As a negative control, other cuttings were treated for 8 h with Hoagland’s solution alone and, as a vehicle control, with Hoagland’s solution (4 h), as well as with Tween 20 (20%,

4 h). After each treatment, the cuttings were allowed to recover for 24 h in Hoagland’s solution; the young inflorescences were collected and fixed in a solution of acetic acid/ethanol (1:3). At least 10 cuttings were scored, and only preparations showing early tetrads were counted. The number of micronuclei in 300 tetrads per slide was counted at a magnification of × 400, and the results are expressed as the percentage Sirolimus in vitro of micronuclei. Six-week-old Balb/c male mice were maintained in a temperature- and humidity-controlled environment (22 ± 2 °C; 55 ± 10% humidity), on a 12/12 h light/dark cycle. Before the experiments, the animals were acclimatized for 1 week, during which

time they had free access to a commercial diet (Purina®) and water. The study was approved by the Animal Research Ethics Committee of the São Paulo State University, College of Pharmaceutical Sciences (res. CEP/FCF/CAr no. 01/2006) Mice were randomly assigned to 9 groups of 8 animals each. Group 1 (negative control) mice received only drinking water (0.6 ml/day by gavage) for 2 weeks before treatment with 0.9% saline solution by i.p. injection. Group 2 (positive control) mice also received only drinking water for 2 weeks but were treated on day 15 with i.p. injections of TSP at 3.75 mg/kg body Neratinib manufacturer weight (BW). Group 3 mice received 0.6 ml Tween 20 (20%) or Tween 80 (6%) by gavage, for 2 weeks, and were treated Dactolisib chemical structure on day 15 with TSP (3.75 mg/kg BW, i.p. The mice in groups 4–9 were treated by gavage (0.6 ml/day) with solutions of ethanolic extract of C. sylvestris (3.9, 7.5, and 15.0 mg/kg BW; groups 4, 5, and 6, respectively) and casearin X (0.3, 0.6, and 1.2 mg/kg BW; groups 7, 8, and 9, respectively) for 2 weeks, all receiving i.p. injections of TSP (3.75 mg/kg BW) on day 15. Mouse bone marrow was collected 24 h after TSP injection. The micronucleus test was carried out as described by Schmid (1975). All slides

were stained with May–Grunwald Giemsa and coded to avoid observer bias. For each experimental result, 1000 polychromatic erythrocytes (PCEs, immature erythrocytes) were scored in order to determine the percentage of micronucleated PCEs. To assess cytotoxicity, the ratio of PCEs to normochromatic erythrocytes (NCEs, mature erythrocytes) was determined in 200 cells. For the comet assay of mouse blood cells, the experimental design was the same as was that for the micronucleus test in mouse bone marrow. Peripheral blood was collected in heparinized capillary vials and kept on ice until use. In brief, 20 μl of blood was homogenized with low-melting-point agarose, spread on a microscope slide pre-coated with normal-melting-point agarose, and coverslipped.

The corresponding commutation superoperators Hˆˆn(C) can be written as differences between left-side and right-side product superoperators Hˆˆn(L) and Hˆˆn(R), defined by their action on a density operator ρˆ: equation(3) Hˆˆ(C)=∑nHˆˆn(C)=∑nHˆˆn(L)-Hˆˆn(R)Hˆˆn(C)ρˆ=[Hˆn,ρˆ]=Hˆnρˆ-ρˆHˆnHˆˆn(L)ρˆ=HˆnρˆHˆˆn(R)ρˆ=ρˆHˆn Their faithful

