Evidence of long term biogeochemical interactions in carbonate weathering: The role of planktonic microorganisms and riverine bivalves in a large fluviokarst system.

The infiltration of organic-rich surface waters towards groundwaters, is known to play a significant role in carbonate weathering and in contributing to the atmospheric continental carbon sink. This paper investigated biogeochemical interactions in karst critical zones, with strong surface water /groundwater interactions, and in particular the role of planktonic microorganisms and riverine bivalves through the analysis of particulate organic matter (OM) oxidation on carbonate weathering. In the large Val d'Orléans fluviokarst aquifer (France), a 20-year monthly dataset of Nitrates, Dissolved Oxygen (DO), dissolved inorganic and organic Carbon (DIC and DOC) fluxes was gathered. The surface water-groundwater comparison of geochemical trends showed that planktonic microorganisms had drastically decreased in surface waters, related to the proliferation of Corbicula bivalves spreading and a decrease in nutrients. This decrease in planktonic microorganisms was followed by a DO increase and an DIC decrease at the karst resurgence. The degradation of planktonic microorganisms consumes DO and produces NO3, dissolved inorganic carbon (DIC) and a proton that in turn, dissolves calcite and produces DIC. Without the input from planktonic microorganisms, the fluviokarst has lost 29 % of this nitrification and 12 % of the carbonate dissolution capacities. Thus, the oxidation of particulate organic matter of planktonic microorganisms, which is part of heterotrophic respiration, appears to be a significant source of the inorganic carbon flux in riverine ecosystems. This shows how weathering can remain active under waters saturated versus calcite and suggests that the oxidation of organic matter can be a more appropriate mechanism than autotrophic respiration to explain the relationship between global warming and DIC flux change in rivers. Through the consumption of plankton, the animal life in rivers thus influences the inorganic carbon in groundwaters, creating a negative feedback in the carbon cycle.

Author Correction: Global karst springs hydrograph dataset for research and management of the world's fastest-flowing groundwater.

An amendment to this paper has been published and can be accessed via a link at the top of the paper.

Global karst springs hydrograph dataset for research and management of the world's fastest-flowing groundwater.

Karst aquifers provide drinking water for 10% of the world's population, support agriculture, groundwater-dependent activities, and ecosystems. These aquifers are characterised by complex groundwater-flow systems, hence, they are extremely vulnerable and protecting them requires an in-depth understanding of the systems. Poor data accessibility has limited advances in karst research and realistic representation of karst processes in large-scale hydrological studies. In this study, we present World Karst Spring hydrograph (WoKaS) database, a community-wide effort to improve data accessibility. WoKaS is the first global karst springs discharge database with over 400 spring observations collected from articles, hydrological databases and researchers. The dataset's coverage compares to the global distribution of carbonate rocks with some bias towards the latitudes of more developed countries. WoKaS database will ensure easy access to a large-sample of good quality datasets suitable for a wide range of applications: comparative studies, trend analysis and model evaluation. This database will largely contribute to research advancement in karst hydrology, supports karst groundwater management, and promotes international and interdisciplinary collaborations.

Short- and long-term gene expression profiles induced by inhaled TiO2 nanostructured aerosol in rat lung.

The number of workers potentially exposed to nanoparticles (NPs) during industrial processes is increasing, although the toxicological properties of these compounds still need to be fully characterized. As NPs may be aerosolized during industrial processes, inhalation represents their main route of occupational exposure. Here, the short- and long-term pulmonary toxicological properties of titanium dioxide were studied, using conventional and molecular toxicological approaches. Fischer 344 rats were exposed to 10 mg/m3 of a TiO2 nanostructured aerosol (NSA) by nose-only inhalation for 6 h/day, 5 days/week for 4 weeks. Lung samples were collected up to 180 post-exposure days. Biochemical and cytological analyses of bronchoalveolar lavage (BAL) showed a strong inflammatory response up to 3 post-exposure days, which decreased overtime. In addition, gene expression profiling revealed overexpression of genes involved in inflammation that was maintained 6 months after the end of exposure (long-term response). Genes involved in oxidative stress and vascular changes were also up-regulated. Long-term response was characterized by persistent altered expression of a number of genes up to 180 post-exposure days, despite the absence of significant histopathological changes. The physiopathological consequences of these changes are not fully understood, but they should raise concerns about the long-term pulmonary effects of inhaled biopersistent NPs such as TiO2.

Experiencing a probabilistic approach to clarify and disclose uncertainties when setting occupational exposure limits.

