Biomedical subjects

G Chevalier

Publications and source records attributed to G Chevalier.

At least 55 records · Page 3Linked to original sources

PubMed1989

Synthesis and characterization of 6-O-(N-heptylcarbamoyl)-methyl-alpha-D-glucopyranoside, a new surfactant for membrane studies.

A new surfactant, 6-O-(N-heptylcarbamoyl)-methyl-alpha-D-glucopyranoside (HECAMEG, molar mass 335.38 g), was synthesized by a simple and low cost procedure from methyl-alpha-D-glucopyranoside. This surfactant is characterized by a high solubility in water (even at 0 degree C), ultraviolet light transparency in the region useful for protein detection, and a high critical micellar concentration (CMC = 19.5 mM), permitting fast elimination by dialysis. Furthermore, the surfactant is colorimetrically titratable by the anthrone technique and its weak interference in protein titration by the Lowry et al. procedure and the bicinchoninic method is easy to overcome. Two membrane proteins (NADH oxidase and succinate dehydrogenase) and a soluble enzyme (lactoperoxidase) retained full activity in the presence of HECAMEG below or above its CMC. The partial inhibition of beta-lactamase (soluble form) by HECAMEG above the CMC was probably only apparent and due to an interference of the surfactant with the substrate rather than a direct effect on the enzyme. HECAMEG was capable of extracting up to 75% of bacteriorhodopsin from the purple membrane of Halobacterium halobium in a nondenatured form as indicated by the spectral properties of the protein. It also solubilized spiralin from the Spiroplasma melliferum membrane with a great selectivity and efficiency, without detectable loss of antigenic properties. These data show that HECAMEG is a very mild surfactant, useful for membrane protein studies.

Bacteria↗

PubMed1989

The response of the pulmonary surfactant-associated alkaline phosphatase following acute cadmium chloride inhalation.

In order to identify sensitive and specific biochemical indicators of pulmonary damages caused by industrial contaminants, male Long-Evans rats were exposed to a cadmium chloride (CdCl2) aerosol (5 mg Cd/m3; MMAD = 1.4 microns; SDg = 1.8) for 1 hr. The rats were sacrificed at 1, 4, 8, and 16 days after treatment. The response of the pulmonary surfactant (SF) system, which prevents alveolar collapse during expiration by lowering the surface tension at the air-liquid interface, was of particular interest. The effect of CdCl2 inhalation on the SF system was monitored by assaying the alkaline phosphatase (AKP) activity and phospholipid (PL) content in an enriched surface active SF fraction purified from bronchoalveolar lavages. The AKP activity of the SF fraction was markedly decreased (99%) on Day 1, indicating an inhibition of AKP by Cd. The PL content remained at control level while the total protein content was significantly increased (199%). On day 4, the high recovery of PL (207%) and AKP activities (639%) may reflect an increased secretion caused by Type II cell hyperplasia. By Day 8 these parameters returned to baseline levels. On Day 16 both the AKP activity and the PL content of the SF fraction were decreased significantly. Concurrently, the activities of the acid phosphatase and the B-N-acetylglucosaminidase followed, but to a lesser extent, the response of the AKP activity on Days 1 and 4. They differed from AKP, however, in that their activities remained significantly elevated on Day 8 and in that they returned to baseline levels on Day 16.(ABSTRACT TRUNCATED AT 250 WORDS)

Acetylglucosaminidase↗

PubMed1988

Toxicity of inhaled cadmium chloride: early responses of the antioxidant and surfactant systems in rat lungs.

In order to establish an animal model for assessing early and sensitive biochemical indicators of pulmonary damage, we studied the effects of inhaled CdCl2 (5 mg/m3.h; mass median aerodynamic diameter (MMAD) = 1.4 microns; SDg = 1.8) on the antioxidant defense and pulmonary surfactant systems of rat lungs. Rats were sacrificed 1, 4, 8, and 16 d after inhalation. Pulmonary edema (wet/dry weight) was observed on d 1. The total activities of the enzymes superoxide dismutase (SOD) and glucose-6-phosphate dehydrogenase (G6PD) in the lung homogenates of the treated animals were significantly throughout the 16-d period. Glutathione reductase (GR) was increased on d 4 and after. The general increases of SOD, GR, and the lysosomal enzymes acid phosphatase and beta-N-acetylglucosaminidase could be attributed to changes in the cellularity of the lung tissue. The significant increase in the specific activity of G6PD on d 4 suggested enzyme stimulation. Concurrently, the response of the surfactant system was measured by assaying the alkaline phosphatase (AKP) and the phospholipid content in the homogenates and in the cell-free bronchoalveolar lavage (BAL) fluids. The AKP activity in the homogenates decreased by 30%, while no activity was detected in the BAL on d 1, suggesting an inhibition of AKP by Cd. The secretion of surfactant seemed altered at this early time: phospholipid in the BAL decreased by 44%, although it increased by 61% in the tissue. The high recovery of phospholipid (312%) in the BAL on d 4 and the important changes in the AKP activity in the BAL from d 4 to 16 may reflect alterations in the processing of the surfactant. The effect of Cd on AKP makes this enzyme a potential marker of the metal redistribution in the pulmonary alveolar region, which could be a useful tool in long-term studies.

