966) and NK-κB (docking score = −9.274) compared to acetylsalicylic acid 3 (docking score for COX-2 = −5.412; for NK-κB = −5.525) [13]. Furthermore, salicylates Galunisertib cost exhibit other biological activities, including anticancer and anti-proliferation [12]. The significance of β-d-salicin 1 molecule may encourage further understanding into its cross-biological function. Therefore, the aim of this article is to explore the mechanistic biosynthetic pathways of β-d-salicin 1, its metabolism and discuss the genetic cross-talk between pants and humans. β-d-Salicin 1 or

2-(hydroxymethyl) phenyl-O-β-d-glucopyranoside is the first phenolic glycoside discovered in nature with a molecular mass of 286.27782 g/mol. Its IUPAC name is (2R,3S,4S,5R,6S)-2-(hydroxymethyl)-6-[2-(hydroxymethyl) phenoxy]oxane-3,4,5-triol. β-d-Glucose 4 moiety of β-d-salicin 1

contributes to all five chiral carbon centres. The chemical structure of β-d-salicin 1 encompasses β-d-glucose 4 and 2-hydroxybenzyl alcohol, or salicyl alcohol 5. β-d-Salicin 1 contains seven oxygen atoms, as H-bond acceptor and five hydroxyl groups, as H-bond donors. It 1 also possesses nine rotational buy Panobinostat bonds that control its conformational structure. In addition, the β-d-glucose 4 and salicyl alcohol 5 moieties are bonded by β-1,1′-d-glycosidic bond. These chemical features contribute to the polarity of β-d-salicin 1. Therefore, the extraction of β-d-salicin 1 requires a polar solvent system, such as boiling water and ethyl alcohol. In addition, the presence of d-glucose 4 moiety contributes to the enhancement of physcochemical properties of β-d-salicin 1. Although there have been long-standing biotic and abiotic interests in β-d-salicin 1, no defined biosynthetic pathway, genes or enzymes have been illustrated in the literature [14] and [15]. Nonetheless, adapting the biotechnological approach and utilising leave tissues and radio labelled precursors have elucidated some biosynthetic

aspects of β-d-salicin 1 in Salix and Populous [16] and [17]. It reveals that the biosynthesis of β-d-salicin 1 is associated with phenylpropanoid pathway that starts with l-phenylalanine 6 ( Scheme 1). Using radiolabled precursors indicate that the biosynthesis of β-d-salicin 1 encompasses five steps: deamination, ortho-hydroxylation, Digestive enzyme β-oxidation, C2 unite elimination and glucosylation [7] and [16]. l-Phenylalanine 6 is available in plants and readily biotransforms into trans cinnamic acid 7 by phenylalanine ammonialyase (PAL) [18]. Thereby, plants produce a large number of organic compounds via this biotransformation [19]. The catalysis of l-phenylalanine 6 involves deamination of the amino group of α-amino acid. The mechanism of this biotransformation involves the formation of an enzyme-substrate complex, generating a carbonium ion intermediate which subsequently induces the elimination of the 3-pro-S proton giving trans-cinnamic acid 7 in a stereospecific manner ( Scheme 2).

, 2010). The phenomenon has been confirmed by Bowley et al. (2010) who PLX3397 mouse had reported 10% of intersex at the same site and found individuals with testis-ova at other contaminated sites of the Harbour. In most of Canadian intersex oocytes were in previtellogenic or vacuolization stages. Whereas, single individuals, from the most contaminated site, showed advanced stages of oocytes development, i.e. late vitellogenic ova ( Bowley et al., 2010 and Marentette et al., 2010) and some of them did not show development of seminiferous lobules ( Marentette et al., 2010). In both studies feminization of urogenital papilla has been shown to be a useful

indicator of exposure to EDCs as it was reported only in males CH5424802 mw collected at contaminated sites, while at less polluted and cleaner sites, chosen as reference sites, no urogenital papilla changes nor intersex in males were observed. Since PAHs and PCBs were the major contaminants in sediments at sites, where endocrine disruptions in N. melanostomus were identified, they are thought to be one of the most likely agents responsible for the observed disruptions ( Bowley et al., 2010 and Marentette et al., 2010). In the Baltic Sea, as particularly susceptible