representations have exponential dimensions, but representations in low correlation order basis sets are cheap [13]. In a given operator basis Oˆk: equation(4) Hˆˆn(L)jk=OˆjHˆˆn(L)Oˆk=TrOˆj†HˆnOˆk=Tr⊗m=1Nσˆj,m†⊗m=1Nσˆn,m⊗m=1Nσˆk,m Because dot products commute with direct products and the trace of a direct product is a product of traces, we have: equation(5) Hˆˆn(L)jk=Tr⊗m=1Nσˆj,m†σˆn,mσˆk,m=∏m=1NTrσˆj,m†σˆn,mσˆk,min which the dimension SB203580 datasheet of individual matrices σˆn,k is tiny and does not depend on the Epacadostat cell line size of the spin system;

the computational complexity of computing Tr[σˆj,m†σˆn,mσˆk,m] is therefore O(1) and the complexity of computing one matrix element is O(N) multiplications, where N is the total number of spins in the system. With O(N2) interactions in the spin system, this puts the worst-case complexity of building the representation of the Hamiltonian in Eq. (3) to O(N3D2), where D is the dimension of the reduced basis set. The sparsity of spin Hamiltonians [19] and the fact that spin interaction networks in proteins are also sparse Tolmetin puts the practically observed scaling closer to O(N2D) – a significant improvement on the O(4N) best-case scaling of the adjoint direct product representation. This improvement is further amplified by the presence of unpopulated states even in the low correlation order subspace [8], by the existence of multiple independently evolving

subspaces [13], and by the fact that not all of the populated states belong to the propagator group orbit of the detection state [11]. Matrix dimension, storage and CPU time statistics for a 512 × 512 point 1H–1H NOESY simulation of ubiquitin (573 protons, ∼50,000 terms in the dipolar Hamiltonian) are given in Table 2. As demonstrated in Fig. 1 and Fig. 2, the simulation is in good agreement with the experimental data. The state space restriction approximation reduces the Hamiltonian superoperator dimension from 4573 ≈ 10345 to 848,530. The reduced Hamiltonian is still sparse, and therefore within reach of modern matrix manipulation techniques – the simulation shown in Fig. 1 took less than 24 h on a large shared-memory computer.

While, as yet, there is a lack of direct evidence examining differences in cortical inhibition in synaesthesia, this offers one plausible mechanism of neural development that may associate synaesthesia, schizotypy, creativity

and mental imagery. Delineating the relative contributions that extended cognitive manifestations and alterations in neural development have on the relationship between synaesthesia and schizotypy will provide important insights into the mechanisms that mediate the developmental of typical and atypical perceptual experiences. MJB is supported by a British Academy Postdoctoral Fellowship. This work was partly supported by an MRC grant to VW. “
“The concept FDA-approved Drug Library molecular weight of the visual word form is one that is well-established within the psychological literature. Cattel (1886) first documented ‘whole word’ reading by demonstrating how briefly presented words were

easier to recall than briefly Linsitinib presented meaningless letter strings, and letters have subsequently been shown to be better identified when presented within a word than individually (Reicher, 1969; Wheeler, 1970) or within a non-word (Grainger et al., 2003). More recently, neuroimaging studies have identified an area within the left fusiform gyrus which is specialised for letter and word recognition and which may constitute the visual word form area (VWFA; Cohen et al., 2000). Given the recency of written relative to spoken language as a cultural invention, it is unlikely that a VWFA would have evolved specifically for reading. However, one suggestion is that accumulated reading experience promotes the specialisation of a pre-existing inferotemporal pathway CYTH4 for higher-order visual processing (McCandliss et al., 2003). The current paper emphasises the extent

of this functional specialisation by demonstrating remarkably preserved reading in the context of profoundly impaired perception of non-word stimuli. Neuropsychological evidence supporting the existence of highly-specialised processes for visual word recognition has been derived from patients exhibiting ‘letter-by-letter reading’ (LBL; also referred to as ‘word form dyslexia’ or ‘pure alexia’; e.g., Shallice and Warrington, 1980; Farah and Wallace, 1991; Binder and Mohr, 1992; Warrington and Langdon, 1994; Hanley and Kay, 1996; Cohen et al., 2000). Such patients exhibit intact letter identification and relatively accurate, but slow, reading, whereby response latencies increase in a linear manner proportionate to word length. LBL reading has been suggested to reflect destruction or inaccessibility of a visual word form system, and is associated with damage to the VWFA (Warrington and Shallice, 1980; Cohen et al., 2000). The attribution of LBL reading to a specific word form deficit has been challenged on two main grounds, namely that the condition and its characteristic word length effects can be accounted for by a general visual deficit and/or a letter identification deficit.