Acetylglucosaminidase↗

PubMed1988

Virus-pesticide interactions with murine cellular immunity after sublethal exposure to dieldrin and aminocarb.

Interaction of two potential immunosuppressive factors, sublethal pesticide exposure and viral inhibition of lymphocyte mitogenesis, was examined in mixed lymphocyte reaction (MLR). Inbred (C57Bl/6 x A/J)F mice, semisusceptible to mouse hepatitis virus 3 (MHV3) infection were exposed to selected pesticides and subsequently infected with the MHV3 virus. The mortality of animals was examined as a function of pesticide exposure. Two pesticides were selected for further studies: the organochlorine pesticide dieldrin, which increased the cumulative mortality of animals, and the carbamate pesticide aminocarb, which did not affect the virus-induced cumulative mortality of animals. Spleen lymphocytes from dieldrin- and aminocarb-exposed C57Bl/6 mice (susceptible to MHV3 infection) were used as responder cells in one-way MLR. A marked immunosuppression of the MLR proliferative response was observed in the dieldrin group, whereas sublethal exposure to aminocarb did not affect the in vitro MLR response. The MLR cultures were subsequently infected in vitro with the MHV3 virus, which resulted in a time-dependent and virus dose-dependent inhibition of lymphocyte proliferation. However, no synergism was observed with the addition of either the MHV3 virus-induced inhibition of in vitro MLR lymphoproliferative response or dieldrin-related immunosuppression, since in vitro MHV3 infection of cells from dieldrin-exposed mice did not aggravate the dieldrin-related immunosuppression. In addition, no "hidden" aminocarb-related damage of the lymphoproliferative response was noted, as the kinetics of the virus-induced inhibition in the aminocarb group were analogous to the control. In conclusion, dieldrin-induced immunosuppression of the cellular immune response, rather than MHV3 virus-induced inhibition of lymphoproliferative activity itself, was the primary factor potentially responsible for the impaired cellular response. Furthermore, the data support the observation that cell-mediated immunity can be a potential target for the adverse effects of pesticide exposure.

Animals↗

PubMed1987

Development of vasoactive intestinal peptide-responsive adenylate cyclase during enterocytic differentiation of Caco-2 cells in culture. Evidence for an increased receptor level.

The purpose of this work was to study vasoactive intestinal peptide (VIP) receptors and the adenylate cyclase response to VIP upon enterocytic differentiation of the human colon adenocarcinoma cell line Caco-2 in culture. The VIP-stimulated enzyme activity is very low, e.g. 20% above basal activity in undifferentiated cells (day 5) and is enhanced markedly at confluency reaching a maximum, e.g. 270%, above basal activity in fully differentiated cells (day 30). VIP potency is also slightly enhanced, the EC50 of VIP ranging from 0.31 nM at day 5 to 0.07 nM at day 30. Modifications of the adenylate cyclase system are not responsible for the development of VIP response. Indeed, forskolin-stimulated adenylate cyclase activity is unchanged during differentiation supporting no alteration of the enzyme catalytic subunit. The same holds true for NaF and guanosine 5'-(beta, gamma-imido)trisphosphate, indicating a constant activity of the guanine nucleotide regulatory unit which mediates hormonal stimulation of adenylate cyclase (Ns). This is further supported by the similar extent of cholera toxin-catalyzed [32P]ADP-ribosylation of the Ns protein that is observed during differentiation. In sharp contrast, a dramatic increase of VIP receptor concentration is observed ranging from 32 fmol/mg of protein at day 5 to 414 fmol/mg of protein at day 30. This is confirmed by affinity cross-linking experiments showing an increased specific incorporation of 125I-VIP in a major 66,000-dalton component during differentiation. A slight increase in receptor affinity is also observed during differentiation with Kd ranging from 0.39 nM at day 5 to 0.08 nM at day 30. These data indicate that one population of VIP receptors accumulates during Caco-2 cell differentiation, representing the crucial event in the development of adenylate cyclase response to the peptide.