to develop intersex in contaminated environment turned out to be Z. viviparus, which since over a decade has been used in research concerning the impact of EDCs in coastal waters of such countries as Germany, Denmark or Sweden ( Förlin, 2012, Gercken and Sordyl, 2002, Gercken and Sundt, 2007 and Strand et al., 2009). Nevertheless, there were no reports or studies concerning the presence of intersex in Z. viviparus, nor in any other fish species, in the Gulf of Gdańsk. If more comprehensive research indicated that the phenomenon

of intersex in N. melanostomus from the Gulf of Gdańsk is a response to EDCs, N. melanostomus could be suggested as a sentinel species in endocrine disruption Aurora Kinase research, not only in the Gulf but also in other regions of the Baltic Sea invaded by this species. In conclusion, this is the first report of intersex in the invasive N. melanostomus from the Baltic Sea as well as intersex fish in Polish coastal waters. The occurrence of intersex individuals and feminization of secondary sexual characteristics might indicate that N. melanostomus inhabiting coastal waters of the Gulf of Gdańsk was exposed to estrogenic EDCs. However, as only two stations were studied and intersex was observed in single individuals, which might suggest occurrence of spontaneous intersex, an extended study need to be carried out in order to determine the range of the occurrence and the baseline levels of N. melanostomus intersex in the Gulf. Investigations are also necessary to better characterize possible endocrine disrupters at the investigated stations and other areas of the Gulf of Gdańsk. Moreover, if it is shown that the occurrence of intersex is the result of exposure to EDCs, N.

Genes were assigned to functional categories using gene ontology in the Database for Annotation, Visualization and Integrated Discovery (DAVID) (Dennis et al., 2003). BMDExpress was used to calculate benchmark doses (BMDs) from gene expression data (Yang et al., 2007). Analyses were performed on genes that were identified as statistically significant by one-way ANOVA (p < 0.05) using four models: Hill, Power, Linear and 2° Polynomial. Models that described the data with the least complexity were selected. A nested chi-square

NVP-BKM120 mw test, with cutoff of 0.05, was first used to select among the linear and 2° polynomial model, followed by comparison of Akaike information criterion (AIC), which measured the relative goodness of fit of a statistical model, between nested models and the power model. The model with the lowest AIC was selected as the best fit. A maximum of 250 Dasatinib iterations and a confidence level of 0.95 were selected. For functional classifications and analyses, the resulting BMD datasets were mapped to KEGG pathways

with promiscuous probes removed (probes that mapped to multiple annotated genes). BMDs that exceeded the highest exposure dose (TSC= 90 μg/ml, MSC = 10 μg/ml) were removed from the analysis. Three RT-PCR pathway specific arrays (cell cycle, apoptosis and stress and toxicity) were used to validate the expression of specific microarray genes (SABiosciences, Frederick, Cediranib (AZD2171) MD, USA). Eight nanograms of total RNA, from the same samples that were used for the microarray study, were reverse transcribed to cDNA using an RT2 First Strand Kit (SABiosciences, Frederick, MD, USA). cDNA was mixed with the RT2 qPCR Master Mixes and aliquoted into 96-well plates containing primers for 84 pathway specific genes. Expression levels

were evaluated using a CFX96 real-time Detection System (BioRad, Philidelphia, PA, USA). Relative gene expression was normalized to the Gapdh housekeeping gene, which remained unaffected under experimental conditions. Fold changes and statistical significance (student’s t-test) were calculated using the REST method for statistical significance ( Pfaffl et al., 2002). For the LDH assay, a sharp increase in toxicity was observed for MSC exposures above 6 μg/ml. The response remained high (approx. 375% of control) for all subsequent concentrations. The MSC response was approximately 3 times greater than that observed for TSC, which showed a gradual increase in toxicity between 3 and 30 μg/ml and high toxicity (above 200% of control) above 30 μg/ml. For the XTT assay, exposure to MSC concentrations greater than 6 μg/ml reduced mitochondrial dehydrogenase levels to below 80% of control values. In comparison, similar reductions required TSC concentrations above 30 μg/ml TSC. For the microarray study, FE1 cells were exposed to 2.5, 5 and10 μg/ml of MSC and 25, 50 and 90 μg/ml of TSC.

