95 research outputs found
Different effects of anthocyanins and phenolic acids from wild blueberry (Vaccinium angustifolium) on monocytes adhesion to endothelial cells in a TNF-alpha stimulated proinflammatory environment
No full textSCOPE:
Monocyte adhesion to the vascular endothelium is a crucial step in the early stages of atherogenesis. This study aims to investigate the capacity of an anthocyanin (ACN) and phenolic acid (PA)-rich fraction (RF) of a wild blueberry, single ACNs (cyanidin, malvidin, delphinidin) and related metabolites (protocatechuic, syringic and gallic acid) to counteract monocytes (THP-1) adhesion to endothelial cells (HUVECs) in a tumor necrosis α (TNF-α) mediated pro-inflammatory environment.
METHODS AND RESULTS:
HUVECs were incubated with different concentrations (from 0.01 to 10 μg mL-1 ) of the compounds for 24 h. Labelled monocytic THP-1 cells were added to HUVECs and their adhesion was induced by TNF-α (100 ng mL-1 ). ACN-RF reduced THP-1 adhesion to HUVECs with a maximum effect at 10 μg mL-1 (-33%). PA-RF counteracted THP-1 adhesion at 0.01, 0.1 and 1 μg mL-1 (-45%, -48.7% and -27.6%, respectively), but not at maximum concentration. Supplementation with gallic acid reduced THP-1 adhesion to HUVECs with a maximum effect at 1 μg mL-1 (-29.9%), while malvidin-3-glucoside and syringic acid increased the adhesion. No effect was observed for the other compounds.
CONCLUSION:
These results suggest that ACNs/PA-RF may prevent atherogenesis while the effects of the single ACNs and metabolites are controversial and merit further exploration
Anthocyanins and phenolic acids from a wild blueberry (Vaccinium angustifolium) powder counteract lipid accumulation in THP-1-derived macrophages
No full textPurpose: Blueberries are a rich source of anthocyanins (ACNs) and phenolic acids (PA), which are hypothesized to protect against development of atherosclerosis. The present study examined the effect of an ACN- and PA-rich fractions, obtained from a wild blueberry powder, on the capacity to counteract lipid accumulation in macrophages derived from monocytic THP-1 cells. In addition, we tested the capacity of pure ACNs and their metabolites to alter lipid accumulation.Methods: THP-1-derived macrophages were incubated with fatty acids (500 μM oleic/palmitic acid, 2:1 ratio) and different concentrations (from 0.05 to 10 μg mL−1) of ACN- and PA-rich fractions, pure ACN standards (malvidin, delphinidin and cyanidin 3-glucoside), and metabolites (syringic, gallic and protocatechuic acids). Lipid accumulation was quantified with the fluorescent dye Nile red.Results: Lipid accumulation was reduced at all concentrations of the ACN-rich fraction tested with a maximum reduction at 10 μg mL−1 (−27.4 %; p < 0.0001). The PA-rich fraction significantly reduced the lipid accumulation only at the low concentrations from 0.05 μg mL−1 to 0.3 μg mL−1, with respect to the control with fatty acids. Supplementation with pure ACN compounds (malvidin and delphinidin-3-glucoside and its metabolic products (syringic and gallic acid)) reduced lipid accumulation especially at the low concentrations, while no significant effect was observed after cyanidin-3-glucoside and protocatechuic acid supplementation.Conclusions: The results demonstrated a potential role of both the ACN- and PA-rich fractions and single compounds in the lipid accumulation also at concentrations close to that achievable in vivo
Biomarkers of DNA Oxidation Products:Links to Exposure and Disease in Public Health Studies
No full textEnvironmental exposure can increase the production of reactive oxygen species and deplete cellular antioxidants in humans, resulting in oxidatively generated damage to DNA that is both a useful biomarker of oxidative stress and indicator of carcinogenic hazard. Methods of oxidatively damaged DNA analysis have been developed and used in public health research since the 1990s. Advanced techniques detect specific lesions, but they might not be applicable to complex matrixes (e.g., tissues), small sample volume, and large-scale studies. The most reliable methods are characterized by (1) detecting relevant DNA oxidation products (e.g., premutagenic lesions), (2) not harboring technical problems, (3) being applicable to complex biological mixtures, and (4) having the ability to process a large number of samples in a reasonable period of time. Most effort has been devoted to the measurements of 8-oxo-7,8-dihydro-2′-deoxyguanine (8-oxodG), which can be analyzed by chromatographic, enzymic, and antibody-based methods. Results from validation trials have shown that certain chromatographic and enzymic assays (namely the comet assay) are superior techniques. The enzyme-modified comet assay has been popular because it is technically simpler than chromatographic assays. It is widely used in public health studies on environmental exposures such as outdoor air pollution. Validated biomarker assays on oxidatively damaged DNA have been used to fill knowledge gaps between findings in prospective cohort studies and hazards from contemporary sources of air pollution exposures. Results from each of these research fields feed into public health research as approaches to conduct primary prevention of diseases caused by environmental or occupational agents. </p