OBJECTIVES: Assessment factors (AFs) are commonly used for deriving reference concentrations for chemicals. These factors take into account variabilities as well as uncertainties in the dataset, such as inter-species and intra-species variabilities or exposure duration extrapolation or extrapolation from the lowest-observed-adverse-effect level (LOAEL) to the noobserved- adverse-effect level (NOAEL). In a deterministic approach, the value of an AF is the result of a debate among experts and, often a conservative value is used as a default choice. A probabilistic framework to better take into account uncertainties and/or variability when setting occupational exposure limits (OELs) is presented and discussed in this paper. MATERIAL AND METHODS: Each AF is considered as a random variable with a probabilistic distribution. A short literature was conducted before setting default distributions ranges and shapes for each AF commonly used. A random sampling, using Monte Carlo techniques, is then used for propagating the identified uncertainties and computing the final OEL distribution. RESULTS: Starting from the broad default distributions obtained, experts narrow it to its most likely range, according to the scientific knowledge available for a specific chemical. Introducing distribution rather than single deterministic values allows disclosing and clarifying variability and/or uncertainties inherent to the OEL construction process. CONCLUSIONS: This probabilistic approach yields quantitative insight into both the possible range and the relative likelihood of values for model outputs. It thereby provides a better support in decision-making and improves transparency. Int J Occup Med Environ Health 2018;31(4):475-489.

In vitro comet and micronucleus assays do not predict morphological transforming effects of silica particles in Syrian Hamster Embryo cells.

Crystalline silica particles and asbestos have both been classified as carcinogenic by the International Agency for Research on Cancer (IARC). However, because of the limited data available, amorphous silica was not classifiable. In vitro, the carcinogenic potential of natural crystalline and amorphous silica particles has been revealed by the Syrian Hamster Embryo (SHE) cell transformation assay. On the other hand, the genotoxic potential of those substances has not been investigated in SHE cells. And yet, genotoxicity assays are commonly used for hazard evaluation and they are often used as in vitro assays of reference to predict a possible carcinogenic potential. The main objective of this study was to compare the genotoxic potential and the carcinogenic potential of different crystalline and amorphous silica particles in SHE cells. Three silica samples of different crystallinity were used: natural amorphous silica, partially crystallized silica and quartz silica particles. Their genotoxicity were tested through the in vitro micronucleus assay and the comet assay in SHE, and their carcinogenic potential through the SHE transformation assay. In addition, silica samples were also tested with the same genotoxicity assays in V79 hamster-lung cells, a common in vitro model for particle exposure. Results obtained in the micronucleus and the comet assays show that none of the silica was capable of inducing genotoxic effects in SHE cells and only the amorphous silica induced genotoxic effects in V79 cells. However in the SHE cell transformation assays, the partially crystallized and quartz silica were able to induce morphological cell transformation. Together, these data suggest that, in vitro, the short-term genotoxic assays alone are not sufficient to predict the hazard and the carcinogenic potential of this type of particles; SHE transformation assay appears a more reliable tool for this purpose and should be included in the "in vitro battery assays" for hazard assessment.

Genotoxicity of synthetic amorphous silica nanoparticles in rats following short-term exposure. Part 2: intratracheal instillation and intravenous injection.

Synthetic amorphous silica nanomaterials (SAS) are extensively used in food and tire industries. In many industrial processes, SAS may become aerosolized and lead to occupational exposure of workers through inhalation in particular. However, little is known about the in vivo genotoxicity of these particulate materials. To gain insight into the toxicological properties of four SAS (NM-200, NM-201, NM-202, and NM-203), rats are treated with three consecutive intratracheal instillations of 3, 6, or 12 mg/kg of SAS at 48, 24, and 3 hrs prior to tissue collection (cumulative doses of 9, 18, and 36 mg/kg). Deoxyribonucleic acid (DNA) damage was assessed using erythrocyte micronucleus test and the standard and Fpg-modified comet assays on cells from bronchoalveolar lavage fluid (BALF), lung, blood, spleen, liver, bone marrow, and kidney. Although all of the SAS caused increased dose-dependent changes in lung inflammation as demonstrated by BALF neutrophilia, they did not induce any significant DNA damage. As the amount of SAS reaching the blood stream and subsequently the internal organs is probably to be low following intratracheal instillation, an additional experiment was performed with NM-203. Rats received three consecutive intravenous injections of 5, 10, or 20 mg/kg of SAS at 48, 24, and 3 hrs prior to tissue collection. Despite the hepatotoxicity, thrombocytopenia, and even animal death induced by this nanomaterial, no significant increase in DNA damage or micronucleus frequency was observed in SAS-exposed animals. It was concluded that under experimental conditions, SAS induced obvious toxic effects but did cause any genotoxicity following intratracheal instillation and intravenous injection.

