012) higher Hif-1α scores in UT-SCC-34 compared with UT-SCC-74A xenografts ( Figure 2B), whereas the lower scores seen in UT-SCC-8 xenografts reached only marginal significance (P = .082). UT-SCC-34 and UT-SCC-74A cells exhibited the highest [18F]EF5 uptake, whereas low uptake was

seen in UT-SCC-25 cells (Figure 3). After 1 hour of exposure to hypoxia, [18F]EF5 uptake increased slightly in all UT-SCC cell lines. However, this uptake declined over time toward the levels detected in the normoxic conditions (Figure 3). One exception to this pattern was detected in UT-SCC-74A cells in which a higher [18F]EF5 uptake was seen at 24 hours after exposure to hypoxia in comparison to normoxic conditions. However, significantly different (P < .0001) [18F]EF5 uptake was already seen between the cell lines under normoxia, except between UT-SCC-34 and UT-SCC-74A, MG-132 research buy which showed similar high uptake. In general, Alectinib the hypoxic environment

increased the uptake of [18F]FDG in UT-SCC cell lines (Figure 4A). The uptake of [18F]FDG observed in UT-SCC-34 cells remained rather stable between 1 to 24 hours of hypoxia exposure. UT-SCC-8, UT-SCC-25, and UT-SCC-74A exhibited a more variable [18F]FDG uptake; UT-SCC-8 increased over time until 6 hours, and UT-SCC-74A increased in a dual-phase manner over time being greatest after 24 hours of hypoxia. UT-SCC-25 cells exhibited the least [18F]FDG uptake of the four cell lines studied. Hif-1α expression was detected during hypoxia, whereas under normoxic conditions, Hif-1α expression was absent or weak (Figure 4A). The expression of Hif-1α in the UT-SCC-74A cell line deviated from the commonly observed expression pattern by exhibiting the strongest expression after 24 hours instead of at 3 to 6 hours of hypoxia. The Hif-1α expression correlated strongly with the [18F]FDG uptake in the UT-SCC-74A cell line (r = 0.984; P = .0004). This correlation was slightly weaker in UT-SCC-34 (r = 0.801; P = .0554), UT-SCC-25 (r = 0.763; P = .0774),

and UT-SCC-8 (r = 0.721; P = .1057) cell lines ( Figure 4B). Our aim in this study was to investigate whether a certain molecular profile might affect [18F]EF5 and [18F]FDG uptake in HNSCC. The main finding of our study is that [18F]EF5 uptake appears to be related to a hypoxia-driven adverse phenotype. The Cell press highest [18F]EF5 uptake was seen in UT-SCC-34 xenografts (Figure 1), which also expressed high amounts of CA IX, Glut-1, and Hif-1α (Figure 2 and Table 2). Moreover, much lower levels of [18F]EF5 uptake and CA IX and Hif-1α expression were detected in UT-SCC-8 xenografts. We consider this difference (P = .091) in [18F]EF5 uptake as a trend toward significance in this limited sample number study. Compared to UT-SCC-8 xenografts, a higher, although not statistically significantly (P = .194), uptake of [18F]EF5 was also detected in UT-SCC-74A xenografts.

Importantly, CD5 was one of only two proteins identified with at least Dasatinib solubility dmso 2 peptides specifically in the VLR32-containing IP compared to the ‘minus-VLR32’ negative control.

The other identified protein, myosin-9 was only identified with 2 spectra from 2 unique peptides, corresponding to a sequence coverage of only 1%. Using this approach we determined that VLR32 immunoprecipitations contained the CD5 antigen (Table 2). We verified these results in parallel experiments testing the reactivity of VLR32 with cells transfected with CD5–GFP fusion constructs, by western blot analysis and immunoprecipitation experiments. VLR32, but not the negative control VLR4, was able to detect CD5–GFP fusion proteins in cell lysates from transiently transfected HEK293T cells (Fig. 3A). This find more reactivity was limited to lysates separated under non-reducing conditions as separation of cell lysates under reducing conditions abolished VLR32 binding (data not shown). In additional experiments, we demonstrated that VLR32 but not the negative control VLR4

precipitated CD5–GFP fusion proteins from cell lysates of transiently transfected HEK293T cells (Fig. 3B) and that VLR32 but not VLR4 stained HEK293T cells transfected with CD5 expression constructs in flow cytometry experiments (Fig. 3C). These experiments demonstrate the CD5-specificity of VLR32. Prior studies of VLR antibodies suggest that binding of the antibody to the antigen is avidity-based and that the affinity of