For most of our history, humans could do little to protect themselves against infectious diseases as dramatically illustrated by the influenza pandemic of 1918–1919. However, over the past four centuries vaccines have had an immeasurable impact on human health. In the 18th century the development of the vaccinia virus vaccine provided a safe approach to protect against the deadly scourge of smallpox. In the 19th century fundamental discoveries CAL-101 supplier in microbiology and immunology led to a basic understanding of how vaccines protect against infectious diseases. Work by Louis Pasteur, Émile Roux and others showed that vaccines containing inactivated or attenuated

microbes could protect against ancient afflictions like rabies, cholera and typhoid. The pace of scientific innovation accelerated in the 20th century in parallel with the development of new vaccines. Novel methods for producing vaccine antigens, including cell culture systems and genetic engineering, www.selleckchem.com/products/ldk378.html were invented and new ways of enhancing vaccine potency, including adjuvants and carrier protein conjugation, were discovered. Between 1913 and 1997, new

vaccines for 20 diseases became available that provided defence against feared childhood diseases, such as diphtheria, pertussis, measles and Haemophilus influenzae type b infection, and other worldwide killers, including influenza, polio and hepatitis B virus. In the first decade of the 21st century alone, 10 new vaccines have been licensed including the first therapeutic vaccine

for a viral infection (herpes zoster), the first adjuvanted prophylactic cancer vaccines (human papillomavirus), the first therapeutic cancer vaccine (prostate cancer), and the first intranasal vaccine (influenza). New technologies, new discoveries and greater understanding of human immunology Tideglusib and microbial pathogenesis will continue to facilitate the development of new and improved vaccines. The field of vaccine research and development has grown increasingly sophisticated and complex. This new textbook, written by internationally recognised vaccine experts, provides a comprehensive overview of the essential aspects of vaccine development. The six chapters of this book examine the fascinating history of vaccine development, provide a comprehensible review of vaccine immunology, elucidate the science of vaccine antigens and vaccine adjuvants, clarify the complex vaccine development pathway from concept to testing to licensure and implementation, and finally the book explores the near future describing the exciting developments that promise to deliver new vaccines for known and yet to be discovered targets as well as vaccines for non-traditional targets such as autoimmune diseases, malignancies and addiction. The editors would like to acknowledge the generations of vaccine researchers whose determination, commitment and brilliance have made the world a better and safer place.

This caused mature kleptocnides to appear out of the intensity range (blue, the colour for overload of measuring range) with an intensity value of 255 i.u. or higher. The highest fluorescence intensity of every single nematocyst within the ten sections of a cnidosac was determined (maximum absolute fluorescence of single nematocysts, fNc). In addition the background fluorescence (fBg) in every section was measured to finally calculate a relative value (fNc/fBg). This value was determined by dividing the maximum absolute fluorescence of a nematocyst by the fluorescence of the surrounding tissue of the same section (Fig. 3A). Additionally, the percentage of kleptocnides

with a higher fluorescence than 255 i.u. was calculated for every time slot (Table 1). Statistical analysis was performed BKM120 with Microsoft Excel and SPSS 15 (IBM). Statistical tests on significance of the changes in fluorescence intensity values see more over time were performed with the non-parametric Mann Whitney U test (SPSS15). The autofluorescence of unstained nematocysts in Aiptasia spec. and in Aeolidiella stephanieae was very low and negligible. The nematocysts became slightly visible when excitation was amplified with settings of PMT1 = 900 V, almost twice as much as used in the Ageladine A staining experiments. Preliminary

staining experiments revealed that Ageladine A easily permeates the nematocysts of gastropods and their Inositol monophosphatase 1 food (Fig. 1B–D, Fig. 2A, B). Undischarged nematocysts with high fluorescence intensity were present in high amounts within the Aiptasia epidermis at the tip of the tentacles and especially in the acontia ( Fig. 2A, B). Lower amounts of fluorescing nematocysts were found along the tentacles and throughout the scapus. Nematocysts exhibiting hardly any fluorescence were found in lower numbers along the tentacles, and in higher numbers in the scapus. Gastropod feeding was used to trigger the discharge of the anemone’s nematocysts. Discharged nematocyst capsules, which could be found around

the two animals (anemone and gastropod) in high numbers, lost their high fluorescence with time, although their threads continued glowing, especially when PMT1 = 500 V is chosen (Fig. 2E). This was also observed in discharged kleptocnides extruded from the cnidosac (Fig. 1D). In the digestive gland and stomach area of the freshly fed gastropod, non-fluorescing nematocysts outnumbered fluorescing ones by far. This became obvious when transmission pictures were compared to fluorescence pictures (Fig. 2C, D). Since the body with the overlying viscera in the gastropod was very thick and optic measurements were difficult, no statistic values could be obtained. To investigate properties of incorporated nematocysts in the gastropod at various times, 47 cnidosacs with 1770 nematocysts in total were measured at five intervals (7, 24, 48, 72 and 96 h) after food uptake.

