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At least 613 records · Page 34Linked to original sources
PubMed1997

Silica induces changes in cytosolic free calcium, cytosolic pH, and plasma membrane potential in bovine alveolar macrophages.

The mineral-dust induced activation of pulmonary phagocytes is thought to be involved in the induction of severe lung diseases. The activation of bovine alveolar macrophages (BAM) by silica was investigated by flow cytometry. Short-term incubation (< 10 min) of BAM with silica gel and quartz dust particles induced increases in the cytosolic free calcium concentration ([Ca2+]i), decreases in intracellular pH (pHi), and increases in plasma membrane potential (PMP). The extent of these changes was concentration dependent, related to the type of dust and was due to Ca2+ influx from the extracellular medium. An increase in [Ca2+]i was inhibited, when extracellular Ca2+ was removed. Furthermore the calcium signal was quenched by Mn2+ and diminished by the calcium channel blocker verapamil. The protein kinase C specific inhibitor bisindolylmaleimide II (GF 109,203 X) did not inhibit the silica-induced [Ca2+]i rise. In contrast, silica-induced cytosolic acidification and depolarization were inhibited by GF 109,203 X but not by removal of extracellular calcium. Addition of TiO2 particles or heavy metal-containing dusts had no effect on any of the three parameters. Our data suggest the existence of silica-activated transmembrane ion exchange mechanisms in BAM, which might be involved in the specific cytotoxicity of silica by Ca(2+)-dependent and independent pathways.

Animals↗
PubMed1988

Fibroblast proliferation induced by silica-exposed human alveolar macrophages.

Inhalation of silica dust is an important cause of pulmonary fibrosis. In these studies, we demonstrate that supernatants of silica-stimulated human alveolar macrophages cause significantly (p less than 0.05) greater amounts of fibroblast proliferation than do supernatants of macrophages stimulated with optimal amounts of endotoxin (LPS). The amount of fibroblast proliferation was similar (p greater than 0.2) in the presence of supernatants of LPS-stimulated macrophages and supernatants of unstimulated adherent macrophages. When macrophages were stimulated with LPS in the presence of indomethacin (to inhibit the cyclooxygenase pathway of arachidonic acid), the supernatants stimulated the same amount of proliferation of fibroblasts as did supernatants of silica-stimulated macrophages. Indomethacin did not increase the growth factor activity of supernatants of silica-stimulated or unstimulated macrophages. Consistent with these observations, supernatants of LPS-stimulated macrophages contained 25.5 +/- 3.8 nM of PGE2, whereas supernatants of silica-stimulated macrophages and unstimulated macrophages contained essentially no PGE2. These findings were confirmed by high performance liquid chromatography. The amounts of PGE2 present in supernatants of LPS-stimulated macrophages were sufficient to cause a 75% reduction in the proliferation of maximally stimulated fibroblasts. These studies suggest that silica may be a very effective stimulus for fibroblast proliferation in vivo since it causes macrophages to release growth factors for fibroblasts without triggering the release of PGE2, an inhibitor of fibroblast proliferation.

Cell Division↗
PubMed1989

Asbestos fibers and silica particles stimulate rat alveolar macrophages to release tumor necrosis factor. Autoregulatory role of leukotriene B4.

Alveolar macrophages (AM) can play a crucial role in the pathogenesis of pulmonary disease via their ability to produce potent inflammatory and fibrogenic mediators. We found that rat AM cultured with 1 to 100 micrograms/ml of silica particles or asbestos fibers produced tumor necrosis factor (TNF) and leukotriene B4 (LTB4) in a concentration-dependent fashion, whereas latex beads, an inert phagocytic stimulus, failed to induce significant augmentation of either TNF or LTB4. In a time course study, AM stimulated for 2 h with silica or asbestos produced an increased amount of LTB4, which preceded the rise in TNF activity detected 7 and 24 h after culture initiation. The induction appears to involve the synthesis of new protein since actinomycin D and cycloheximide abrogate the majority of the stimulatory effect. We next examined the role of LTB4 in mineral-dust-induced TNF production. The lipoxygenase inhibitors nordihydroguaiaretic acid (NDGA) and AA861 used at 1 to 50 micrograms/ml reduced in a concentration-dependent fashion asbestos- or silica-stimulated TNF release. On the other hand, "reconstitutive" experiments in which we added exogenous LTB4 (10(-14) to 10(-8) M) to AM treated with lipoxygenase inhibitors showed partial restoration of TNF production induced by chrysotile or silica, with peak effect at 10(-10)M LTB4. The present study demonstrated that AM incubated in the presence of chrysotile A or silica can produce both LTB4 and TNF and that endogenous lipoxygenase metabolites as well as exogenous LTB4 can act to amplify TNF production. These observations suggest a common mechanism by which asbestos and silica may modulate the production of inflammatory and fibrogenic cytokines.