the individual antigen-binding unit to the antigen is often comparatively low (Herrin et al., 2008 and Kirchdoerfer et al., 2012). To investigate the affinity versus avidity-based binding of VLR32 to the CD5 antigen, we generated monomeric VLR32 antibodies by deleting the C-terminal 42 residues of the VLR antibody. As PLEKHM2 expected, the resulting individual VLR units displayed a slightly faster migration pattern compared to full-length VLR proteins (Fig. 3B). Only the multimeric VLR32 was able to bind to CD5 efficiently as shown for immunoprecipitation (Fig. 3B) and flow cytometry analyses (Fig. 3D). VLR binding was not detected by flow cytometry using the monomeric VLR32 (Fig. 3D) and only a weak signal was obtained for immunoprecipitated CD5–GFP using the monomeric VLR32 (Fig. 3B). These data indicate an avidity-based contribution to the binding of the VLR32 lamprey antibody to human CD5. In this study, we demonstrate for the first time that monoclonal lamprey VLR antibodies can be used for purification and mass spectrometry-based identification of cell surface expressed protein antigens. Unlike conventional immunoglobulin-based antibodies, VLR antibodies utilize their leucine-rich repeats as basic structural units, resulting in a fundamentally different protein architecture of antigen receptors.

The review of the patients’ charts identified 46 staff members who were directly involved in the care of either patient. Their histories and clinical examinations did not reveal any sore throat, skin, rectal or vaginal symptoms suggestive of GAS. Identification of GAS alone in the health care workers was not sufficient to link them to the outbreak; DNA typing of the three strains indicated that the strains of the patients were identical, and those of the two staff members were not epidemiologically linked to each other or to the outbreak strain [12]. Both staff members with GAS were removed from direct patient contact and were treated orally with a ten-day course of clindamycin. The success of their decolonization

status was assessed at the end of therapy and at three, six, nine and twelve months thereafter before they were learn more reassigned to their routine work. In some published reports, recurrence of an outbreak was traceable to a colonization of family members of the index case [18], [24] and [25]. Unfortunately, in this study, the husband of the second patient was the only family member of either patient

who was available for interview, and his surveillance culture was negative. No further GAS infection was detected thereafter. The literature also indicates that environmental screenings Proteasome inhibitor should be considered [26], especially in cases with there is a lack of evidence of infection among hospital personnel. These screenings were Interleukin-3 receptor all uneventful. As has

been previously reported, early infection control intervention after the detection of the second case was the key measure behind the successful control of this outbreak [27] Strict adherence to infection control practices, such as contact isolation; enhancement of standard precautions; cleaning, disinfection, and sterilization of instruments; and the proper environmental cleaning of the operating theatres were strictly implemented. Relevant educational programs for all hospital personnel were equally important. Moreover, timely and regular reports regarding the progress of the outbreak to all concerned had a significant impact on the implementation of the infection control precautions and demonstrates the vital importance of engaging all hospital personnel in the management of any outbreak. Invasive GAS TSS is a serious disease with a high case fatality rate. Unfortunately, in spite of extensive investigations of all involved personnel and of the environment, the mode of transmission to the second patient could not be established. Droplet or airborne transmission could not be ruled out. The infection control service of the hospital had a significant role in stopping the outbreak and preventing any new cases of GAS during the 24 months following the first case. More data are needed to prove and to accurately define the magnitude of the airborne and/or environmental transmission of GAS. Funding: No funding sources.

3-fold higher at the 1:9 ratio of M6:NM1. These results indicated that NM1 enhanced the transcriptional expression of the genes involved in methane oxidation when NM1 was more abundant than M6, consistent with the population and methane oxidation rate results. Relative expression of FADH was about 2-fold lower than the expression levels of the pMMO and MDH genes. We speculate that some of the formaldehyde produced was used for biosynthesis because formaldehyde has

a central role as an intermediate in catabolism and anabolism [9]. Increased transcriptional expression of these genes was likely responsible for the increased oxidation rate measured at the 1:9 ratio of M6:NM1. Similarly, [11] reported that the amount of mRNA copies was correlated with the activity in the reactor. Enzalutamide We demonstrated that NM1 concurrently enhanced the population growth of M6 and the expression of the methane-oxidation genes in a density-dependent manner. The two types of bacterial cells were mixed on the basis of cell number. Because the mass of NM1 cells is 5.7-fold less than that of M6, the mass-ratio of NM1 to M6 was estimated