Mice exposed to HQ showed augmented levels of MDA and enhanced ROS generation by neutrophils in comparison to samples obtained from vehicle-exposed animals (Fig. 1A and B, respectively). On the contrary, no differences were detected in the two animal groups with regard to global DNA fragmentation (Fig. 1C). In vivo exposure to HQ at 12.5, 25 or 50 ppm did not modify the number of circulating Selleckchem EPZ015666 leukocytes after LPS challenge. The number of neutrophils and mononuclear cells (MN) was not statistically different in vehicle- and HQ-exposed

animals ( Table 1). Normal values of polymorphonuclear leukocytes (PMN) in mouse blood are around 15–20%, and they are highly elevated after acute inflammation. This pattern of response was detected in both groups of animals, indicating that neutrophil mobilization from storage compartments was not affected by HQ exposure. It is noteworthy that the levels of PMN and MN in vehicle- and HQ-exposed animals ( Table 1) must be compared in groups of animals submitted

to the same concentration exposure, since assays were performed on different days and total leukocyte numbers for the mice ranges about 3500–6000/mm3. Corroborating that HQ exposure does not affect neutrophil delivery from bone marrow or cell maturation steps, cell cycle was equivalent in circulating cells obtained Crizotinib molecular weight from vehicle- or HQ-exposed animals ( Fig. 2). On the other hand, exposure to 12.5, 25 or 50 ppm of HQ reduced the neutrophil numbers recovered in BALF (Fig. 3A), and these cells seemed to persist inside the lung tissue, since MPO levels of lung were higher than those obtained for vehicle-exposed animals (Fig. 3B). Numbers of neutrophils in BALF, obtained in vehicle-exposed and non-inflamed animals, was almost 50% less in comparison to the LPS-stimulated control group (Fig. 3A, dotted line), indicating the efficiency of LPS in inducing lung inflammation and that circulating neutrophils from

vehicle-exposed animals were able to migrate to the alveolar compartment. As the three concentrations of HQ similarly reduced the number of PMN in the BALF, and 25 ppm exposure next promoted more homogenous responses, the following study was conducted with animals exposed to 25 ppm of HQ. As IL-1β, TNF-α and IL-6 are involved in leukocyte migration by inducing the expression of adhesion molecules and secretion of chemoattractant factors (Barreiro et al., 2010), the effects of HQ exposure on these cytokines in BALF were investigated using ELISA. The data obtained demonstrated that HQ did not modify the baseline or LPS-induced secretion of these cytokines (Fig. 4). In vivo exposure to HQ did not modify the LPS-induced expression of endothelial E- and P-selectins ( Fig. 5A) and ICAM-1, VCAM-1 and PECAM-1 ( Fig. 5B). Baseline expression of these molecules was very low in lung tissue and did not differ between the two animal groups studied (data not shown).

In the vials with faecal pellets, these blank values represented between 22 and 50% of the total carbon demand. Once the FP carbon demand is withdrawn, this represents an increase of the chl a max microbial carbon demand

by a factor of 1.8 to 8, and an increase of the 90 m microbial carbon demand by a factor of 1.1 to 5. When incubated in 0.2 μm FSW, the FP-CSD was 2.0% d− 1 for in situ pellets and 5.9% d− 1 for culture pellets ( Figure 2). We interpret this FP-CSD as the respiratory result of bacteria from the faecal pellet matrix. Both treatments – water type and faecal pellet origin – had significant effects on the FP-CSD, although their interaction did not have a significant effect (two-way ANOVA, water type F2.23 = 8.783, p < 0.05, chl a max significantly LBH589 higher than FSW and 90 m, LSD post-hoc PF-02341066 purchase both p < 0.05, no difference between FSW and 90, p = 0.966; faecal pellet origin F1.23 = 10.030, p < 0.05, culture significantly higher, LSD post-hoc test

p < 0.05, Table 1). For both pellet types, FP-CSDs in water from the chl a max were significantly higher than in 0.2 μm FSW or 90 m water (one-way ANOVA, LSD post-hoc test all p < 0.05, Figure 2). Since the FP-CSD in 0.2 μm FSW is due to the activities from the bacteria of the faecal pellet matrix, the difference between chl a max FP-CSD and FSW FP-CSD provides information on the FP-CSD due to the free-living bacteria and protozooplankton, which represents about 40% and 70% of the total FP-CSD from the culture and in situ faecal pellets