Animals↗
PubMed1995

Hydroxyl radical production and lung injury in the rat following silica or titanium dioxide instillation in vivo.

The hydroxyl radical (.OH) is a highly reactive oxygen free radical that has been implicated as a cause of lung injury following exposure to silica and silicates. Despite evidence that silica generates .OH in vitro, there has been no previous demonstration of in vivo production of .OH after exposure to nonfibrous mineral oxide dusts. We tested the hypothesis that instillation of silica into rat lungs is associated with greater .OH production and acute lung inflammation in vivo relative to the instillation of a less toxic nonsilicate particle, titanium dioxide. The production of .OH in the lungs following dust instillation was measured using sodium salicylate as an .OH trap. Seven days after dust exposure, the rats were given intraperitoneal salicylate, the lungs isolated, and salicylate hydroxylation products (2,3- and 2,5-dihydroxybenzoic acid), reflecting .OH, were measured. There was significantly more 2,3-dihydroxybenzoic acid in silica-exposed lungs compared with lungs instilled with titanium dioxide. In addition, the instillation of silica into rat lungs in vivo was associated with a greater acute inflammatory response. We conclude that following in vivo exposure, silica stimulates greater .OH production relative to the less toxic particle, titanium dioxide. These differences in .OH generation correspond to disparities in acute lung inflammation.

Animals↗
PubMed1999

Upregulation of the p75 but not the p55 TNF-alpha receptor mRNA after silica and bleomycin exposure and protection from lung injury in double receptor knockout mice.

We have investigated a potential role for tumor necrosis factor (TNF)-alpha and its two receptors (p55 and p75) in lung injury. We used several varieties of mice exposed endotracheally to two fibrogenic agents, silica (0.2 g/kg) and bleomycin (4 U/kg). The lungs were analyzed at 14 and 28 d after exposure to bleomycin or silica, respectively, for TNF and TNF receptor (TNFR) messenger RNA (mRNA), hydroxyproline content, and histopathology. Silica induced increased (over saline-treated animals) expression of TNF mRNA in double TNFR knockout (Ko), C57BL/6, BALB/c, and 129/J mice. In contrast, bleomycin increased expression in all but BALB/c mice, which are resistant to the fibrogenic effects of this drug. mRNA expression of both receptors was constitutively expressed in all of the normal murine strains. Silica upregulated expression of the p75 receptor, but not the p55 receptor, in the C57BL/6, BALB/c, and 129/J mice. In comparison, bleomycin had little effect on either receptor in the bleomycin-resistant BALB/c mice. Hydroxyproline content of the lungs after treatment followed this same pattern, with significant increases caused by silica in the C57BL/6, BALB/c, and 129/J mice, whereas bleomycin caused no apparent increases in the BALB/c mice. Even though silica and bleomycin induced increases in TNF in the TNFR Ko mice, the mice were protected from the fibrogenic effects of these agents. This study supports the concept that TNF is a central mediator of interstitial pulmonary fibrosis.

Animals↗
PubMed1998

Expression of plasminogen activator inhibitors type-1 and type-2 in the mouse lung after administration of crystalline silica.