Dissemination of acrylamide monomer from polyacrylamide-based flocculant use--sand and gravel quarry case study.

Aggregate quarries play a major role in land settlement. However, like all industrial operations, they can have impacts on the environment, notably due to the use of polyacrylamide (PAM)-based flocculants, which contain residual acrylamide (AMD), a carcinogenic, mutagenic, and reprotoxic monomer. In this study, the dissemination of AMD throughout the environment has been investigated in a French quarry. The presence of AMD has been determined in the process water and in the sludge, as well as in the surrounding surface water and groundwater. From the results of several sampling campaigns carried out on this case study, we can (a) confirm that the AMD contained in the commercial product is found in the quarry's water circuit (0.41 to 5.66 µg/l); (b) show that AMD is transported to the surrounding environment, as confirmed by the contamination of a pond near the installation (0.07 to 0.08 µg/l) and the presence of AMD in groundwater (0.01 to 0.02 µg/l); and (c) show that the sludge in both the current and former settling basins contains AMD (between 4 and 26 µg/kg of dry sludge). Therefore, we demonstrated in this case study that using PAM-based flocculants leads to the release of AMD to the environment beyond the treatment plant and creates a reserve of AMD in sludge basins.

Water and acrylamide monomer transfer rates from a settling basin to groundwaters.

The aim of this paper was to estimate the potential leakage of acrylamide monomer, used for flocculation in a settling basin, towards the groundwaters. Surface-groundwater interactions were conceptualized with a groundwater transport model, using a transfer rate to describe the clogged properties of the interface. The change in the transfer rate as a function of the spreading of the clogged layer in the settling basin was characterized with respect to time. It is shown that the water and the Acrylamide transfer rate are not controlled by the spreading of the clogged layer until this layer fully covers the interface. When the clogged layer spreads out, the transfer rate remains in the same order of magnitude until the area covered reaches 80 %. The main flux takes place through bank seepage. In these early stage conditions of a working settling basin, the acrylamide flux towards groundwaters remains constant, at close to 10 g/year (±5).

Genotoxicity of styrene-7,8-oxide and styrene in Fisher 344 rats: a 4-week inhalation study.

The cytogenetic alterations in leukocytes and the increased risk for leukemia, lymphoma, or all lymphohematopoietic cancer observed in workers occupationally exposed to styrene have been associated with its hepatic metabolisation into styrene-7,8-oxide, an epoxide which can induce DNA damages. However, it has been observed that styrene-7,8-oxide was also found in the atmosphere of reinforced plastic industries where large amounts of styrene are used. Since the main route of exposure to these compounds is inhalation, in order to gain new insights regarding their systemic genotoxicity, Fisher 344 male rats were exposed in full-body inhalation chambers, 6 h/day, 5 days/week for 4 weeks to styrene-7,8-oxide (25, 50, and 75 ppm) or styrene (75, 300, and 1000 ppm). Then, the induction of micronuclei in circulating reticulocytes and DNA strand breaks in leukocytes using the comet assay was studied at the end of the 3rd and 20th days of exposure. Our results showed that neither styrene nor styrene-7,8-oxide induced a significant increase of the micronucleus frequency in reticulocytes or DNA strand breaks in white blood cells. However, in the presence of the formamidopyridine DNA glycosylase, an enzyme able to recognize and excise DNA at the level of some oxidized DNA bases, a significant increase of DNA damages was observed at the end of the 3rd day of treatment in leukocytes from rats exposed to styrene but not to styrene-7,8-oxide. This experimental design helped to gather new information regarding the systemic genotoxicity of these two chemicals and may be valuable for the risk assessment associated with an occupational exposure to these molecules.

Cytotoxicity and genotoxicity of nanosized and microsized titanium dioxide and iron oxide particles in Syrian hamster embryo cells.