ALK inhibitor to be 0.02, 0.19, and 1.68 at the 9:1, 1:1, and 1:9 ratios of M6:NM1. NM1 only had significant effects on the activity and growth of M6 at the 1:9 ratio of M6:NM1, indicating that NM1 had a significant effect on M6 only when it was present at higher mass than M6. Previous studies have shown that a few vitamins and organic acids can enhance methanotrophic growth [31]. For instance, [13] reported that cobalamin (vitamin B12) produced by Rhizobium stimulated the growth and activity of several methanotrophs, including Methylomonas and Methylovulum. Xing et al. [31] reported that riboflavin and organic acids (maleate, succinate, malate, and citrate) induced the population growth of Methylosinus. Thus, we hypothesize that extracellular substances from NM1 enhanced the population growth of M6 as well as the expression of the methane-oxidation enzymes in M6. Further investigations of the metabolic interactions between these two organisms are warranted. Our results also imply

that methane oxidizers may Baricitinib commonly interact with other organisms in natural environments. This is the first study to report that the non-methanotrophic bacterium Sphingopyxis enhances the activity of the type II methanotroph Methylocystis. We demonstrated that NM1 enhanced the population growth of M6 as well as the expression of the genes involved in the methane oxidation pathway in a density-dependent manner. These results can be used to develop and guide management and enhancement strategies for methanotrophic biotechnological processes. For instance, this stimulation can be used for accelerating start-up in methanotrophic systems. This research was supported by the Basic Science Research Program through the National Research Foundation of Korea (NRF) funded by the Ministry of Science (2012R1A2A2A03046724) and by the Ministry of Education (2013R1A1A2061015).

, 2005). All metrics are given as mean ± SEM and compared using paired or unpaired Student’s t-tests or one-way ANOVA followed by a Bonferroni’s post-test as appropriate. Significance was accepted at P < 0.05; n denotes the number of animals studied in each experimental group. Pharmacological agents were purchased from Sigma–Aldrich (UK), Dorsomorphin nmr except CPA (Ascent Scientific) and MnTMPyP (Calbiochem), and were dissolved in Holman’s buffer, except

apocynin and indomethacin (absolute ethanol), and CPA and DHE (DMSO). Responses evoked by CPA in the presence of L-NAME/indomethacin were unaffected by exposure to 30 μM arsenite for 30 min, whereas exposure to 100 μM arsenite for 30 min caused a leftward shift in the concentration–relaxation curve, such that pIC50 increased from ∼4.8 to ∼5.2 without change in Rmax ( Fig. 1A; Table 1). EDHF-type relaxations evoked by ACh were similarly potentiated by exposure to 100 μM arsenite for 30 min, exhibiting a significant increase in pEC50 from ∼6.8 to ∼7.0 without change in Rmax ( Fig. 1B; Table 1). In control rings with intact endothelium incubated in the absence of L-NAME/indomethacin,

the additional contribution of NO to CPA- and ACh-evoked relaxations was evidenced by pIC50 values of ∼5.0 and ∼7.3, and increases in Rmax to ∼90% from ∼80% and ∼70% compared to the corresponding EDHF-type concentration–relaxation curves ( Table 1). Responses to CPA and ACh were Selleck Ku-0059436 unaffected by

incubation with 100 μM arsenite for 30 min Carnitine palmitoyltransferase II ( Fig. 2A and B; Table 1). In control rings incubated in the absence of L-NAME/indomethacin, the magnitude of the constrictor response to 1 μM PE was unaffected by exposure to 30 μM arsenite for 30 min, but was reduced by ∼15% following exposure to 100 μM arsenite for 30 min (from 30.1 ± 1.7 mN to 26.7 ± 1.8 mN, pooled data from all experiments n = 21, P < 0.01). Incubation with L-NAME/indomethacin increased PE-induced constriction by ∼15% and this increment in tone was reversed by exposure to 100 μM arsenite for 30 min (from 35.3 ± 1.2 mN to 30.0 ± 1.1 mN, pooled data from all experiments n = 73, P < 0.01), such that constriction then matched the level observed in the absence of L-NAME/indomethacin. No attempt was made to correct for these small overlapping effects on pre-relaxation tone. Maximal relaxations evoked by CPA and ACh in aortic rings with intact endothelium were equivalent to ∼70% of PE-induced tone and were mediated by NO because no significant EDHF-type component was evident in the presence of L-NAME/indomethacin (Fig. 3A). Rmax and pIC50/pEC50 values for concentration–relaxation curves constructed for CPA and ACh were unaffected by incubation with 100 μM arsenite for 30 min ( Table 2). As in the RIA, this incubation protocol reduced PE-induced constriction by ∼15% (from 26.9 ± 1.6 mN to 22.9 ± 1.3 mN, pooled data from all experiments n = 14, P < 0.01).