Altered expression of plasminogen activator inhibitors (PAIs) is of potential relevance to the process of lung fibrosis. To clarify the involvement of PAIs in interstitial lung diseases, we examined whether alterations in PAI-1 and PAI-2 were induced in response to a single intratracheal administration of a fibrosing dose of crystalline silica in mice (5 mg x animal(-1)). The time course of changes in PAI activity and PAI-1 protein were characterized in bronchoalveolar lavage fluid (BALF) and changes in PAI-1 and PAI-2 messenger ribonucleic acid (mRNAs) were monitored by reverse transcriptase polymerase chain reaction (RT-PCR) in BALF cells and lung tissue up to the fibrotic stage of the disease. Substantial levels of PAI activity were found in BALF of control animals, whereas no PAI-1 protein was detected. In response to silica treatment, we observed an acute increase of PAI activity and PAI-1 protein levels in BALF (day 1), associated with an induction of PAI-1 and PAI-2 mRNA levels in lung tissue. In alveolar macrophages, silica treatment induced a persistent upregulation of PAI-2 mRNA only. One month after silica treatment, PAI activity was undetectable in BALF while substantial PAI activity was still present in controls. At the same time point, sustained upregulation of PAI-1 and PAI- 2 mRNAs was, however, noted in lung tissue of animals treated with silica. These findings support the possible implication of PAIs in the remodelling process induced by silica in the lung.

Animals↗
PubMed2005

Overexpression of cathepsin K during silica-induced lung fibrosis and control by TGF-beta.

BACKGROUND: Lung fibrosis is characterized by tissue remodeling resulting from an imbalance between synthesis and degradation of extracellular organic matrices. To examine whether cathepsin(s) (Cat) are important in the development of pulmonary fibrosis, we assessed the expression of four Cat known for their collagenolytic activity in a model of silica-induced lung fibrosis. METHODS: Different strains of mice were transorally instilled with 2.5 mg crystalline silica or other particles. Cat expression (Cat K, S, L and B) was quantified in lung tissue and isolated pulmonary cells by quantitative RT-PCR. In vitro, we assessed the effect of different cytokines, involved in lung inflammatory and fibrotic responses, on the expression of Cat K by alveolar macrophages and fibroblasts. RESULTS: In lung tissue, Cat K transcript was the most strongly upregulated in response to silica, and this upregulation was intimately related to the fibrotic process. In mouse strains known for their differential response to silica, we showed that the level of Cat K expression following silica treatment was inversely related to the level of TGF-beta expression and the susceptibility of these strains to develop fibrosis. Pulmonary macrophages and fibroblasts were identified as Cat K overproducing cells in the lung of silicotic mice. In vitro, Cat K was downregulated in mouse and human lung fibroblasts by the profibrotic growth factor TGF-beta1. CONCLUSION: Altogether, these data suggest that while Cat K may contribute to control lung fibrosis, TGF-beta appears to limit its overexpression in response to silica particles.

Animals↗
PubMed2001

Silica-induced cytokine release from A549 cells: importance of surface area versus size.

Physical and chemical properties such as structure, composition and surface reactivity determine the biological activity of mineral particles. Long-term exposure to crystalline silica is known to cause persistent pulmonary inflammation leading to adverse health effects. There is less information about the potential health effects of amorphous (noncrystalline) silica. In this study, the inflammatory and cytotoxic potency of crystalline and amorphous silica in relation to particle size and surface area was assessed. Human epithelial lung cells (A549) were exposed to different size fractions of quartz ( aerodynamic diameter 0.5, 2 and 10 microm) and amorphous silica (diameter 0.3 microm). All particles induced increased release of the proinflammatory cytokines interleukin (IL)-6 and IL-8. When cells were exposed to equal masses of quartz, the smallest size fraction was the most potent. These differences, however, disappeared when cytokine release was related to equal surface areas. When amorphous silica and quartz were compared, the amorphous silica was most potent to induce IL - 6 regardless of how exposure was expressed, whereas the smallest size fraction of quartz was the most potent inducer of IL-8. Thus, the surface area seems to be the critical determinant when potency of different sizes of quartz is compared.

Cell Line↗
PubMed1994

Introduction of luminol-dependent chemiluminescence as a method to study silica inflammation in the tissue and phagocytic cells of rat lung.