Potential differences in the toxicological properties of nanosized and non-nanosized particles have been notably pointed out for titanium dioxide (TiO(2)) particles, which are currently widely produced and used in many industrial areas. Nanoparticles of the iron oxides magnetite (Fe(3)O(4)) and hematite (Fe(2)O(3)) also have many industrial applications but their toxicological properties are less documented than those of TiO(2). In the present study, the in vitro cytotoxicity and genotoxicity of commercially available nanosized and microsized anatase TiO(2), rutile TiO(2), Fe(3)O(4), and Fe(2)O(3) particles were compared in Syrian hamster embryo (SHE) cells. Samples were characterized for chemical composition, primary particle size, crystal phase, shape, and specific surface area. In acellular assays, TiO(2) and iron oxide particles were able to generate reactive oxygen species (ROS). At the same mass dose, all nanoparticles produced higher levels of ROS than their microsized counterparts. Measurement of particle size in the SHE culture medium showed that primary nanoparticles and microparticles are present in the form of micrometric agglomerates of highly poly-dispersed size. Uptake of primary particles and agglomerates by SHE exposed for 24 h was observed for all samples. TiO(2) samples were found to be more cytotoxic than iron oxide samples. Concerning primary size effects, anatase TiO(2), rutile TiO(2), and Fe(2)O(3) nanoparticles induced higher cytotoxicity than their microsized counterparts after 72 h of exposure. Over this treatment time, anatase TiO(2) and Fe(2)O(3) nanoparticles also produced more intracellular ROS compared to the microsized particles. However, similar levels of DNA damage were observed in the comet assay after 24 h of exposure to anatase nanoparticles and microparticles. Rutile microparticles were found to induce more DNA damage than the nanosized particles. However, no significant increase in DNA damage was detected from nanosized and microsized iron oxides. None of the samples tested showed significant induction of micronuclei formation after 24 h of exposure. In agreement with previous size-comparison studies, we suggest that in vitro cytotoxicity and genotoxicity induced by metal oxide nanoparticles are not always higher than those induced by their bulk counterparts.

Bio-distribution study of 1,2-diethylbenzene and its main metabolites by whole-body autoradiography and tissue homogenates.

The bio-distribution of the neurotoxic 1,2-diethylbenzene (1,2-DEB) was studied in male Sprague-Dawley rats after intravenous administration of [(14)C] 1,2-DEB (1 mg kg(-1)). The highest concentrations of [(14)C] non-volatile metabolites, determined by whole-body auto-radiography, were in the nasal cavity, ethmoid turbinates and in kidney. Whatever the time after dosing, the [(14)C] concentrations in the cerebrum, cerebellum, spinal cord and lung were lower than those in the blood. In contrast, after killing of batch of administered rats, the [(14)C] concentrations in the brain homogenates were higher than in plasma for 5-15 min. In addition, the [(14)C] concentrations in the lung were higher than in the plasma for 24 h post-dose. Moreover, the concentrations of unchanged 1,2-DEB and one of its metabolites, 1-(2'-ethylphenyl)ethanol (1,2-EPE) in the brain, were higher than in the plasma until 1 h post-dose. The concentrations of 1,2-DEB in the blood cells were tenfold higher than in the plasma. The clearance of unchanged 1,2-DEB in the whole blood and in the blood cells was 6.4 and 3.9 ml min(-1), respectively. The apparent half-life of unchanged 1,2-DEB in plasma is very fast (5 min) which suggests a quick distribution and/or metabolism in liver and/or other tissues such as the lung. In conclusion, unchanged 1,2-DEB has a high affinity for the brain and blood cells and its concentrations in plasma and brain decreased rapidly with time.

Bitumen fume-induced gene expression profile in rat lung.

Exposure to bitumen fumes during paving and roofing activities may represent an occupational health risk. To date, most of the studies performed on the biological effect of asphalt fumes have been done with regard to their content in carcinogenic polycyclic aromatic hydrocarbons (PAH). In order to gain an additional insight into the mechanisms of action of bitumen fumes, we studied their pulmonary effects in rodents following inhalation using the microarray technology. Fisher 344 rats were exposed for 5 days, 6 h/day to bitumen fumes generated at road paving temperature (170 degrees C) using a nose-only exposition device. With the intention of studying the early transcriptional events induced by asphalt fumes, lung tissues were collected immediately following exposure and gene expression profiles in control and exposed rats were determined by using oligonucleotide microarrays. Data analysis revealed that genes involved in lung inflammatory response as well as genes associated with PAH metabolization and detoxification were highly expressed in bitumen-exposed animals. In addition, the expression of genes related to elastase activity and its inhibition which are associated with emphysema was also modulated. More interestingly genes coding for monoamine oxidases A and B involved in the metabolism of neurotransmitters and xenobiotics were downregulated in exposed rats. Altogether, these data give additional information concerning the bitumen fumes biological effects and would allow to better review the health effects of occupational asphalt fumes exposure.