Adenylyl Cyclases↗

PubMed1987

A and H blood group antigens as markers of sucrase-isomaltase from the enterocyte-like differentiated human colon carcinoma cell lines HT-29 and Caco-2.

The purpose of this work was to investigate whether sucrase-isomaltase from enterocyte-like differentiated human colon carcinoma cell lines carries blood group antigens of the ABH system. Six cultured lines of blood group A (HT-29, SW-480, Co-115) or O phenotype (Caco-2, HRT-18, HCT-8R) were studied. Only HT-29 cells grown in the absence of glucose (HT-29 Glc-) and Caco-2 cells express an enterocytic differentiation with the presence of sucrase-isomaltase on the apical surface of the cells. Binding of anti-A antibodies to HT-29 Glc- and of UEA-I to Caco-2 cells gave the same apical immunofluorescence pattern of staining as did anti-sucrase-isomaltase antibodies, whereas only a membrane binding was observed in nondifferentiated cells. Sucrase-isomaltase immunoisolated from HT-29 Glc- and Caco-2 cells reacted with anti-A antibodies and Ulex europaeus agglutinin-I (UEA-I), respectively, at sodium dodecyl sulfate-polyacrylamide gel electrophoresis and immunoblot. Immunoprecipitation of solubilized brush border-enriched fractions from the same cells with UEA-I or anti-A antibodies resulted in an inhibition of sucrase activity which reached congruent to 80% for Caco-2 cells with UEA-I and approximately equal to 50% for HT-29 cells with anti-A antibodies. Similar results were obtained in the corresponding tumors in nude mice: anti-A antibodies in HT-29 and UEA-I in Caco-2 tumors bound to the same apical structures as did anti-sucrase-isomaltase antibodies; sucrase-isomaltase immunoisolated from the tumors bound anti-A antibodies (HT-29) or UEA-I (Caco-2). These results support the hypothesis that sucrase-isomaltase from enterocyte-like differentiated human colon cancer cells carries blood group antigens of the ABH system. These findings suggest that colon cancers which have been shown to display an apical pattern of expression of ABH antigens should be screened for their possible enterocytic differentiation.

ABO Blood-Group System↗

PubMed1987

Immunosuppression in mice after inhalation of cadmium aerosol.

Aerosol cadmium (CdCl2) exposure of female C57Bl/6 mice was performed to assess the in vivo effects of cadmium on the cellular and humoral immune responses of splenic lymphocytes. Primary cellular and humoral responses of lymphocytes were examined at 5-18 days after a single, 60 min exposure to 0.88 mg Cd/m3 (MMAD = 0.7 +/- 0.3 micron, sigma g = 3.43). Significant decrease of in vitro lymphoproliferative response to allogeneic antigens, LPS and PHA antigens, and inhibition of the primary IgM response to sheep erythrocytes were correlated with a marked decrease in spleen cell viability at 5-8 days after aerosol cadmium exposure. This type of cadmium-induced immunosuppression, which correlated with the direct cytotoxicity of effector cells, appeared to be different from the chronic, oral cadmium-induced suppression of the primary IgM response, in which acute cytotoxicity of the spleen cell population was not observed.

Administration, Inhalation↗

PubMed1986

Pulmonary toxicity of the insecticide fenitrothion in the rat following a single field exposure.

The pulmonary toxicity of the organophosphorus insecticide fenitrothion was evaluated following a single exposure of rats to the field formulation, at the site of an aerial spraying. Four groups of 40 Sprague-Dawley rats (including a control), set in wood enclosures, were placed under the aerial lines of the spraying aircraft. The degree of exposure was monitored at the ground level by air sampling and visual evidence of droplet activity deposition. Plasma pseudocholinesterase activity and pulmonary alveoli ultrastructure were used as indices to the fenitrothion exposure. Rat lungs were examined under light and electron microscopy at days 3, 7, 21, 60 and 180 after the exposure. Although a few signs of toxic lung injury were observed at days 3 and 7 there was no cholinergic crisis nor an effect on the pseudocholinesterase activity within 12 h in the exposed animals, when compared with controls. The alveolar toxic reaction was limited to small and discrete foci, and was entirely reversible within a period of 2 months. On a morphological basis it is thus concluded that a single field exposure to fenitrothion did not induce any permanent change in the alveolar area of the rat lung.

