OBJECTIVETo explore the integrative quantitative index of the extent of pneumoconiotic changes by dusts and to evaluate the extent of pulmonary injury by the dusts containing different contents of free silica.

METHODSIn accordance with the morphometric principle, the areas of each kind of pathologic changes in the lung tissue sections of pneumoconiosis model were measured by utilizing a computer-aided graphic analyzer, and the volume density of each pathologic change and the value of pulmonary injury by dust(VPID) were calculated. Meanwhile the extent of pulmonary injury were compared among the rat groups treated with the dusts containing different contents of free silica.

RESULTSThere were significant differences among each groups in the volume density of some pathologic changes in the same exposed periods. There were significant correlation between VPID and the content of free silica dust or the lung collagen content (r = 0.535-0.849, P < 0.005 or P < 0.01). Furthermore, the degree of cor relationship of VPID with both of the latter were higher than the sum of unweighted volume density of the various pathologic changes in lung.

CONCLUSIONIt is suitable, reasonable and simple to use VPID an index to indicate the extent of pulmonary injury by dust and to diagnose pneumoconiosis in pathology, and the extent of pulmonary injury by dust may be aggravated with the increasing of the content of free silica.

Animals ; Dust ; Lung ; pathology ; Pneumoconiosis ; pathology ; Rats ; Silicon Dioxide ; toxicity

Animals ; Lung/metabolism* ; Rats ; Silicon Dioxide/toxicity* ; Thioredoxins/metabolism*

OBJECTIVE: To investigate the toxicology and biodynamics of silica nanoparticle. METHODS: The silica nanoparticles were injected into mice through tail vein, and the mice were amphimixised, the urine was collected in different time, variations of pathology in organs and tissues of the mice were detected. At the same time, the silica nanoparticles' distribution in the tissues was observed through electron microscope. RESULTS: The silica nanoparticles were detected in all tissues and urine of the mice. The injected mice can reproduce as normal. CONCLUSION The silica nanoparticles do not have toxicity and can be used in vivo.
Animals ; Female ; Male ; Materials Testing ; Mice ; Nanostructures ; toxicity ; Rats ; Silicon Dioxide ; pharmacokinetics ; toxicity ; Tissue Distribution ; Transfection

Dust ; Humans ; Maximum Allowable Concentration ; Occupational Exposure ; adverse effects ; Research Report ; Silicon Dioxide ; toxicity

OBJECTIVETo investigate the autophagy of effector cells in lung tissue at different time points when rats were exposed to free SiO2 dust.

METHODSSixty Wistar rats (220∼230 g) were selected and allocated to experimental group (n = 30) and control group (n = 30). In the experimental group, a rat silicosis model was established by infusing SiO2 suspension into the trachea of rats. Six rats in each group were sacrificed on days 1, 7, 14, 21, or 28 of dust exposure. Lung tissue samples were collected to prepare lung tissue sections. The pulmonary inflammation and fibrosis were observed by HE staining. The proautophagosome, autophagosome, and autophagolysosome in lung tissue sections were observed under a transmission electron microscope.

RESULTSOn day 1 of dust exposure, many proautophagosomes and autophagosomes were seen in both experimental group and control group. On day 7 of dust exposure, the experimental group had more autophagosomes in lung tissue than the control group. On day 14 of dust exposure, the experimental group had fewer autophagosomes than the control group. On days 21 and 28, autophagolysosomes were seen in macrophage plasma in both experimental group and control group; the autophagolysosomes in experimental group showed cloudy swelling and expansion, and some were vacuolated, and these changes were more significant on day 28.

CONCLUSIONFree SiO2 dust can induce autophagy in the lung tissue of rats, with varying degrees at different time points of dust exposure.

Animals ; Autophagy ; drug effects ; Dust ; Lung ; drug effects ; pathology ; Male ; Rats ; Rats, Wistar ; Silicon Dioxide ; toxicity

Objective: To construct a recombinant lentiviral vector for mouse miR-204 overexpression, and to verify the targeted regulation of miR-204 and DVL3 in silica (SiO(2)) -induced mouse lung epithelial cells (MLE-12 cells) . Methods: In October 2019, the pre-miR-204 gene was amplified from the mouse genome by the polymerase chain reaction (PCR) method. After sequencing, the amplified product was cloned into the pLenti-CMV-EGFP lentiviral vector. The positive clones were identified by PCR screening and sequencing. The miR-204 overexpressed lentiviral vector was transfected into 293T cells, and lentiviral packaging and titer determination were performed. The experiment was divided into SiO(2) control group, virus control group, and miR-204 virus group, and the expressions of miR-204 and DVL3 gene were detected by real-time PCR. Results: The miR-204 lentiviral expression vector Lv-miR-204-5p was constructed and identified correctly by PCR and sequencing, and a virus dilution with a titer of 9.57×10(8) IU/ml was obtained. The results of real-time PCR showed that the expression of miR-204 in MLE-12 cells of the miR-204 virus group was higher than that of SiO(2) control group and virus control group, and the expression of DVL3 gene was lower than that of SiO(2) control group and virus control group, the differences were statistically significant (P<0.05) . Conclusion: Overexpression of miR-204 by lentiviral vector may inhibit the expression of DVL3 gene in silica-induced mouse lung epithelial cells.
Animals ; Epithelial Cells ; Genetic Vectors ; Lentivirus/metabolism* ; Lung ; Mice ; MicroRNAs/metabolism* ; Silicon Dioxide/toxicity* ; Transfection

OBJECTIVETo study the pulmonary toxicity to rats induced by the nanosized SiO(2) or the standard SiO(2).