Both maximum parsimony analysis and Bayesian inference were congruent and only the Bayesian phylogenetic tree is presented with posterior probability and MP bootstrap values. The resulting tree was midpoint rooted, based on sequences of wsp from S. invicta, S. saevissima, S. geminata, and S. megergates ( Table 1) as well as on sequences from Wolbachia strains from other hosts of the genus Solenopsis retrieved from the GenBank ( Table 4). Six Wolbachia strains of the supergroup A were found

in S. invicta and three in S. saevissima. Two strains (AF243435 and AY446997) found in S. invicta retrieved from the GenBank were grouped in the branch of Wolbachia strains of this ant, forming a derived polytomy. At the base of this clade, a group of Wolbachia strains forms a polytomy Idelalisib in vivo with strains from S. saevissima retrieved from the GenBank (EU251431 and EU251432). Within supergroup B, fifteen Nutlin-3a purchase strains were found in S. invicta, three in S. saevissima, and two in S. megergates. Three strains, termed H23 and H26; and H31 were also found in S. invicta and S. saevissima,

respectively. Supergroup B was separated in two groups. One of them exhibited a unresolved node (polytomy) formed by a Wolbachia sequence found in S. daguerrei retrieved from GenBank (AY878102), along with Wolbachia strains from S. invicta and S. megergates. The second group was a sister group of the first group, formed by Wolbachia strains found in S. invicta (H22) at the base, followed by a branch

from strains found in S. invicta retrieved from GenBank (AF217722), and a strain found in S. megergates and another in S. invicta. A derived group in relation to the previous ones was comprised by strains found in S. daguerrei (AY878101, AY878107), followed by a group of strains found in S. invicta, forming a polytomy with strains found in S. invicta and S. daguerrei retrieved from GenBank (AF243436, DQ842483, and AY878106). The analysis of Wolbachia sequences of different species of Solenopsis indicates a higher frequency of supergroup B rather than A, unlike the observed by Ahrens and Shoemaker (2005) in S. invicta. These authors reported a similar occurrence of the two supergroups in some South-American populations. In the distribution of these supergroups in the network generated and in the reconstructed phylogeny, there is a complete L-NAME HCl separation of supergroups, in agreement with the described by Zhou et al. (1998) and Ahrens and Shoemaker (2005), the variants H1–H16 ( Fig. 2) correspond to strains of the group A and H17–H46 correspond to strains of the group B. The number of strains was very high and was not associated with the number of Solenopsis species examined (S. invicta, S. saevissima, S. megergates; S. geminata, and S. pusillignis), which might be indicative of horizontal transmission within the genus Solenopsis, as suggested by Ahrens and Shoemaker (2005). Similarly, Souza et al. (2009) suggested horizontal transmission in Brazilian populations of S.

A consequence of the choice of scope and models is that possible impacts are reduced to a temporary

impact because the choice of scientific approach includes an ABT-199 manufacturer assumption that the cod stock will, given time, recover from an oil spill. But experience, for example on the overfishing of Northern cod [54] or the effects of the Exxon Valdez oil spill [51], suggests that major impacts can cause changes in the ecosystem structure which make it difficult, maybe impossible, for stocks or ecosystems to recover. Weinberg [55, p. 209] introduced the concept of ‘trans-science’, defined as “questions that can be asked of science and yet which cannot be answered by science”. Risk assessment is in the realm of trans-science: first, a sound empiric basis for calculating a

worst-case scenario and its probability would have required decades, at least, to provide a sufficient number of comparable blowouts and second, due to the complexity of ecosystems, a complete assessment of impacts is not achievable. This means that choices, of which some will not be science based, need to be made on how to approach the problem of whether petroleum production in the Lofoten area constitutes an acceptable risk to the environment, and if so, in which localities and with what safeguards. A pressing question is whether the present choice of approach, resulting in a quite narrow scope of risk assessments, is relevant for policy making. As argued above, quantified measures for risk assessments from and its associated uncertainties are impossible to achieve without, perhaps Selleckchem INK 128 considerable, uncertainty. Still, risk assessments may indicate important perspectives on risks. It is reasonable to assume that in case the area is opened, simulation studies may indicate sites that are likely to cause less harm than others in case of a major oil spill. The oil industry has proven to hold technological equipment and knowhow to drill horizontally for quite some distance and has used this technology to avoid drilling close to vulnerable benthic communities such

