possible pharmacological effects of organotin(II) complexes

Antitumour, antifertility and histopathological investigations were carried out on male rats by the use of organotin complexes. The organotin complexes were synthesized by the alkylation of [Sn(TAML(n))Cl(2)] (n=1-4 and TAML(n) represents the tetraazamacrocyclic ligands) in the presence of CH(3)I or C(2)H(5)Br. The structures of all the complexes have been established on the basis of elemental analyses, conductivity measurements, IR, (1)H NMR, (13)C NMR, (119)Sn NMR and X-ray spectral data. The antitumour effect of the compounds was examined on swiss mice. The results obtained clearly indicated that the compounds, [C(2)H(5)Sn(TAML(3))C(5)H(5)N] and [C(2)H(5)Sn(TAML(4))C(5)H(5)N] display effective antitumour activity. The emphasis has been given on in vivo study on male albino rats (Rattus norvegicus) by performing serum analyses, blood analyses and fertility test.     

The genotoxic effects of 2,4,5-T

2,4,5-T (2,4,5-trichlorophenoxyacetic acid) is a herbicide that is used primarily for brush and weed control on rangelands and pastures, and rights-of-way. Commercial formulations contain up to 0.1 ppm of the contaminant dioxin (TCDD) which has been shown to cause birth defects and tumors in animals when administered in concentrations below 100 ppt. In many studies (especially in literature prior to 1970) it is not clear whether the reported genotoxic effects are the result of the 2,4,5-T per se, the TCDD contaminant, or a combination of both.The possible harmful effects of 2,4,5-T to humans and wildlife came into prominence during the Vietnam war when the American Army used Agent Orange (equal parts of 2,4-D and 2,4,5-T) for defoliation purposes. The reported increases in the incidence of congenital malformations and certain types of cancer in defoliant-treated regions led to the Bionetics Research Laboratory study in which 2,4,5-T was reported to cause developmental abnormalities in rats.Subsequent research showed that 2,4,5-T is a clastogen producing chromosome aberrations including bridges and micronuclei in a variety of animal and plant species. In addition, 2,4,5-T induces cell enlargement, lengthens the duration of the mitotic cycle, extends DNA synthesis, induces mitosis and causes chromosome contraction, stickiness, and sticky bridges, all at low concentrations. C-Mitoses, multinucleate cells, polyploidy, reduced fertility, and species resistance have also been reported. In vivo production of chromosome aberrations in humans is inconclusive. The emulsifiers and solvents in commercial preparations of 2,4,5-T have also been shown to induce chromosome aberrations. 2,4,5-T is only weakly mutagenic with positive reports recorded in only 2 of 4 sex-linked lethal tests in Drosophila and in one of two studies on Saccharomyces cerevisiae. Only two studies on carcinogenicity from 2,4,5-T are reported with contradictory results. While the data on teratogenicity are not clear-cut, the number of positive reports suggest that 2,4,5-T is definitely teratogenic both with and without TCDD and that 2,4,5-T and TCDD may potentiate teratogenic activity. Further studies, including epidemiological investigations of human groups exposed to 2,4,5-T, are required to supplement insufficient data and to resolve contradictory evidence.     