The inhalation of silica has been shown to produce a dramatic inflammatory and toxic response within the lungs of humans and laboratory animals. A variety of cellular and biochemical parameters are used to assess the silica-induced lung injury. The purpose of this paper is to introduce the use of luminol-dependent chemiluminescence as a new method to study inflammation in both phagocytic cells and lung tissue recovered from silica-exposed animals. Chemiluminescence, or the emission of light, accompanies the release of reactive forms of oxygen when phagocytic cells are challenged. In this study, male Fischer 344 rats were intratracheally instilled with either silica (10 mg/100 g bw) or saline vehicle. One day after the instillations, a marked increase in the chemiluminescence was observed in the lung tissue and bronchoalveolar lavage cells recovered from the silica-treated animals when compared with the saline controls. The light reaction was markedly decreased by either superoxide dismutase of N-nitro-arginine methyl ester hydrochloride. Superoxide dismutase is involved in the enzymatic breakdown of superoxide anion, while N-nitro-L-arginine methyl ester hydrocholoride, a nitric oxide synthase inhibitor, prevents the formation of nitric oxide. When superoxide anion and nitric oxide react, they form the highly oxidizing substance peroxynitrite. This study then implicates peroxynitrite as an agent that may be responsible for some of the oxidant lung injury that is associated with silica exposure. The use of luminol-dependent chemiluminescence may prove valuable as a method to measure the earliest events in the inflammatory process, and may be an adjunct in studying the mechanisms that produce inflammation.

Animals↗
PubMed1997

Localization of intercellular adhesion molecule-1 (ICAM-1) in the lungs of silica-exposed mice.

Intercellular adhesion molecule-1 (ICAM-1) is expressed on a variety of cells including endothelial cells, alveolar epithelial cells, and alveolar macrophages. Endothelial/epithelial cell ICAM-1 participates in the migration of leukocytes out of the blood in response to pulmonary inflammation, whereas alveolar macrophage ICAM-1 may represent cell activation. Our previous studies have shown that there is increased expression of ICAM-1 in lung tissue during acute inflammation following intratracheal injection with silica particles (2 mg/mouse). This increased expression was shown to play a role, in part, in the migration of neutrophils from the circulation into the tissue parenchyma. The aim of the current work is to localize expression of ICAM-1 during acute inflammation in lungs of mice exposed to either silica or the nuisance dust, titanium dioxide. In silica-exposed mice, a significant increase in ICAM-1 was detected on day-1 and localized by immunohistochemistry to aggregates of pulmonary macrophages and to type II epithelial cells. Areas of the lung with increased ICAM-1 expression also showed increased tumor necrosis factor alpha expression. Immunocytochemical staining of bronchoalveolar lavage (BAL) cells demonstrated increased ICAM-1 expression associated with alveolar macrophages 3, 5, and 7 days following silica exposure. Finally, soluble ICAM-1 levels in the BAL fluid were significantly increased in mice exposed to silica on the same days. Titanium dioxide exposure elicited a minimal increase in expression of ICAM-1 in the lungs. These data demonstrate that exposure to the toxic particle silica specifically increases ICAM-1 expression localized to pulmonary macrophages and type II epithelial cells.

Animals↗
PubMed2005

Silica induces human cyclooxygenase-2 gene expression through the NF-kappaB signaling pathway.

Silica is a causative factor of acute cell injury in pulmonary fibrosis. Inducible cyclooxygenase-2 (COX-2) was suggested to play a role in the process of inflammation and fibrosis. We report that silica induces COX-2 expression in WI-38 fibroblasts. Further analysis showed that silica activated the transcription of COX-2 gene primarily via a nuclear factor (NF)-kB binding site in the promoter. NF-kB-inducing kinase (NIK) and TGF-k activated kinase 1 (TAK1), the upstream signaling molecules of NF-kB, are involved in the silica-mediated COX-2 expression. The Electrophoretic Mobility Shift Assay (EMSA) showed that silica induced the direct binding of NF-kB on the putative binding site in COX-2 promoter. These results suggest that silica activates the human COX-2 gene transcription through the induction of NF-kB activity.

Binding Sites↗
PubMed2006

Diffusivities of tris(2,2'-bipyridyl)ruthenium inside silica-nanochannels modified with alkylsilanes.