However, HDN restored the elevated levels significantly (P < 0.05) to within normal range in these animals

when compared to their respective control groups. The changes in the levels of serum and tissue lipids in normal and experimental rats are illustrated in Table 3. The levels selleck chemical of serum and tissue (Liver & Kidney) total cholesterol, triglycerides (TGs), free fatty acids (FFAs) and phospholipids (PLs) were highly altered in Fe treated rats when compared with control group. Oral administration of HDN to Fe intoxicated rat changes in the levels of serum and tissue total cholesterol, TGs, FFAs and PLs were near to normal. Table 4 shows the levels of lipid peroxidative markers (measured by the levels of thiobarbituric acid reactive substances and lipid hydroperoxides) were significantly increased in the plasma and tissue (Liver & Kidney) of Fe treated rats. Administration of HDN significantly (p < 0.05) decreased the levels of thiobarbituric acid reactive substances and lipid hydroperoxides on iron intoxicated rats Table 5 illustrates the activities of enzymatic antioxidants namely superoxide dismutase, catalase, glutathione GSK2118436 manufacturer peroxidase, glutathione-S-transferase in tissue (Liver & Kidney) of control and experimental rats. A significant (P < 0.05) depletion in the activities of enzymatic antioxidants in Fe treated rats was observed. Treatment of HDN along with Fe increased the levels of enzymatic antioxidants in

tissue (Liver & Kidney). Table 6 shows the changes in the levels of plasma and tissue (Liver & Kidney) non-enzymatic antioxidants

namely reduced glutathione, vitamin C and vitamin E. A significant (P < 0.05) decrease in the levels of non-enzymatic Calpain antioxidants was noticed in rats treated with Fe when compared to control rats. Treatment with HDN (80 mg/kg body weight) along with Fe restored the levels of non-enzymatic antioxidants to near normal. Histological analysis showed that Fe administration induces the pathological changes in liver. The liver of control rats (Fig. 3A) and HDN (Fig. 3B) treated rats showed a normal architecture. Fe exposure resulted in changes in liver architecture as indicated by focal necrosis, inflammatory cell infiltration and giant cell formation (Fig. 3 C). Fe along with HDN administration (Fig. 3D) showed near normal hepatocytes with mild portal inflammation. Histological studies showed that Fe administration induces the pathological changes in kidney. The focal areas of hemorrhage and inflammation of renal cells (Fig. 4C) were observed in Fe alone intoxicated rats. Rats administered with HDN along with Fe showed near normal appearance of glomerulai and tubules (Fig. 4D). Administration of HDN to normal rats did not produce any pathological changes in kidney (Fig. 4B) when compared with normal control rats (Fig. 4A). The objective of the present work was to investigate the protective effects of hesperidin on iron induced toxicity in rats.

We show a good match to estimated wave heights, but these might be further refined by adjusting the slide parameters further, as per Bondevik et al. (2005). The Fluidity modelling presented here assumes one particular type of slide movement as a single rigid block. It is unclear how somewhat more realistic slide behaviour would affect tsunami magnitudes and inundation heights around surrounding coastlines. More work is required in order to attempt

to improve the veracity of the model by altering the slide initiation and shape and to study the effects of such BKM120 supplier changes and how they compare to the changes described here with respect to resolution. The effects of bathymetric and coastline resolution are important in determining accurate simulated run-up heights of tsunamis. We have shown that the higher resolution coastline and bathymetric simulations produce simulated wave heights that are in closer agreement to inferred wave heights from observational data and have some sense of numerical convergence. Overall numerical resolution is important to minimise numerical errors and for this simulation a fixed mesh of 12.5 km is sufficient with coarse coastlines to reproduce the work of Harbitz (1992). However, as along-coastline resolution