Plant extracts as modulators of genotoxic effects

Higher plants used extensively in traditional medicines are increasingly being screened for their role in modulating the activity of environmental genotoxicants. The property of preventing carcinogenesis has been reported in many plant extracts. The observation of a close association between carcinogenesis and mutagenesis has extended the survey to include plant extracts and plant products able to modify the process of mutagenesis, which involves alteration in the genetic material. Natural plant products may, apart from inducing mutations, modify the action of other known mutagens on the living organisms by 1) activating the existing mutagens within the cell, 2) inhibiting the production of mutagens in the cell, 3) synergising the activity of existing mutagens, or 4) activating the promutagens within the cell into mutagens. This review deals with data obtained in the course of research on the modulatory effects of plant extracts on mutagenesis and clastogenesis, two genotoxic phenomena associated with carcinogenesis. In screening for antimutagenic effects, extracts of different plant parts have been used, ranging from leafy vegetables, fruits, and underground storage organs to whole plants. The extracts were prepared mainly in water or organic solvents. Several of these assays have indicated the involvement of certain factors that are intrinsic components of the extracts, ranging from specific compounds like ascorbic acid to vegetable fibres which could act as nonspecific redox agents, free radical scavengers, or ligands for binding metals or toxic principles. The possible ways in which inhibitors of mutagenesis can act include the inhibition of interaction between genes and biochemically reactive mutagens and the inhibition of metabolic activation of indirectly acting mutagens. The effects of toxicants can be observed at the level of chromosomes (clastogenesis) through alterations in chromosome structure (chromosomal aberrations) and number (aneuploidy, polyploidy). A wide range of short-term and long-term screening procedures is available. The most common ones use higher plants or rodents in vivo as test systems for monitoring chromosomal aberrations. Experiments with a number of crude vegetable and fruit extracts have demonstrated their anticlastogenic activities against known cytotoxic agents. The individual components of the extracts—e.g., sulfhydryl and flavonoid compounds, gallic acid, ellagic acid, mucic acid, citric acid, reducing sugars, tannin—are observed to have an additive interaction with the major constituents chlorophyll and ascorbic acid, when modulating the effects of the clastogens. Under certain conditions, plant products may induce mutagenic effects, due to the presence of multiple biological properties. Some inhibitors can stimulate simultaneously both enhancing and detoxifying mechanisms, e.g., inducers of coordinated enzyme activities. Many oxidants can, depending on the redox potential, either accept or donate electrons, rendering them protective or harmful. Plants also play an active role in the accumulation, metabolism, and environmental distribution of xenobiotics. The property of plants to activate promutagens that may enter the food chain is of great significance in view of the large number and types of chemicals to which the plants are exposed. A promutagen is a chemical that is not mutagenic itself but that can be biologically transformed by a plant system into a mutagen. Several methods for studying promutagens from plants were developed both in vivo and in vitro, including plant cell-free systems. Both mutagens and antimutagens can be extracted from the same plant extract depending on the nature of solvents used for extraction. Interaction between inhibitors may lead to synergistic effects. Such combined action may take place through the different inhibitors acting at different levels or being localised at different cellular areas. The greater protection afforded by crude plant extract as compared with an equivalent amount of the purified or synthetic ingredients, as observed withPhyllanthus emblica L. andBeta vulgaris L. var.benghalensis Hort., may be related to this phenomenon. Specific biological action of a drug is due to its specific binding to a functional molecular receptor. In complex plant extracts, the variable observed effects can be attributed to the many chemically reactive species that are formed during the processing and ingestion of the extract, which could act as non-specific redox agents, scavengers of free radicals, and ligands for binding to toxicants. The final effects are obviously the outcome of interactions between the components and their individual and collective interaction with the toxicant. The specificity and efficacy of such responses will be influenced also by the physiological factors influencing the plants and the process of administration of the extract. In utilizing pharmacologically active herbs, both beneficial and potential adverse effects must be taken into account. The actual dose and form of the plant also need to be worked out.     

Selenium metabolism in a strain ofFusarium

Fusarium sp. was isolated from Sinai soil at Egypt. It showed tendency to tolerate high concentrations of selenium in the form of sodium selenite up to 3.5% (w/v). The microscopic examination revealed some morphological distortions. However, the fungus was capable to circumvent the toxic effect of selenium. The fungus possesses strong reducing ability as high quantities of elemental selenium were precipitated within the fungal cells as well as on the surface of the fungal hyphae and spores. The presence of selenium increased the cellular contents of carbohydrates, proteins, and lipids. Labeling studies indicate the incorporation of selenite into certain amino acids: selenocysteine and selenocysteic acid. Moreover, the presence of selenium induced the biosynthesis of several types of low molecular weight proteins. The results demonstrated different modes of detoxification of selenium toxicity.     

Antimutagenic effects and possible mechanisms of action of vitamins and related compounds against genotoxic heterocyclic amines from cooked food.