The apparent diffusion coefficients of tris(2,2'-bipyridyl)ruthenium ([Ru(bpy(3))](2+)) are estimated in silica-nanochannels which are assembled inside columnar alumina pores in an anodic alumina membrane, and are modified with alkylsilanes such as trimethylchlorosilane (C1), butyldimethylchlorosilane (C4), and dodecyldimethylchlorosilane (C12). The estimation is performed by observing the lag-time, which is defined as the time required for [Ru(bpy)(3)](2+) to diffuse through alkylsilane-modified silica-nanochannels in the alumina membrane. When ethanol is used as a solvent, the apparent diffusion coefficients of [Ru(bpy)(3)](2+) are estimated as 2.1 x 10(-10) and 3.2 x 10(-10) cm(2) s(-1) in the C1- and C4-modified silica-nanochannels, respectively. These values are about 10(4) times smaller than that obtained in bulk ethanol. Based on the experimental results on the solvent dependency of the lag-time, the hydrogen-bonding interaction between ethanol molecules is considered to be stronger in the C1- and C4-modified silica-nanochannels than in bulk ethanol, and the hydrogen-bonding interaction plays a critical role for the slow diffusivity in those nanochannels. In contrast, the apparent diffusion coefficient in the C12-modified silica-nanochannel is at least two orders of magnitude larger than those in the C1- and C4-modified silica-nanochannels. This relatively fast diffusion is most likely explained by the presence of a long alkyl chain of C12, which reduces a hindrance effect that is originates in the hydrogen-bonding interaction.

Journal Article↗
PubMed1993

Silicon-zinc interactions and potential roles for dietary zinc and copper in minimizing silica urolithiasis in rats.

Two 8-wk experiments were conducted with Sprague-Dawley weanling rats to determine whether interactions occurring between Zn and Si, or a nutritional deficiency of either Cu or Zn, affect silica urolith formation. In Exp. 1, concentrations of 0, 540, and 2,700 mg of Si/kg of diet from tetraethylorthosilicate were used with dietary Zn concentrations of 4, 12, and 500 mg/kg of diet in a 3 x 3 factorial arrangement. In Exp. 2, copper at 1 or 5 mg/kg of diet and Zn at 4, 12, and 500 mg/kg of diet were used in a 2 x 3 factorial arrangement. All diets in Exp. 2 contained 2,700 mg of Si/kg. Silica uroliths occurred in all treatments providing, 2,700 mg of Si/kg of diet. There was a trend (P = .17) toward a reduction of silica urolith incidence with increasing concentrations of dietary Zn in Exp. 1. In Exp. 2, a deficiency of Zn, and a Cu deficiency exacerbated by 500 mg of Zn/kg of diet, increased (P < .05) silica urolith formation. An antagonism between Si and Zn, as demonstrated previously in the rat, may not be of a sufficient magnitude to be applicable to the prevention of silica urolithiasis. The data further demonstrate that Zn deficiency and, to a lesser extent, Cu deficiency contributed to silica urolith formation in rats fed diets having a high content of absorbable Si. However, 540 mg of Si/kg of diet may potentiate the metabolic activity of Zn, as indicated by a 23% Si-mediated weight gain response in Zn-deficient rats.

Alkaline Phosphatase↗
PubMed1989

Functional and morphologic comparison of silica- and elastase-induced airflow obstruction.

We have previously shown that intratracheally instilled silica (quartz) produces both morphologic evidence of emphysema and small-airway changes, and functional evidence of airflow obstruction. To further define the nature of the airflow-associated lesions induced by silica, we compared silica-exposed rats to rats given intratracheal elastase, a standard model of emphysema. Both silica and elastase produced increases in RV and FRC along with upward shifts in the pressure-volume curves. Flows were decreased in both groups, but the changes were more severe in the silica-treated animals. Morphologically, the two treatments produced about the same degree of airspace enlargement, present in both alveoli and alveolar ducts, as well as decreased alveolar and alveolar duct surface area/unit lung volume. Elastic fiber length per unit volume was also decreased in both groups. However, small-airway walls were markedly thickened in the silica-treated compared to the elastase-treated group. We conclude that, in the parenchyma, both these agents produce morphologically similar airspace dilatation, and both induce destruction of elastic fibers. These lesions appear to correlate with abnormalities in the pressure-volume curve. Flow reductions seem to be primarily correlated with changes in small-airway wall structure.

Animals↗
PubMedDate not supplied

Intrathoracic distribution and transport of aerosolized silica in the rat.

Short-term exposure of rats to aerosols of the silicon dioxide, cristobalite, leads to pulmonary inflammation persisting several months. Clearance of particles occurs during the first two weeks after cessation of exposure, after which there is little additional clearance in the whole lung. In the present studies, quantitation of silica in lung compartments at selected times following exposure indicated movement of particles between the alveolar space and the lung tissue per se, with increased alveolar silica content associated with decreased silica content in the tissue compartment. Further, changes in the silica content in the alveolar compartment were generally associated with fluctuations in the alveolar macrophage population. Silica accumulated linearly in the mediastinal lymph nodes and thymus for several months after cessation of exposure, while negligible amounts were found in kidney, spleen, liver, and blood. A compartmental model was used to describe the distribution and translocation kinetics of the inhaled silica in the lung and extrapulmonary tissues.