increases, commensurately higher mesh resolution is required around the coasts. Assumptions of the slide AZD1208 acting as a rigid block, accelerating to 35 m/s, are similar to previous studies, but as the Storegga slide is thought to be retrogressive and disintegrate as it moved, more work is required to ascertain the effects of this on wave run-up heights. In establishing the spatial resolution of coastlines and palaeobathymetry required to adequately model the Storegga slide-generated tsunami, this work provides a foundation on which simulations examining the effect of complex slide parameters can build. Given the simplicity of our slide model and the absence of an inundation model, our multiscale models of the Storegga submarine slide generated tsunami shows remarkable agreement with inferred wave-heights from sediment deposits along the Norwegian and Scottish coasts.

The agreement within the Faroe Islands is less good, with a simulated wave height that is around a 6 m too small, but consistent with previous studies (Bondevik et al., 2005). Our multiscale not model simulates the Storegga tsunami for 15 h, tracking the wave propagation into the southern North Sea, predicting wave heights of less than 1 m for the northern coast of mainland Europe. The addition of palaeobathymetric information, neglected in previous studies, aids the match to observed data within the region where our data is valid and makes a substantial difference in the southern North Sea region and around the Shetland Islands. However, the use of realistic palaeobathymetry makes little difference along the Norwegian coast, which was the primary focus of previous studies.

More information is needed to determine if repeated exposure is toxic, if animals become SGI-1776 research buy habituated, or if consumption is only related to the availability of alternative forage. This work was funded by the National Institute of Science and Technology for Control of Plants Poisoning, CNPq grant number 573534/2008-0. The author acknowledges Prof. Odaci de Oliveira, Federal University of the Semiarid (UFERSA), for identifying the Jatropha species.

“
“The 17th World Congress of the International Society on Toxinology (IST) and Venom Week 2012 (4th International Scientific Symposium on All Things Venomous) are being combined into a multi-disciplinary scientific meeting on animal, plant and microbial toxins. The meeting will be held July 8 – 13, 2012, in Honolulu, Hawaii at the Hilton Hawaiian Village, a world-class hotel, right on Waikiki beach, and with special conference rates. The meeting will contain state-of-the-art toxinological research and practice, with platform

and poster sessions on animal, plant and microbial toxinology, proteomics, genomics, pharmacology, pathophysiology, venoms, antivenoms, clinical toxinology, veterinary PFT�� mw toxinology, venomous animal collections issues, and more! The meeting website can be found at: http://www.istworldcongress17-venomweek2012.org/ “
“The 17th World Congress of the International Society on Toxinology (IST) and Venom Week 2012 (4th International Scientific Symposium on All Things Venomous) are being combined into a multi-disciplinary scientific meeting on animal, plant and microbial toxins. The meeting will be held July 8 – 13, 2012, in Honolulu, Hawaii at the Hilton Hawaiian Village, a world-class hotel, right on Waikiki Paclitaxel research buy beach, and with special conference rates. The meeting will contain state-of-the-art toxinological research and practice, with platform and

poster sessions on animal, plant and microbial toxinology, proteomics, genomics, pharmacology, pathophysiology, venoms, antivenoms, clinical toxinology, veterinary toxinology, venomous animal collections issues, and more! The meeting website can be found at: http://www.istworldcongress17-venomweek2012.org/ “
“Bothrops alcatraz is a pitviper found only in the Alcatrazes Archipelago, off the northern coast of São Paulo state in southeastern Brazil. This species feeds primarily on invertebrates (centipedes) and vertebrates (amphibians) since these islands are devoid of small rodents, the main prey of mainland Bothrops spp. B. alcatraz differs from Bothrops jararaca primarily by its darker coloration, lower number of ventral, subcaudal, and infralabial scales, number and shape of anterior cephalic scales, shape of hemipenal spines and body size ( Marques et al., 2002). As a geographically and ecologically isolated species, B. alcatraz has a high potential for morphological variation and divergence in its venom composition compared to other Bothrops species.