respectively. FP-CSD of the culture pellets were statistically higher than for the in situ pellets when incubated in FSW and 90 m (factors of 2.3 and 2.6 respectively, one-way ANOVA p < 0.05 for both, Figure 2), and had a tendency to be higher for chl a max, though not significantly ( Figure 2). Although previous studies have diglyceride used microbial volumes of bacteria and protozooplankton for assessing their carbon demand (i.e. Shinada et al. 2001), in the present study at the same temperature, the same microbial community (chl a max or 90 m) increased its carbon demand by a factor up to 8 in the presence of 30 faecal pellets in the 5 ml vials. In natural conditions, it is unlikely that 30 faecal pellets may occur at the same time in such a small volume; however, it is important to consider that respiration and carbon demand depend on the available carbon sources, and in particular the presence of faecal pellets.

0004). Blood glucose was 34% higher in SL than in NL group (P < 0.0004). To investigate circulating levels of acylated ghrelin, we measured these after 4 h of fasting. SL group presented significantly decreased plasma acylated ghrelin levels (98.64 ± 23.1 pg/mL) compared with NL mice (201.1 ± 20.7 pg/mL) (p < 0.01) ( Table 1). Many biological actions of ghrelin are started by the binding of ghrelin to its cognate cell surface receptor GHSR-1a [53]. SL animals had a markedly higher (2.9-fold) GHSR-1a content than their counterparts (P < 0.0004) ( Fig. 5A and B), and higher PI3K association with GHSR-1a in SL than NL groups (P < 0.05) ( Fig. 5B). In addition, GHSR-1a mRNA was increased in SL-hearts as compared

to NL ventricles (P < 0.05, Fig. 6). We examined the basal phosphorylation state of AKT-Ser473 in the left ventricles of NL and SL mice (Fig. 7). Fig. 7A shows that AKT content in SL mTOR inhibitor mice was 42.7% higher when compared to NL mice (P < 0.03). Furthermore, AKT was highly phosphorylated in left ventricles of SL mice (57.1%), when compared to NL mice ( Fig. 7B). We investigated AMPK content and activation. Fig. 8(A and B), shows that there were no significant difference among the groups with respect to AMPK content and phosphorylation. Early life overnutrition induced Olaparib supplier a significant increase in body weight in adult mice. This observation confirms previous results from our and other groups [9],

[26], [28], [35] and [37]. Basically, obesity resulted in a significant accumulation of retroperitoneal and epididymal fat masses when the mice reach adulthood. In addition, we observed increased ratio of body weight to tibia length in early life overnourished

mice, showing that the difference between groups was in body weight, not in length. In others words, early life overnutrition induced a metabolic profile where energy storage was privileged. Thus, these data reinforces the theory that the development of obesity, diabetes, and cardiovascular disease IKBKE is an expected output in adulthood of the animals submitted to disturbed nutrition in early life [9], [26], [28], [35], [37] and [45]. Therefore, we hypothesized that in hearts of these obese mice, the signaling process of the gut-derived hormone ghrelin should be altered. In this context to explain this process we firstly showed the presence of the ghrelin receptor GHSR-1a in left ventricles confirming results from other authors [8]. And, as original data, we clearly demonstrated that obesity induced in early life increases heart ghrelin receptor expression (GHSR-1a) in adulthood. In other words, these result confirmed evidences indicating that cardiovascular tissue is rich in ghrelin receptors, reinforcing results in the literature in which increases are found in ghrelin receptor mRNA of human cardiomyocytes, rat cardiomyocytes and cardiovascular vessels [13].

In the latest study Price et al. [41] combined FRAP in a mouse tibia with computational modeling and was able to predict the peak computational fluid velocity during cyclic

loading, 60 μm/s, and also estimate the peak resultant fluid shear stress ~ 5 Pa. These predictions are based on a three compartment model which considers the pericellular matrix surrounding the osteocyte cell processes in their canaliculi. In the original fluid flow hypothesis [9] the activation of the osteocytes was proposed to be due to fluid shear stress acting on the cell process membrane. Numerous experimental studies were subsequently conducted exposing bone cells in culture to steady and pulsatile wall shear stresses in selleck the range 0.6 to 3.0 Pa predicted by the model in [9]. A typical in vitro study [42] is conducted in a two-dimensional (2D) environment on surface attached MLO-Y4 osteocyte-like cells as opposed to the three-dimensional (3D) in vivo environment of bone matrix where the osteocyte morphology and pericellular flow environment are different. There are several differences between the flow-induced activation Selleck Y 27632 of bone cells in vivo and in vitro. In vivo the cells are attached to their mineralized matrix either through tethering filaments, or perhaps through integrin-based focal adhesions. β3 integrins have been observed on the cell processes and β1 integrins are