as coral reefs [56]. A different aspect of developing risk assessments is that the cooperation between sectors on developing criteria for these has already facilitated new discussions and reflections on knowledge and uncertainty. Taken together, the development of risk assessments based on the worst-case scenarios has a certain potential. However, it is disputable whether worst-case scenarios can be used as a key instrument for deciding whether to open the Lofoten area or not. How well do effects on cod larvae represent the effects on the ecosystem? And how can the attention these risk assessments get from the experts and the public be understood? There is a need to look closer at the role of risk assessments and their uncertainties. First of all it must be clear what it is. A worst-case scenario is not a worst imaginable scenario.

, 2004 and Milligan and Watkins, 2009), and we have recently shown that Ca2+ signalling in astrocytes is disturbed when influenced by inflammatory stimuli (Hansson, 2010). Two substances with proposed anti-inflammatory properties at extremely low concentrations, naloxone and ouabain, demonstrate an ability to limit the inflammatory Torin 1 induced alterations in astrocytes (Forshammar et al., 2011). We conclude that this is a note-worthy step in understanding astrocyte responses and neuroinflammatory mechanisms. There are more substances that have been proposed to have anti-inflammatory qualities and up-regulate or restore parameters related to inflammation especially

at extremely low concentrations in astrocytes. In the present study we wanted to examine a number of substances, which have anti-inflammatory effects on astrocytes, and we wanted to test them in LPS-activated microglia. The substances MK-2206 cost tested were naloxone, ouabain, and bupivacaine. We also

used some well-known classical anti-inflammatory substances, dexamethasone and corticosterone, as control substances. They attenuated both TNF-α and IL-1β releases. Glucocorticoids prevent swelling of cells and release of pro-inflammatory cytokines (Chao et al., 1992 and Lekander et al., 2009), and decrease the number of activated microglia (Hinkerohe et al., 2010). These two glucocorticoids are frequently used in acute pain states (De Oliveira et al., 2011). On the other hand, glucocorticoids can also cause extracellular accumulation of glutamate, which could cause excitotoxicity and acute stress (Jacobsson et al., 2006). Naloxone at ultralow concentration, prevented LPS induced down-regulation of Na+/K+-ATPase

(Forshammar et al., 2011), and down-regulated LPS-induced endomorphin stimulated Ca2+ transients in astrocytes (Block et al., 2012), as well as reversed down-regulation of the Na+ dependent glutamate transporter (Tsai et al., 2009). So far naloxone has not been able to decrease the release Ribociclib purchase of pro-inflammatory cytokines in LPS-activated astrocytes or microglia. Instead a small increase of TNF-α was observed in microglia. Ouabain also enhances LPS down-regulated iNOS activity in peritoneal macrophages (Sowa and Przewlocki, 1997). It decreased the IL-1β release in astrocytes ( Forshammar et al., 2011), but showed a small increase of TNF-α in microglia. It can be speculated in if the increased release of TNF-α with ultralow concentrations of naloxone or ouabain might have a protective effect. Exogenous TNF-α as well as TNF-α produced by astrocytes, induces production of neurotrophic factors such as nerve growth factor (NGF) and glial cell line-derived neurotrophic factor GDNF by astrocytes ( Kuno et al., 2006). TNF-α as well as IL-1β are considered to initiate a cascade of activation of cytokines and growth factors.

Thus PH suffers not only from an acquired disruption of synchronisation, but also a violation of perceptual unity of timing across different aspects of the same pairing of auditory and visual stimuli. Neurologically normal individuals also showed a comparable opponency between our

two measures (in speech and non-speech and in both directions of audiovisual influence): thus if one subject showed auditory lagging for TOJ, the McGurk measure tended to show auditory leading (or vice versa). Altogether, these counterintuitive findings suggest that perception of synchrony and integration depend on distinct rather than common synchronising mechanisms, and reveal one strategy by which the brain might achieve near-veridical perception of the timing of multisensory learn more events, at least on average, despite the evident temporal disunity of sensory processing. If specialised mechanisms existed to synchronise senses in normal brains, one would expect to find more cases of acquired sensory desynchronisation when such mechanisms are lesioned (Wiener et al., 2011).