Genotoxic effects of bitumen fumes in Big Blue transgenic rat lung.

Road paving workers are exposed to bitumen fumes (CAS No. 8052-42-4), a complex mixture of volatile compounds and particles containing carcinogenic and non-carcinogenic polycyclic aromatic hydrocarbons. However, epidemiological and experimental animal studies failed to draw unambiguous conclusions concerning their toxicity. In order to gain better insights on their genotoxic potential, we used an experimental design able to generate bitumen fumes at road paving temperature (temperature: 170 degrees C, total particulate matter: 100mg/m3) and perform a nose-only exposure of Big Blue transgenic rodents 6h/day for five consecutive days. The mutagenic properties of bitumen fumes were determined by analyzing the mutation frequency and spectrum of the neutral reporter gene cII inserted into the rodent genome. We previously observed in mouse lung, that bitumen fumes did not induce an increase of cII mutants, a modification of the mutation spectrum, nor the formation of DNA adducts. Since DNA adducts were found in the lungs of rats exposed to asphalt fumes in similar conditions, we decided to carry out an analogous experiment with Big Blue rats. A DNA adduct was detected 3 and 30 days after the end of treatment suggesting that these genetic alterations were quite steady. Thirty days after exposure, the cII mutant frequency was similar in control and exposed rats. In addition, a slight but not significant modification of the mutation spectrum associated with an increase of G:C to T:A and A:T to C:G transversions was noticeable in the treated animals. Then, these data failed to demonstrate a pulmonary mutagenic potential for bitumen fumes generated at road paving temperature in our experimental conditions despite the presence of a DNA adduct. These results may provide information concerning the pulmonary mechanism of action of this aerosol and may contribute to the occupational health hazard assessment.

TDI can induce respiratory allergy with Th2-dominated response in mice.

Toluene diisocyanate (TDI), a highly reactive industrial chemical is one of the leading causes of occupation-related asthma in industrialized countries. The pathophysiology of TDI-induced asthma, however, remains poorly understood, in part due to a lack of appropriate animal models. In this study, four models of TDI-sensitised mice were investigated. In model number 1, the mice were sensitised for 4 h/day on four consecutive days to 3 ppm inhaled TDI and challenged twice for 4 h each time with 0.3 ppm inhaled TDI. In model number 2, the sensitising condition was similar to that of model 1, but the challenge conditions involved an initial inhalation of 2 ppmTDI for 4h and then tracheal instillation with 50 microg/mouse albumin-TDI. In model number 3, the mice were sensitised first to 25% TDI (sc) and then three times for 4 h each time to 1 ppm inhaled TDI and challenged twice for 4h each time with 0.1 ppm inhalated TDI. In model number 4, the mice were first sensitised to 1% TDI by skin application and then with 0.2% TDI by tracheal instillation and challenged tree times by tracheal instillation of 0.1% TDI. In model number 4, skin application followed by tracheal instillations of TDI led to local and systemic Th2-dominated immune responses that were characterized: (1) in the lung-associated lymph nodes by a decrease in Th1 cytokine (IFN-gamma) production associated with an increase in Th2 cytokine (IL-4, IL-5, IL-3) production; (2) in the lungs by an allergic inflammation throughout the conducting airways: goblet cell proliferation and eosinophil influx and; (3) in the serums by increased total and specific IgE levels, 17.5- and 3.5-fold higher than that of the controls, respectively. The conditions used for sensitisation in the other models, i.e. inhalation or subcutaneous administration plus inhalation, failed to induce a strong Th2 response like that observed in model number 4. The findings indicate that TDI can induce a Th2-dominated response in mice when administered by topical application plus tracheal instillation for sensitisation and by intra-tracheal instillation for challenge (model number 4). This mouse Th2 model of TDI-induced airway allergy can, in several aspects, mimic occupational TDI asthma in humans and may prove to be useful in determining the mechanistic basis behind this disease.

Surface reactivity, cytotoxicity, and transforming potency of iron-covered compared to untreated refractory ceramic fibers.