METHODSSeventy-two male SD rats were divided into three groups: the nanosized SiO(2) group, the standard SiO(2) group and the control group. 24 rats each group. The nanosized SiO(2) group and the standard SiO(2) group were instilled intratracheally with 0.5 ml suspension of 0.6 mg/ml nanosized SiO(2) or standard SiO(2) respectively while the control group was instilled with 0.5 ml physiological saline. On the 3rd, 7th, 14th, and 28th day after exposure, six rats were sacrificed at each time point and the total white cells counts and total protein in BALF and the histopathological changes were observed. The pulmonary toxicities of the two SiO(2) dusts were compared.

RESULTSNanosized SiO(2) caused significant increase at 3rd, 7th, 14th day after the exposure [(16.0 +/- 6.0) x 10(6), (11.1 +/- 4.0) x 10(6), (12.2 +/- 4.6) x 10(6)] compared with saline (P < 0.05 or P < 0.01) in the total numbers of white cells and on the 3rd after the exposure compared with standard SiO(2) [(5.7 +/- 3.7) x 10(6), P < 0.01]. Meanwhile, Nanosized SiO(2) significantly increased the total protein on the 14th, 28th day after the exposure (0.41 +/- 0.14, 0.41 +/- 0.19 g/L) compared with saline or standard SiO(2) and nanosized SiO(2) on the 3rd, 7th day after the exposure (P < 0.05 or P < 0.01). Nanosized SiO(2)-treated rats showed marked white cell infiltration in alveolar space or around brondum the blood vessel. Standard SiO(2) caused similar but less severe responses compared with nanosized SiO(2). Van Gieson's-stained sections showed no significant fibrosis in these dust-exposed rats at 28th day after the exposure.

CONCLUSIONNanosized SiO(2) can cause severer and longer pulmonary toxicity in rats than standard SiO(2). The pulmonary particle load threshold of nanosized SiO(2) may be lower than that of standard SiO(2).

Animals ; Male ; Nanoparticles ; toxicity ; Particle Size ; Pulmonary Fibrosis ; chemically induced ; Rats ; Rats, Sprague-Dawley ; Silicon Dioxide ; toxicity

OBJECTIVETo access rat lung toxicity of nano silica particles.

METHODSTransmission electron microscope was used to observe size, shape and dispersibility of two silica particles; Size of two particles in water and RPMI 1640 containing 1% FBS were measured using Zeta Potential Analyzer. LDH activities of rat type I-like alveolar epithelial cell line R3/1 cells after 6, 24 and 48 h incubation with 2.5, 5.0, 10.0, 20.0 microg/ml of two silica nano particles were detected by spectrophotometric method; protein carbonylation and MIP-2 release of R3/1 cells after 24 h incubation with 2.5, 5.0, 10.0, 20.0 microg/ml of two silica nano particles were measured using ELISA kits.

RESULTSTEM image showed nano silica particles were round and dispersed evenly; the average sizes of the two silica particles were (43+/-4.2) and (68+/-5.7) nm. Two silica particles had similar size in water and RPMI 1640 containing 1% FBS, respectively. Both nano silica particles in 2.5 approximately 20.0 microg/ml dose range did not cause significant increase of LDH activities (P>0.05), did not elevate protein carbonylation and MIP-2 levels in R3/1 cells (P>0.05).

CONCLUSIONTwo nano silica particles do not have lung toxicity in 2.5 approximately 20.0 microg/ml dose range.

Alveolar Epithelial Cells ; drug effects ; metabolism ; Animals ; Cells, Cultured ; L-Lactate Dehydrogenase ; metabolism ; Nanoparticles ; toxicity ; Rats ; Silicon Dioxide ; toxicity ; Toxicity Tests

OBJECTIVETo investigate the subchronic oral toxicity of silica nanoparticles (NPs) and silica microparticles (MPs) in rats and to compare the difference in toxicity between two particle sizes.

METHODSSprague-Dawley rats were randomly divided into seven groups: the control group; the silica NPs low-, middle-, and high-dose groups; and the silica MPs low-, middle-, and high-dose groups [166.7, 500, and 1,500 mg/(kg•bw•day)]. All rats were gavaged daily for 90 days, and deionized water was administered to the control group. Clinical observations were made daily, and body weights and food consumption were determined weekly. Blood samples were collected on day 91 for measurement of hematology and clinical biochemistry. Animals were euthanized for necropsy, and selected organs were weighed and fixed for histological examination. The tissue distribution of silicon in the blood, liver, kidneys, and testis were determined.

RESULTSThere were no toxicologically significant changes in mortality, clinical signs, body weight, food consumption, necropsy findings, and organ weights. Differences between the silica groups and the control group in some hematological and clinical biochemical values and histopathological findings were not considered treatment related. The tissue distribution of silicon was comparable across all groups.

CONCLUSIONOur study demonstrated that neither silica NPs nor silica MPs induced toxicological effects after subchronic oral exposure in rats.

Administration, Oral ; Animals ; Dose-Response Relationship, Drug ; Female ; Male ; Nanoparticles ; toxicity ; Particle Size ; Rats ; Rats, Sprague-Dawley ; Silicon Dioxide ; toxicity ; Toxicity Tests, Subchronic

Animals ; Male ; Particle Size ; Rats ; Rats, Sprague-Dawley ; Respiratory Distress Syndrome, Adult ; chemically induced ; Silicon Dioxide ; chemistry ; toxicity