Possible antimutagenic activity of 26 vitamins and related compounds - ascorbic acid, beta-carotene, cyanocobalamin, folic acid, nicotinic acid, nicotinamide, pantothenic acid, pyridoxale, pyridoxamine, pyridoxine, retinal, retinol, retinoic acid, retinyl acetate, retinyl palmitate, riboflavin, riboflavin 5'-phosphate, flavin adenine dinucleotide (FAD), alpha-tocopherol, alpha-tocopherol acetate, vitamins K(1), K(3), K(4), 1, 4-naphthoquinone, and coenzyme Q(10) - was tested against six heterocyclic amine (HCA) mutagens, i.e., 2-amino-3-methyl-imidazo[4, 5-f]quinoline (IQ), 2-amino-3,4-dimethyl-imidazo[4,5-f]quinoline (MeIQ), 2-amino-3,8-dimethyl-imidazo[4,5-f]quinoxaline (MeIQx), 2-amino-1-methyl-6-phenylimidazo[4,5-b]pyridine (PhIP), 2-amino-6-methyl-dipyrido[1,2-a:3',2'-d]imidazole (Glu-P-1) and 3-amino-1-methyl-5H-pyrido[4,3-b]indole (Trp-P-2) in the Salmonella/reversion assay using tester strains Salmonella typhimurium TA 98 and TA 100. Retinol, retinal, riboflavin, riboflavin 5'-phosphate, FAD, vitamins K(1), K(3), K(4), 1, 4-naphthoquinone, and coenzyme Q(10) caused a concentration-dependent decrease in the mutagenicity of all six mutagens in both tester strains. Quantification of antimutagenic potencies by calculating ID(50)1000; vitamin K(1): 401-740; vitamin K(3) (menadione): 85-590; vitamin K(4): 45-313; 1,4-naphthoquinone: 170-290; coenzyme Q(10): 490-860. In general, there were no major differences between HCAs tested except in part with Trp-P-2 nor between the two tester strains. In enzyme kinetic experiments with Salmonella, retinol, vitamins K(3), and K(4) behaved as competitive inhibitors of IQ induced mutagenesis. However, at the highest concentration of menadione (200 nmol/plate) and of riboflavin 5'-phosphate (2000 nmol/plate), non-competitive inhibition was observed. At other concentrations of riboflavin 5'-phosphate and at all concentrations of FAD, meaningful interpretation of enzyme kinetics were not possible. Reduction of the activity of 7-ethoxy- and 7-methoxyresorufin-O-dealkylases with IC(50) values of 2.03-30.8 microM indicated strong inhibition of 1A1 and 1A2 dependent monooxygenases by menadione and retinol. Riboflavin 5'-phosphate and FAD were less effective (IC(50): 110-803.7 microM). Nicotinamide-adenine-dinucleotidephosphate (NADPH) cytochrome P-450 reductase was not affected by retinoids but stimulated by naphthoquinones and both riboflavin derivatives up to about 50 and 80%, respectively. Again, the mutagenic activity of N-hydroxy-2-amino-3-methyl-imidazo[4,5-f]quinoline (N-OH-IQ) in Salmonella was not suppressed by K-vitamins but marginally reduced by retinol, retinal, and FAD but distinctly by riboflavin 5'-phosphate. In various experiments designed for modulation of the mutagenic response, inhibition of metabolic activation of IQ to N-OH-IQ was found to be the only relevant mechanism of antimutagenesis of menadione while a weak contribution of an other way seemed possible for retinol and FAD.     

Preventive effects of supplemental dietary zinc on heat-induced damage in the epididymis of boars