Administration, Inhalation↗

PubMed1986

Nigral modulation of cerebello-thalamo-cortical transmission in the ventral medial thalamic nucleus.

In the rat, the highly active GABAergic neurons of the substantia nigra pars reticulata (SNR) are known to exert a tonic inhibitory influence on cells in the ventral medial thalamic nucleus (VM). Considering that this nucleus is involved in the transfer of cerebellar signals towards motor cortex, we investigated the role played by SNR in that transmission. For this purpose we examined how changes in nigral background activity are reflected in the reactivity of VM cells to their cerebellar input. We report here that a GABA induced nigral pause increases the efficacy of cerebellar afferent volleys in VM, whereas an increase of nigral background by bicuculline, interrupts cerebello-thalamo-cortical transmission. It is concluded that nigrothalamic neurons subserve a permanent gating of cerebello-thalamo-cortical transmission in VM.

Action Potentials↗

PubMed1986

Effect of chronic exposure to an acidified environment on the urophysis of the brook trout, Salvelinus fontinalis.

The activity of the caudal neurosecretory system including its neurohemal organ, the urophysis, was assessed in six populations of brook trout (Salvelinus fontinalis)--three from acidified lakes and three from nonacidified lakes (Laurentides Parc, Québec). The acidified lakes were characterized by low pH (mean annual value around 5.5), poor buffering capacity and low conductivity. The activity of the caudal neurosecretory cells was evaluated by morphometry (cell and nuclear sizes). The urophysial content of the neuropeptide urotensin II was measured by isolated trout rectum bioassay. Fish from acidified lakes showed markedly larger cell and nuclear sizes and a lower content of urotensin II than fish from nonacidified lakes. An acidified environment appears to stimulate the synthetic activity of caudal neurosecretory neurons and promote release of urotensin II from the urophysis. This modified endocrine activity in brook trout may reflect adjustment to adverse external ionic conditions.

Animals↗

PubMed1985

Disinhibition as a basic process in the expression of striatal functions. I. The striato-nigral influence on tecto-spinal/tecto-diencephalic neurons.

The striato-nigro-collicular pathway is one of the neuronal circuits through which basal ganglia can influence ocular and cephalic motricity. Through this pathway striatal signals are conveyed to a major collicular efferent system i.e. the tecto-spinal/tecto-diencephalic neurons (TSD). A striking particularity of the striato-nigro-collicular connection is to present an assemblage of two successive GABAergic inhibitory links. To analyze how striatal information is expressed through this double inhibitory system we made use of concomitant unitary recordings of substantia nigra pars reticulata (SNR) and TSD activity while nigral and/or striatal activity was changed by local applications of pharmacological agents. We observed (1) that an intranigral application of GABA which transiently abolishes the tonic discharge of SNR cells, causes the TSD cells to discharge vigorously. During this period of increased excitability the responsiveness of TSD cells to somatosensory input is significantly enhanced; (2) that an intrastriatal injection of glutamate which silences the nigro-collicular cells, causes the TSD cells to discharge. This striatally induced tectal firing being sensitive to intranigral application of a GABA antagonist (bicuculline), led us to the conclusion that striatum exerts a facilitatory influence on TSD cells by releasing these neurons from the tonic inhibitory nigral influence. The functional implication of such a mechanism is discussed in the light of the current knowledge on the involvement of basal ganglia in eye/head orienting movements.

Animals↗

PubMed1985

Disinhibition as a basic process in the expression of striatal functions. II. The striato-nigral influence on thalamocortical cells of the ventromedial thalamic nucleus.

Besides the nigro-collicular pathway, the nigro-thalamic projection to the ventromedial thalamic nucleus represents another efferent system of the basal ganglia through which striatum can influence motor centers. Since the striato-nigrothalamic circuit is composed of two successive GABAergic inhibitory links and the SNR is tonically active, we tested that by inhibiting nigrothalamic cells, the striatum may exert a facilitatory influence on VM-thalamocortical cells. We show that a transitory block of SNR (substantia nigra pars reticulata) firing (induced by either intranigral application of GABA or by stimulating the inhibitory striato-nigral pathway), causes a perfectly time-locked increase of activity in a large number of VM cells projecting to motor cortex. Moreover, the striatally evoked excitation of VM-thalamocortical cells requires the functional integrity of the GABAergic striato-nigral link. We conclude that the double inhibitory striato-nigrothalamic pathway acts on VM-thalamocortical cells through a disinhibitory mechanism. The functional implication of such a mechanism is discussed.