Untreated and iron-coated refractory ceramic fibers (RCFs) 1, 3, and 4 were examined for their potential to generate free radicals and to catalyze hydrogen peroxide decomposition in cell-free assays and were compared for cytotoxic and transforming potencies in Syrian hamster embryo (SHE) cell system. Coating with a high quantity of iron increased the capability of RCFs to generate hydroxyl radicals and to catalyze the decomposition of hydrogen peroxide. In the SHE cells, the untreated RCFs had varying ability to induce inhibition of cell proliferation, cytotoxicity (as measured by the colony-forming efficiency, CE) and morphological transformation, in a concentration-dependent manner. According to cytotoxic and transforming potencies, they ranged as follows: RCF3 > RCF1 > RCF4. The lethal concentration 50 (LC50; decrease of CE to 50% of controls after 7 d of treatment) expressed per number of RCF3 and RCF1/cm(2) of culture dish was 2.5 x 10(4) and 3.7 x 10(4), respectively, whereas RCF4 was not cytotoxic up to the highest concentration tested (23.7 x 10(4) fibers/cm(2)). At LC50, RCF3 was 1.4-fold more transforming than RCF1, and the weakest, RCF4, induced less than 1% transformation. Iron coating of RCF1 and RCF3 markedly attenuated their cytostatic, cytotoxic, and transforming potencies without a linear concentration-transformation relationship. In contrast, iron coating of RCF4 affected slightly its low transforming potency, although the growth inhibitory effect was reduced. The observed decrease rather than increase in the cytotoxic and transforming potencies of the active samples RCF1 and RCF3 by their coating with large amounts of ferric iron suggests that it is not the quantity or any form of iron on the surface of fibers but the iron, even in trace, in a particular redox and coordinate state that might play a role in the fiber's surface reactivity with regard to the biological material. Surface chemical functions involved in the interaction with the cell could be inactivated by the deposition of a high quantity of Fe(III) on the surface of fibers. Physicochemical studies correlated to biological effects is an approach for understanding the properties of solids related to a given biological response and for elucidating the cellular and molecular mechanisms.

Lack of genotoxicity of bitumen fumes in transgenic mouse lung.

During hot application of bitumen containing materials, e.g. in hot paving or roofing, fumes are emitted that contain polycyclic aromatic compounds. Previous studies with rodents exposed to bitumen and coal-tar fume condensates showed formation of DNA adducts. In order to clarify the genotoxicity of bitumen fumes, we designed a study by using mice carrying a reporter gene for mutagenesis analysis and exposed by nose-only to a constant and reproducible aerosol of bitumen fumes. We analyzed the genotoxic activity of inhaled bitumen fumes generated under those controlled conditions through the induction of mutation and DNA adducts in Big Blue mice. Mice were exposed to bitumen fumes (100 mg/m(3) total particulate matter) 6 h per day during 5 days by nose-only in an inhalation chamber designed in our laboratory. Following a 30-day fixation period, the experiment was terminated and lung DNA was extracted for mutant frequency and adduct determinations. The mutant frequency was determined using the cII and the lacI mutant analysis systems. In, addition, 61 and 54 mutants were sequenced in control and exposed groups, respectively. The study did not show any mutation or adduct induction in the exposed group compared to the control group: cII mutant frequencies were 11.0+/-4.5x10(-5) and 11.0+/-4.8x10(-5) in control and exposed lungs, respectively. Identically, using the lacI mutation detection system, the mutant frequencies were 6.4+/-3.1x10(-5) and 5.8+/-2.0x10(-5). The mutation spectra of both series were quite similar with regard to transition and transversion frequencies. The absence of genotoxicity in the group exposed to 100 mg/m(3) bitumen is discussed with regard to dosage of inhaled polycyclic aromatic compounds and species.

Estudo quantitativo em microscopia óptica de luz do gânglio pterigopalatino no rato / Light microscopical quantitative study of the pterygopalatine ganglion in rat

Determinaçoes morfométricas estereológicas foram feitas em microscopia óptica de cortes semifinos de gânglio pterigopalatino (GP) do rato. Os seguintes parâmetros do pericário foram analisados: diâmetro equatorial (D), densidade volumétrica (Vv), densidade da superfície por volume (Sv) e densidade numérica (Nv). Os resultados obtidos do estudo de três animais, foram (média + desvio padrao): D = 23,93 + 6,46 mum; Vv = 53,83 + 7,40 por cento; Sv = 0,173 + 0,026 mum1; Nv (x 10(-5)) = 5,38 + 1,26 mum(-3). Os gânglios parassimpáticos cranianos apresentam variaçoes na mesma espécie, e entre diferentes espécies, quanto ao Nv e o tamanho das células.