Therefore, the GPS may be considered insufficient for prognostication. There is INK 128 an increasing evidence that platelet count and NLR can be used for prognostication in patients with several types of cancer [11] and [12]. Recently, Ishizuka et al. [13] showed that COP-NLR is considered to be a useful predictor of postoperative survival in patients with colorectal cancer. They showed that COP-NLR is easy to measure routinely because of its low cost and convenience [13]. Therefore, we conducted a study to determine whether COP-NLR is useful for predicting long-term survival in patients with ESCC. In our study, we demonstrated

that COP-NLR (P = .003) was significantly associated with CSS. Moreover, our study showed a similar HR between COP-NLR and GPS. In addition, the AIC and BIC values were similar between COP-NLR and GPS, indicating that COP-NLR predicts survival in ESCC similar to GPS. The potential limitations of the present study include the use of a retrospective analysis and the Caspase inhibitor in vivo short duration of the mean follow-up duration. In addition, we excluded patients who had adjuvant chemotherapy and/or radiotherapy, which may have influenced our analysis. Furthermore, AIC and BIC values were not correct if follow-up differed between patients, and the results of the study should therefore be regarded with caution. Thus, larger prospective studies will need to be performed to confirm

these preliminary results. In summary, our study showed that both GPS and COP-NLR are associated with tumor progression and can be considered as independent markers in patients with ESCC. We conclude that COP-NLR predicts survival in ESCC similar to GPS. However, larger prospective studies will need to be performed to confirm these preliminary results. The authors declare that they have no competing interests. “
“Melanoma is a malignant tumor of melanocytes, with a high potential to develop metastases. In the last few decades, the incidence of melanoma has increased cAMP substantially worldwide [1] and [2].

The annual growth rate of incidence is approximately 3% to 5%. Genetic, phenotypical, and environmental factors are involved in melanoma developing [3]. The manifestation and prognosis are significantly different between Asian and white populations. The subtype of superficial spreading melanoma is common in white patients, which is clearly associated with sunlight exposure [4]. Studies have confirmed that mutations of p16 located in the chromosome 9 or CDKN2A is the main genetic susceptibility of melanoma [5]. However, the most frequent subtypes of melanoma in Asian patients are acral lentiginous melanoma (AM) and mucosal melanoma (MM) [6] and [7]. The primary lesions were not always exposed to the ultraviolet, so the specific causative factor for increasing melanoma incidence in China was still unclear [6]. Lysosome-associated protein transmembrane 4 beta (LAPTM4B), is a new gene first cloned in hepatocellular carcinoma [8].

Grade-3 febrile neutropenia developed in 22 patients (26.8%). Nonhematological toxicities were generally mild and no evidence of cardiotoxicity of AMR was found in this study (Table 4). Pneumonitis was observed in nine patients (grade 4, n = 1; grade 3, n = 2; grade 2, n = 3; selleck chemical and grade 1, n = 3), and seven (grade 4, n = 1; grade 3, n = 2; grade 2, n = 2; and grade 1, n = 2) discontinued treatment because of unacceptable toxicity levels. The incidence rate of pneumonitis was higher in patients with history of thoracic radiation therapy than in others (38.5% v 5.8%, respectively), but one grade 4 pneumonitis case was observed in a patient without a history of thoracic radiation therapy. G-CSF was