Hyperthermia in boars reduces growth performance and sperm production. Zinc is an essential trace element in animal nutrition. Here we investigate the effects of dietary zinc on epididymal structure and function in Bama miniature pigs treated with heat exposure and investigate approaches to improve the reproductive performance in summer. Male Bama miniature pigs (n=18; aged 6 months; bodyweight=10.79±0.06 kg) were randomly allocated to 3 groups: control group (Control), heat treatment group (HT), and the diet-supplemented and heat treatment group (H+Zn). The Control and HT groups were fed with basal diet and the H+Zn group were fed with basal diet plus 1500 mg/kg zinc daily. After being fed with these 2 different diets for 30 days, pigs in the HT and H+Zn groups were exposed to 5 h of 40 °C heat treatment for 8 days. Rectal temperature and jugular venous blood were collected 3 h after onset of heat exposure on days 1, 4 and 8. Pigs were sacrificed after the termination of heat exposure. Heat treatment increased serum testosterone concentration on day 1 and 4 (P<0.01). In addition, the HT group displayed an increase in the clear cell count and a decrease in epithelium thickness in the caput epithelium (P<0.01, P<0.05), and dietary zinc protected the boars from these impairments (P<0.01, P=0.29). Evaluation of oxidative states showed that heat exposure increased the levels of malondialdehyde (MDA) and glutathione (GSH) in the epididymis (P<0.01, P<0.05), while dietary zinc reduced this elevation (P<0.01, P<0.01). Heat exposure enhanced the glucocorticoid receptor (GR) expression in the nuclei of principal and basal cells (P<0.01, P<0.01) while dietary zinc attenuated the GR immunoreactivity intensity (P<0.01, P<0.01). These results demonstrate that dietary zinc protects the epididymis from high temperature-induced impairment, alleviates oxidative stress, restores the integrity of the caput epithelium and decreases the stress response.     

The occurrence ofFusarium andAlternaria on faba bean seed

The studies on the occurrence ofFusarium andAlternaria in faba bean seed have been conducted for three years. The fungal flora in seed lots from healthy plant and from plant inoculated withAscochyta fabae were determined. In addition the occurrence ofFusarium andAlternaria in three parts of seed: testa, cotyledones, and embryo axis were investigated. It was found thatFusarium andAlternaria were present in faba bean seed, but the frequency of occurrence varied depending upon cultivar and experimental year.     

Absence of genotoxic effects of nonasbestos mineral fibers

The biological activity of natural and synthetic mineral fibers has been examined. Natural attapulgite [(Mg, Al)₂Si₄O₁₀(OH).4H₂0], synthetic xonotlite [Ca₃Si₃O₈(OH)₂] and natural sepiolite [Mg₂Si₃O₈.2H₂O] were selected. Genotoxic effects were investigated by means of a well established cellular model based upon the measurement of unscheduled DNA synthesis (UDS) in rat hepatocytes in primary culture. The intrinsic capacity of the fibers (1 and 10 µ/ml) to induce UDS was first tested. None of the fiber types showed detectable UDS-eliciting activity. Also, the possible modulation of the cellular response to genotoxic agents by the materials was examined by exposing the cells to mixtures of 2-acetylaminofluorene (AAF) (0.05 and 0.25 µg/ml) and fibers (1 and 10 µg/ml). In these experiments, the UDS response was significantly diminished in the presence of xonotlite. This phenomenon may reflect changes in the uptake and/or metabolism of AAF or may result from an inhibition of DNA repair processes, the latter suggesting a possible cocarcinogenic potential for this synthetic silicate. These results point to the immediate necessity of studying more extensively the biological effects of fibrous materials that can be used as substitutes for asbestos.Abbreviations AAF 2-acetylaminofluorene - DMSO dimethyl-sulfoxide - FBS fetal bovine serum - IRDA Institut de Recherche et de Développement sur l'Amiante - LDH lactate dehydrogenase - UDS unscheduled - DNA synthesis - WME Williams' Medium E This work was supported by the Institut de Recherche et de Développement sur l'Amiante (IRDA), Sherbrooke, Canada.     

A study on the genotoxic effects of 8-Cl-cAMP on human lymphocytes in vitro

8-chloro-cyclic adenosine 3',5'-monophosphate (8-Cl-cAMP) is the most potent cAMP analogue that selectively inhibits a variety of cancer cell lines in vitro and tumors in vivo. Its action toward a variety of tumors, especially when coupled with other antitumor agents, have lead to phase I clinical investigations and recently phase II clinical investigations. Until today very little was done to evaluate its genotoxic potential. In order to evaluate its genotoxic potential we used the cytogenetic and cytokinesis block micronucleus assay in vitro on peripheral blood lymphocytes of healthy individuals. Using three concentrations (1 microM, 5 microM and 15 microM), 8-Cl-cAMP in normal human peripheral blood lymphocytes did not induce any cytogenetic aberrations of the structural type [chromatid breakage, isochromatid breakage and gaps], but did induce premature centromere separation (PCS) in all respective doses and increased the frequency of micronuclei (p <0.05) only in the highest dose (15 microM). Antiproliferative action of 8-Cl-cAMP was estimated by using the cytokinesis block nuclear division index (NDI). The results showed a decrease in the NDI of cells exposed to all doses of 8-Cl-cAMP when compared to control. Therefore, the overall results show a genotoxic potential of 8-Cl-cAMP in peripheral blood lymphocytes in vitro.     