found to be ubiquitous [43]. In vitro there is no pericellular matrix surrounding the cell and the attachments to the substrate are all integrin-based. The second difference is the flow environment itself. As shown in [41] the fluid drag forces on the pericellular matrix surrounding the cell process in vivo are 20-fold those of the fluid shear stress acting on the cell process membrane. In vitro the fluid shear stress in nearly all experiments is the same on the cell processes and the cell body. This raises the important issue, which part of the osteocyte is its mechanosensing selleck chemical organelle, its process or its cell body, which we discuss in the next paragraph.

Third, osteocytes seeded on a flat, stiff surface spread out and build up strong basal attachments to their substrate. It has been shown that round non-adherent osteocytes are an order of magnitude more sensitive to a mechanical stimulus than a flat adherent osteocyte [44]. The mechanosensitivity of osteocytes with a more 3D morphology, such as occurs in vivo, may thus differ from that of adherent osteocytes. In summary, experiments with osteocytes cultured in 2D on flat surfaces may not suffice to unravel the intricate mechanisms used by osteocytes to transduce a mechanical signal into a chemical response. However, in vitro experiments undoubtedly do provide valuable insights into which signaling molecules are produced by osteocytes in response to a mechanical stimulus.

P < 0.05 was assumed as statistically significant. Six protocols were considered to establish the hepatocytes dissociation method for P. lineatus. The non-enzymatic dissociation with EDTA (2 mM in PBS) was unsuccessful due to lyses of most cells during the procedure.

The same drawback happened after using the trypsin (0.05%) and pancreatin (0.25%) enzymes. However, collagenase IV (0.25 U ml−1), collagenase IV (0.15 U ml−1) associated with dispase (0.5 U ml−1), and only dispase (1 U ml−1) presented satisfactory results considering cell yield and viability ( Table 1). The protocol using collagenase IV resulted in 88% of cell viability and 1.01 × 107 hepatocytes per gram of liver, whereas collagenase IV and dispase enzymes resulted in about 3-fold increase in hepatocytes yield ( Table 1) maintaining similar cell viability. However, 97% of cell viability Bortezomib mw and 6.36 × 107 hepatocytes per gram of liver were obtained using dispase ( Table 1). On this way, the latter protocol was selected for further tests of cell attachment. Hepatocytes adhered properly on two of the three culture flask brands tested, TTP® and Biofil®. However, there was no improvement in hepatocyte attachment selleck screening library with coat pretreatments and four days were necessary for cell attachment after seeding, as evidenced by the clustering

of hepatocytes in large groups ( Fig. 1 and Fig. 2). On this way, we adopted the following protocol for investigation of cylindrospermopsin effects. Hepatocytes were dissociated with dispase, seeded on TTP® flasks, cultured during four days for cell recovery and attachment, and then exposed to cylindrospermopsin through replacement of culture medium. Cell viability decreased 8% in hepatocytes exposed to the two lowest concentrations of purified cylindrospermopsin (0.1 and 1 μg l−1), but not at the highest concentration of 10 μg l−1 (Fig. 3A). Cells exposed to the three concentrations of cylindrospermopsin have similar GST and G6PDH activities in comparison to the control

group (Fig. 3B and C), although Tukey post test indicated that the GST activity of GPX6 the hepatocytes exposed to 10 μg l−1 was 12% lower than of those exposed to 1 μg l−1 (Fig. 3B). Similarly, this post test showed that the G6PDH activity of the hepatocytes exposed to cylindrospermopsin at 10 μg l−1 was 19% lower than of those exposed to 0.1 and 1 μg l−1 (Fig. 3C). No significant alterations were observed for GSH concentration (53.6 ± 15.8 μmoles of non protein thiols per mg of protein) and also for the 2GSH/GSSG ratio (p > 0.7188) after exposure ( Fig. 3D), despite of the 25% increase of reactive oxygen/nitrogen species levels (mainly hydrogen peroxide) in all cylindrospermopsin-exposed groups in comparison to the control group ( Fig. 3E). Likewise, MXR activity decreased in about 22% in exposed groups, but without a concentration–response relation ( Fig. 3F), demonstrating that cylindrospermopsin may be able to make hepatocytes of P.