administered to 51 (62.2%) patients and blood transfusions were necessary in 9 (11.0%). No treatment-related death was observed in this GKT137831 study. This single-arm confirmatory study was conducted to confirm the efficacy and safety of AMR in patients with refractory SCLC. In the present study, the primary endpoint was the ORR, which was 32.9%. This data supported the result that the ORR of AMR therapy was significantly better than that of topotecan therapy, in accordance with that previously reported in a randomized phase II study by Inoue et al. [9]. A possible limitation

of this study is related to its design, which was not a randomized phase III study, but rather a nonrandomized single-arm confirmatory study. Although there was potential for selection bias as a result of this study design, ORR was sufficiently higher than that for topotecan therapy in previous studies [8] and [11]. The secondary endpoints, PFS and OS, were also favorable, and Fenbendazole no

treatment-related deaths occurred in this study. On the basis of these results, we conclude that AMR monotherapy is suitable as an effective and safe treatment option for refractory SCLC. Jotte et al. [15] reported the results of a randomized phase III trial of AMR versus topotecan as second-line treatment for SCLC. The study randomized 637 patients in a 2:1 ratio for treatment with AMR (n = 424) or topotecan (n = 213). Treatment with AMR and topotecan showed similar OS periods (median, 7.5 v 7.8 months; hazard ratio for death, 0.880; 95% CI, 0.733–1.057; P = 0.17); however, higher ORRs (31.1% v 16.9%; P = 0.0001) and PFS periods (median, 4.1 v 3.5 months; hazard ratio for death or disease progression, 0.802; 95% CI, 0.667–0.965; P = 0.0182) were found with AMR therapy, and toxicity levels were more acceptable than those with topotecan therapy. Furthermore, in a subset analysis of 295 patients with refractory SCLC, AMR therapy demonstrated a modest improvement in OS (median, 6.2 v 5.7 months; hazard ratio for death, 0.766; 95% CI, 0.589–0.997; P = 0.0469). These results support our assertion that AMR monotherapy is a reasonable treatment option for patients with refractory SCLC.

The properties of these CALs, except for their molecular

masses that apparently are underestimated due to interactions on the chromatographic column, are similar to those described before ( Terra and Ferreira, 2012). Predatory hemipterans are usually thought to rely on pre-oral digestion Target Selective Inhibitor Library carried out by salivary enzymes. Although trypsin is usually described in salivary glands and considered to be responsible for prey tissue digestion, there is a lack of comparative work dealing with actual salivary hydrolase activities vis a vis midgut ones. Thus, unless this is done, one can not discount the possibility that prey tissues are pre-orally disrupted, but true digestion occurs only inside the midgut. For example, previous work on P. nigrispinus ( Oliveira et al., 2006) and B. tabidus ( Azevedo et al., 2007) implied a salivary trypsin on pre-oral digestion. Nevetheless, they did not rule out the possibility that they were assaying a cathepsin L instead of trypsin, nor evaluated the activity of this enzyme vis a vis the other proteinases to estimate its significance. Prey digestive enzymes are sometimes considered to play a role in digestion by predators,

although there is no experimental support for this. For instance, Pascual-Ruiz et al. (2009) suggested that P. maculiventris may well take advantage of prey proteolytic SD-208 nmr enzymes for digestion. Their conclusion is based on the increase of trypsin and chymotrypsin activity observed in P. maculiventris feeding on lepidopteran larvae in comparison to those feeding on beetles or dipteran pupae. As their proteolytic assays were done at pH 10, which favor lepidopteran enzymes ( Terra and Ferreira, 1994 and Terra and Ferreira, 2012) and maintain inactive hemipteran proteinases (this paper), their conclusions need to be re-evaluated. Our findings showed that prey muscle fibers are observed inside P. nigrispinus midguts and that they are no longer visible at

the posterior midgut. GNE-0877 This suggests that pre-oral digestion is restricted to tissue disruption. Midgut proteinases are found only in middle and posterior midgut, what discount the possibility that these enzymes are injected into prey. The only salivary proteinase with significant activity in comparison with midgut enzymes is collagenase. Thus, it is probable that collagenase-containing saliva is injected into the prey. This enzyme acting on the extracellular matrix disrupts tissues. Isolated cells or cell aggregates, like the observed muscle fibers, are then ingested by the bugs. True protein digestion then occurs inside the midgut under the action of cathepsin L-like enzymes and aminopeptidase. Although carboxypeptidases and dipeptidases have not been assayed, it is highly probable that they are also involved in protein digestion ( Terra and Ferreira, 1994 and Terra and Ferreira, 2012).