There has only been one previous report, of patient AWF (Hamilton et al., 2006). However the similarity with PH is difficult to assess, as the direction of AWF’s acquired ‘temporal mismatch’ was not specified, and he was only tested with Veliparib supplier synchronous stimuli. AWF showed no McGurk effect while PH did when tested with asynchronous (auditory leading) stimuli. AWF’s lesions are also in a quite different

location, in right parietal cortex, while PH’s lesions are in mid-brain and brainstem. We can at least claim that the present case is the first to be reported of an acquired subjective auditory lead, which is speech-specific and accompanied by an auditory lag for optimal McGurk integration. Surprisingly, some healthy participants also showed large deviations of PSS; indeed for some, synchronous stimuli were just-noticeably asynchronous. Thus it seems PH is not so unusual in terms of experiencing a mismatch in audiovisual timing. Such ubiquitous sensory asynchrony further undermines support for the existence of specialised synchronisation mechanisms. selleck kinase inhibitor It also raises the obvious question of why only PH is aware of his asynchrony in his everyday life. It is possible that our TOJ results from normal participants are specific to our laboratory conditions. In the outside world we learn to expect that when auditory and visual events originate from the same source, they are also very likely to occur simultaneously, regardless of their sensory timing. Under this unity assumption (Vatakis and Spence, 2007; Welch and Warren, 1980) our perception might tend to rely more on this expectation than any sensory evidence of asynchrony. Our paradigm, by contrast, presented a randomised range of asynchronous stimuli with no feedback about which was actually synchronous.

Further studies are needed to identify the molecular mechanism underlying PHT-induced genotoxic effects. We wish to thank CNPq, CAPES,

Instituto Claude Bernard, FUNCAP and FINEP for their financial support in the form of grants and fellowship awards. We are also grateful to Dr. A. Leyva for English editing of the manuscript. “
“Over 800,000 tons of dyestuffs selleck inhibitor are annually produced throughout the World, of which 60–70% are azo dyes (Anliker, 1977 and Combes and Haveland-Smith, 1982). At least 3000 azo dyes were in use in the 1990s (Chung and Cerneglia, 1992), produced by the diazotization of aromatic amines, and used to provide color in products manufactured by the textile, leather, printing, paper, food and cosmetic industries. It has been estimated that 10–15% of the total amount of dyes are released selleck kinase inhibitor into the environment

during manufacturing (Nam and Renganathan, 2000, Moutaouakkil et al., 2003 and Mansour et al., 2007), such a discharge being undesirable for esthetic reasons and also because many azo dyes and their breakdown products are toxic, mutagenic and carcinogenic to both humans and aquatic life (Spadaro et al., 1992, Van Der Zee et al., 2001, Pinheiro et al., 2004 and Seesuriyachan et al., 2007). The toxic effects of azo dyes, mainly their mutagenicity, can be caused by both the dyes themselves and by their metabolites, such as arylamines and free radicals (Collier et al., 1993 and Weisburger, 1997). One of the criteria used to classify a dye as harmful to humans is its ability to reductively cleave, and consequently to form aromatic amines when

in contact with sweat, saliva or gastric juices. Some of these aromatic amines are carcinogenic and can accumulate in food chains (Pielesz, 1999 and Pielesz et al., 2002). Examples of such aromatic amines are the biphenylamines such as benzidine and 4-biphenylamine, which are present in the environment, constituting a threat to human health and to the ecosystems in general (Choudhary, 1996 and Chung et al., 2000). After the oral ingestion of an azo dye, it can be reduced to free aromatic amines by anaerobic intestinal microflora and possibly by mammalian azo reductase almost in the intestinal wall or in the liver (Umbuzeiro et al., 2005). Such a biotransformation can occur in a wide variety of mammalian species including both Rhesus monkeys ( Rinde and Troll, 1975 and Prival and Mitchell, 1982) and humans ( Watabe et al., 1980). The activation of azo dyes involves nitro reduction and azo reduction (Umbuzeiro et al., 2005), and thus it is reasonable that the intestinal microflora play an important role in this activation process (Chung, 1983, Chung et al., 1992 and Lima et al., 2007), and the CYP450 enzymes present in the intestine could also play a part in the activation of these dyes (Umbuzeiro et al., 2005 and Lima et al., 2007).