Animals↗

PubMed1985

The intracellular accumulation of UDP-N-acetylhexosamines is concomitant with the inability of human colon cancer cells to differentiate.

The relationship between the intracellular concentration of various nucleotides as measured by high-performance liquid chromatography analysis, and the differentiation of 2 human colon cancer cell lines was studied. HT-29 cells were induced to undergo both structural and functional enterocytic differentiation (as determined by electron microscopy and the presence of brush-border specific enzymes, respectively) by changing the carbon source or adding Na butyrate to standard tissue culture media. This differentiation occurred after the cells reached confluency when they were cultured in galactose, uridine, inosine, or without nucleosides (all in the absence of glucose) and in the presence of glucose plus Na butyrate. Cells cultured in 25 mM fructose or glucose +/- nucleosides did not differentiate. In all culture conditions where HT-29 cells did not differentite, the intracellular concentrations of 2 compounds which co-migrated with UDP-N-acetylglucosamine and UDP-N-acetylgalactosamine rose approximately equal to 10-fold at confluency and remained elevated throughout the stationary phase, whereas their concentrations remained constant and low after confluency in cells that underwent differentiation. This indicated that the accumulation of these compounds is associated with the inability of these cells to differentiate since other nucleotides and nucleotide sugars did not change in a similar fashion. Purification of the presumed UDP-N-acetylhexosamines, followed by the identification of the products from their chemical and enzymatic hydrolysis, confirmed the identity of these two peaks. Nucleotide analysis of Caco-2 cells, which undergo enterocytic differentiation after they reach confluency even when cultured on glucose, revealed the same pattern of UDP-N-acetylhexosamine levels as differentiated HT-29 cells, with its concentration remaining relatively constant and very low, even after the cells were confluent. The significance of the accumulation of UDP-N-acetylhexosamines in cells unable to differentiate is discussed.

Adenocarcinoma↗

PubMed1985

Enterocytic differentiation of a subpopulation of the human colon tumor cell line HT-29 selected for growth in sugar-free medium and its inhibition by glucose.

In order to study the effect of glucose on the differentiation of cultured human colon cancer cells, a subpopulation of HT-29 cells was selected for its capacity to grow in the total absence of sugar. These cells (Glc-cells) exhibit, after confluency, an enterocytic differentiation, in contrast to cells grown with glucose (Glc+ cells), which always remain undifferentiated. The differentiation is characterized by a polarization of the cell layer with apical brush borders and tight junctions, and by the presence of sucrase-isomaltase. The differentiation of Glc- cells is reversible: the addition of glucose to postconfluent cultures of Glc- cells results in an inhibiting effect on the expression of sucrase-isomaltase; switching growing cultures of Glc- cells to the Glc+ medium for several passages results in a progressive reversion to the undifferentiated state, which is completed after seven passages. The dedifferentiation process is associated with a parallel, passage-related, increase in the rates of glucose consumption and lactic acid production, and decreases of intracellular glycogen content, which return to the values of the undifferentiated original Glc+ cells. The values of these metabolic parameters are correlated, at each passage, with the degree of dedifferentiation of the cells. When these dedifferentiated cells, after having been cultured in Glc+ medium for 20 passages, are switched back to the Glc- medium, they readily grow without mortality, and reexpress the same enterocytic differentiation as the parent Glc- cells. These results show that the capacity of this subpopulation to grow and differentiate in the absence of sugar is a stable characteristic. They further suggest that glucose metabolism interferes with the program of differentiation of HT-29 cells.

Cell Differentiation↗

PubMed1985

Enterocytic differentiation and glucose utilization in the human colon tumor cell line Caco-2: modulation by forskolin.