Wir schließen daraus, dass die Demethylierung von MeHg zu Hg2+ nicht der Mechanismus ist, der für die Entwicklung neurologischer Effekte im Verlauf der chronischen Latenzphase während der Exposition verantwortlich ist. Clarkson und Magos [2] schlugen vor, dass die Demethylierung von MeHg ein Teil der Verteidigungsstrategie der Gliazellen sein könnte, was einmal mehr die Bedeutung der interzellulären click here Abhängigkeit zwischen Neuronen

und Gliazellen betont. Wir haben bereits auf die Bedeutung von SH-Gruppen für die Bindung von Quecksilber hingewiesen, durch die wiederum die Konzentration von „freiem” Quecksilber verringert wird, das eine Interaktion mit sensitiven zellulären Bindungsstellen eingehen kann. Purkinje-Zellen sind reich an SH-Gruppen [120], die als inerte Bindungsstellen fungieren und so ein Quenching der Wirkung von Hg im Zellinnern herbeiführen können, was den Zellen eine höhere Toleranz gegenüber Hg verleiht [121] and [122]. Bei einer MeHg-Behandlung von Astrozyten im Cerebellum ist eine stärkere Depletion von GSH

beobachtet worden als bei Astrozyten im Kortex [123]. Der Grund für die höhere Produktion CB-839 order von ROS in cerebellären Astrozyten war der höhere Gehalt an GSH in kortikalen Astrozyten im Vergleich zu cerebellären Astrozyten. Jedoch wurden keine Unterschiede hinsichtlich der zellulären Verteilung von GSH zwischen Körner- und Purkinje-Zellen festgestellt [124]. Nach Exposition gegenüber MeHg wurde vor allem in Bergmann-Gliazellen, Purkinje-Zellen, Astrozyten und Gliazellen der weißen Substanz Metallothionein (MT) nachgewiesen, nicht dagegen in Körnerzellen [103]. Metallothioneine bestehen aus etwa 62 Aminosäuren, wobei 20 davon Cysteinreste sind. Dies verleiht dem Protein eine außerordentlich hohe Kapazität für die Chelierung von Metallen, die an SH-Gruppen binden. Daher

stellen Metallothioneine einen wichtigen Faktor dar, der die Bindung von Quecksilber an funktionell bedeutsame SH-Gruppen Phosphoglycerate kinase reduzieren kann. Dies sind wichtige Gesichtspunkte im Hinblick auf die unterschiedlichen Effekte in Neuronen sowie im Zusammenhang mit indirekten Wirkungen auf Neuronen als Ergebnis von Effekten, die in Gliazellen ausgelöst werden. Zusammenfassend lässt sich also sagen, dass der Gehalt an SH-Gruppen die MeHg-bedingten toxischen Effekte beeinflussen und zum Teil die unterschiedliche Sensitivität der verschiedenen Zelltypen erklären kann, die sich z. B. anhand von Befunden zur Synthese von Makromolekülen zeigen lässt [125], [126] and [127]. MeHg stört die Synthese von DNA, RNA und Proteinen. Der Mechanismus ist nicht bekannt, jedoch kann angenommen werden, dass die Bindung an wichtige SH-Gruppen bei diesen Veränderungen eine bedeutende Rolle spielt, z. B. durch sekundäre Veränderungen an DNA und RNA sowie Konformationsänderungen bei ribosomalen Proteinen [128].