Aerosols↗
PubMedDate not supplied

Subchronic pulmonary inflammation and fibrosis induced by silica in rats are attenuated by amiodarone.

A previous study demonstrated that the acute phase of silica-induced lung injury in rats can be attenuated by concomitant administration of amiodarone, a cationic amphiphilic drug that inhibits phospholipase activity in the lungs. The purpose of the present study was to determine whether continued amiodarone administration could inhibit subchronic silica-induced lung injury and fibrosis. Male Fischer-344 rats were administered amiodarone (150 mg/kg, p.o., 5 days/week) for 14 days and were then instilled with silica (100 mg/kg) intratracheally. Amiodarone treatment then continued for 60 days. Injury was evaluated by parameters in bronchoalveolar lavage fluid and fibrosis was assessed by lung hydroxyproline content and trichrome staining of collagen. Within the bronchoalveolar lavage fluid, amiodarone treatment resulted in significant decreases in silica-induced elevations in albumin levels, lactate dehydrogenase activity, beta-glucuronidase activity, and neutrophil influx. Amiodarone treatment resulted in significant reductions in silica-induced increases in lung weight and hydroxyproline levels; the diminution of fibrosis due to amiodarone treatment was confirmed histologically. These results indicate that subchronic pulmonary inflammation and fibrosis induced by silica in the rat can be attenuated by the concomitant administration of amiodarone.

Albumins↗
PubMed2001

Silica-induced activation of c-Jun-NH2-terminal amino kinases, protracted expression of the activator protein-1 proto-oncogene, fra-1, and S-phase alterations are mediated via oxidative stress.

Crystalline silica has been classified as a group 1 human carcinogen in the lung. However, its mechanisms of action on pulmonary epithelial cells which give rise to lung cancers are unclear. Using a nontransformed alveolar type II epithelial cell line (C10), we show that alpha-quartz silica causes persistent dose-related increases in phosphorylation of c-Jun-NH2-terminal amino kinases (JNKs) that are inhibited by antioxidants (P < or = 0.05). Increases in activator protein-1 (AP-1) binding to DNA and transactivation of AP-1-dependent gene expression by silica were accompanied by increases in steady-state mRNA levels of the AP-1 family members, c-jun, junB, fra-1, and c-fos at 8 h and elevated mRNA levels of fra-1 at 24 h (P < or = 0.05). Addition of tetramethylthiourea inhibited silica-associated increases infra-1 and proportions of cells in S-phase (P < or = .05). Our findings indicate that silica induces JNK activity, AP-1-dependent gene expression, ie., fra-1, and DNA synthesis via oxidative stress. Moreover, they suggest that silica may act mechanistically as a mitogen or tumor promoter, rather than a genotoxic carcinogen, in the development of lung cancers.

Animals↗
PubMed1989

Secular change in chert distribution: a reflection of evolving biological participation in the silica cycle.

In the modern oceans, the removal of dissolved silica from sea water is principally a biological process carried out by diatoms, with lesser contributions from radiolaria, silicoflagellates, and sponges. Because such silica in sediments is often redistributed locally during diagenesis to from nodular or bedded chert, stratigraphic changes in the facies distribution of early diagenetic chert provide important insights into the development of biological participation in the silica cycle. The abundance of chert in upper Proterozoic peritidal carbonates suggests that at this time silica was removed from seawater principally by abiological processes operating in part of the margins of the oceans. With the evolution of demosponges near the beginning of the Cambrian Period, subtidal biogenetic cherts became increasingly common, and with the Ordovician rise of radiolaria to ecological and biogeochemical prominence, sedimented skeletons became a principal sink for oceanic silica. Cherts of Silurian to Cretaceous age share many features of facies distribution and petrography but they differ from Cenozoic siliceous deposits. These differences are interpreted to reflect the mid-Cretaceous radiation of diatoms and their subsequent rise to domination of the silica cycle. Biogeochemical cycles provide an important framework for the paleobiological interpretation of the organisms that participate in them.

Animals↗