The human colon cancer line Caco-2 exhibits after confluency a concomitant increase of glycogen accumulation and an enterocytic differentiation. The purpose of this work was to investigate whether forskolin (FK), an activator of adenylate cyclase, would induce a permanent glycogenolysis and, if so, whether it would result in modifications of the differentiation pattern of the cells. FK activates adenylate cyclase in Caco-2 cells with an ED50 of 7 X 10(-6)M. Three different treatment protocols with FK (10(-5)M) were applied: 1) the cells were treated during all the time in culture (20 days); 2) the treatment was started after confluency; 3) the treatment was interrupted after confluency. The presence of FK results in a permanent stimulation of cAMP accumulation (10 to 20 fold the basal values) and in a permanently reduced glycogen content (30 or 50% of the control values). The rates of glucose consumption are increased three and five fold in protocols 1 and 3 respectively. These metabolic changes are associated with morphological changes (tightening of the intercellular spaces and shortening of the brush border microvilli) and with a dual inhibition of the activities of brush border hydrolases: a) an inhibition of the post-confluent increase of activity of sucrase, aminopeptidase N and alkaline phosphatase in the brush border enriched fraction; b) an inhibition of the post-confluent increase of activity of sucrase in the cell homogenate. A comparison of the results obtained in each protocol shows that the morphological modifications and the decrease of the enzyme activities in the brush border fraction are regularly associated with an increased cAMP accumulation, whereas the inhibition of the differentiation of sucrase is a direct consequence of the increase in glucose consumption and decrease in glycogen stores.

Cell Line↗

PubMed1985

Absence of genotoxic effects of nonasbestos mineral fibers.

The biological activity of natural and synthetic mineral fibers has been examined. Natural attapulgite [(Mg, Al)2Si4O10(OH).4H2O], synthetic xonotlite [Ca3Si3O8(OH)2] and natural sepiolite [Mg2Si3O8.2H2O] were selected. Genotoxic effects were investigated by means of a well established cellular model based upon the measurement of unscheduled DNA synthesis (UDS) in rat hepatocytes in primary culture. The intrinsic capacity of the fibers (1 and 10 micrograms/ml) to induce UDS was first tested. None of the fiber types showed detectable UDS-eliciting activity. Also, the possible modulation of the cellular response to genotoxic agents by the materials was examined by exposing the cells to mixtures of 2-acetylaminofluorene (AAF) (0.05 and 0.25 micrograms/ml) and fibers (1 and 10 micrograms/ml). In these experiments, the UDS response was significantly diminished in the presence of xonotlite. This phenomenon may reflect changes in the uptake and/or metabolism of AAF or may result from an inhibition of DNA repair processes, the latter suggesting a possible cocarcinogenic potential for this synthetic silicate. These results point to the immediate necessity of studying more extensively the biological effects of fibrous materials that can be used as substitutes for asbestos.

Animals↗

PubMed1985

Ultrastructural study of mineral fiber uptake by hepatocytes in vitro.

Cellular interactions of a series of fibrous materials were examined by the use of a well established in vitro system. Primary cultures of hepatocytes were exposed to natural attapulgite, synthetic xonotlite and natural sepiolite. Ultrastructural analyses revealed that hepatocytes can engage in the phagocytosis of all 3 types of fibers over an exposure period of 20 h. Attapulgite fibers were found in plasma membrane invaginations, and deeper in the cytoplasm, in vesicles exhibiting various shapes. Xonotlite was also incorporated in plasma membrane invaginations; furthermore, these fibers were present in large vacuoles where they were circumscribed by membranes and appeared somewhat isolated from the cytoplasm. Sepiolite fibers were also taken up by the cells and could likewise be identified in the previously described structures. These observations point to the relevance of the hepatocyte model for investigating the effects of fibrous materials at the cellular level.

Animals↗

PubMed1985

Genotoxicity of dimethylnitrosamine in the presence of chrysotile asbestos UICC B and xonotlite.

Interactions of particulates with chemical genotoxic agents may play an important role in the induction of carcinogenesis. With respect to bronchogenic cancer, the synergism associated with combined exposure to asbestos and tobacco smoke is a well-documented phenomenon. The present work focused on chrysotile asbestos and xonotlite. The latter is a fibrous calcium silicate which is increasingly being used to replace asbestos in various industrial applications. The study was aimed at testing the possible interaction of these materials with dimethylnitrosamine (DMN), a genotoxic component of tobacco smoke. The capacity of fibers to interfere with the genotoxic response elicited by DMN in the UDS/hepatocyte assay system specifically designed for sensitive detection of short-patch DNA repair, was looked for. The properties of the selected fibers with respect to binding affinity towards DMN were also examined.

2-Acetylaminofluorene↗