A study on the genotoxic effects of 8-Cl-cAMP on human lymphocytes in vitro

8-chloro-cyclic adenosine 3′,5′-monophosphate (8-Cl-cAMP) is the most potent cAMP analog that selectively inhibits a variety of cancer cell lines in vitro and tumors in vivo. Its action toward a variety of tumors, especially when coupled with other antitumor agents, have lead to phase I clinical investigations and recently phase II clinical investigations. Until today, very little was done to evaluate its genotoxic potential. In order to evaluate its genotoxic potential we used the cytogenetic and cytokinesis block micronucleus assay in vitro on peripheral blood lymphocytes of healthy individuals. In three concentrations (1 μM, 5 μM and 15 μM), 8-Cl-cAMP in normal human peripheral blood lymphocytes did not induce any cytogenetic aberrations of the structural type (chromatid breakage, isochromatid breakage and gaps), but did induce premature centromere separation (PCS) at all respective doses and increased the frequency of micronuclei (p < 0.05) only at the highest dose (15 μM). Antiproliferative action of 8-Cl-cAMP was estimated by using the cytokinesis block nuclear division index (NDI). The results showed a decrease in NDI of cells exposed to all doses of 8-Cl-cAMP when compared to control. Therefore, the overall results show a genotoxic potential of 8-Cl-cAMP in peripheral blood lymphocytes in vitro. This article was submitted by the authors in English.     

Cytotoxic and genotoxic effects of sodium hypochlorite on human peripheral lymphocytes in vitro

Chlorination is widely used method in the disinfection of drinking and utility water worldwide. In this study, cytotoxic and genotoxic effects of sodium hypochlorite were investigated by the cytokinesis-block micronucleus assay and chromosomal aberration analysis on human peripheral lymphocytes in vitro. A significant increase in chromosomal aberration frequency was observed in all treatments of NaOCl (0.030, 0.065, 0.100, 0.25, 0.5, 1, 2, 4 μg/mL) at 24 and 48 h compared with the negative control and mitomycin C (MMC, 0.3 μg/mL), which was used as a positive control. NaOCl significantly increased the frequency of micronuclei in a dose dependent manner. The results showed that there was a significant correlation between NaOCl concentration and chromosomal aberration, micronuclei frequency, necrotic cells, apoptotic cells and binucleated cells.     

Clostridial ADP-ribosylating toxins: effects on ATP and GTP-binding proteins

The actin cytoskeleton appears to be as the cellular target of various clostridial ADP-ribosyltransferases which have been described during recent years.Clostridium botulinum C2 toxin,Clostridium perfringens iota toxin andClostridium spiroforme toxin ADP-ribosylate actin monomers and inhibit actin polymerization.Clostridium botulium exoenzyme C3 andClostridium limosum exoenzyme ADP-ribosylate the low-molecular-mass GTP-binding proteins of the Rho family, which participate in the regulation of the actin cytoskeleton. ADP-ribosylation inactivates the regulatory Rho proteins and disturbs the organization of the actin cytoskeleton.     

Investigations of genotoxic activity of antimicrobial/antiviral agent FS-1 in human lymphocytes and tumor cell

A very promising antiviral and antimicrobial agent FS-1 was studied for its ability to induce DNA damage and micronuclei in human tumor cell lines HeLa and Caco-2 at concentrations of 200, 500 and 1000 microg/ml without exogenous metabolic activation. The compound was additionally tested for DNA damaging ability in human lymphocytes at concentrations of 200, 400 and 800 microg/ml. Neither DNA damage nor micronucleus formation was observed after treatment of all types of cells with FS-1. Based on these results, FS-1 can be further studied for its safety to humans for potential application in clinical medicine as an antimicrobial/antiviral drug.