Gastrointestinal tract exposure to particles and DNA damage in animals:A review of studies before, during and after the peak of nanotoxicology
No full textHumans ingest particles and fibers on daily basis. Non-digestible carbohydrates are beneficial to health and food additives are considered safe. However, titanium dioxide (E171) has been banned in the European Union because the European Food Safety Authority no longer considers it non-genotoxic. Ingestion of microplastics and nanoplastics are novel exposures; their potential hazardous effects to humans have been under the radar for many years. In this review, we have assessed the association between oral exposure to man-made particles/fibers and genotoxicity in gastrointestinal tract cells and secondary tissues. We identified a total of 137 studies on oral exposure to particles and fibers. This was reduced to 49 papers with sufficient quality and relevance, including exposures to asbestos, diesel exhaust particles, titanium dioxide, silver nanoparticles, zinc oxide, synthetic amorphous silica and certain other nanomaterials. Nineteen studies show positive results, 25 studies show null results, and 5 papers show equivocal results on genotoxicity. Recent studies seem to show null effects, whereas there is a higher proportion of positive genotoxicity results in early studies. Genotoxic effects seem to cluster in studies on diesel exhaust particles and titanium dioxide, whereas studies on silver nanoparticles, zinc oxide and synthetic amorphous silica seem to show mainly null effects. The most widely used genotoxic tests are the alkaline comet assay and micronucleus assay. There are relatively few results on genotoxicity using reliable measurements of oxidatively damaged DNA, DNA double strand breaks (γH2AX assay) and mutations. In general, evidence suggest that oral exposure to particles and fibers is associated with genotoxicity in animals.Humans ingest particles and fibers on daily basis. Non-digestible carbohydrates are beneficial to health and food additives are considered safe. However, titanium dioxide (E171) has been banned in the European Union because the European Food Safety Authority no longer considers it non-genotoxic. Ingestion of microplastics and nanoplastics are novel exposures; their potential hazardous effects to humans have been under the radar for many years. In this review, we have assessed the association between oral exposure to man-made particles/fibers and genotoxicity in gastrointestinal tract cells and secondary tissues. We identified a total of 137 studies on oral exposure to particles and fibers. This was reduced to 49 papers with sufficient quality and relevance, including exposures to asbestos, diesel exhaust particles, titanium dioxide, silver nanoparticles, zinc oxide, synthetic amorphous silica and certain other nanomaterials. Nineteen studies show positive results, 25 studies show null results, and 5 papers show equivocal results on genotoxicity. Recent studies seem to show null effects, whereas there is a higher proportion of positive genotoxicity results in early studies. Genotoxic effects seem to cluster in studies on diesel exhaust particles and titanium dioxide, whereas studies on silver nanoparticles, zinc oxide and synthetic amorphous silica seem to show mainly null effects. The most widely used genotoxic tests are the alkaline comet assay and micronucleus assay. There are relatively few results on genotoxicity using reliable measurements of oxidatively damaged DNA, DNA double strand breaks (γH2AX assay) and mutations. In general, evidence suggest that oral exposure to particles and fibers is associated with genotoxicity in animals.</p
Exposure to nanoplastic particles and DNA damage in mammalian cells
No full textThere is concern about human exposure to nanoplastics from intentional use or degradation of plastics in the environment. This review assesses genotoxic effects of nanoplastics, defined as particles with a primary size of less than 1000 nm. The majority of results on genotoxicity come from studies on polystyrene (PS) particles in mammalian cell cultures. Most studies have measured DNA strand breaks (standard comet assay), oxidatively damaged DNA (Fpg-modified comet assay) and micronuclei. Twenty-nine out of 60 results have shown statistically significant genotoxic effects by PS exposure in cell cultures. A statistical analysis indicates that especially modified PS particles are genotoxic (odds ratio = 8.6, 95 % CI: 1.6, 46) and immune cells seems to be more sensitive to genotoxicity than other cell types such as epithelial cells (odds ratio = 8.0, 95 % CI: 1.6, 39). On the contrary, there is not a clear association between statistically significant effects in genotoxicity tests and the primary size of PS particles, (i.e. smaller versus larger than 100 nm) or between the type of genotoxic endpoint (i.e. repairable versus permanent DNA lesions). Three studies of PS particle exposure in animals have shown increased level of DNA strand breaks in leukocytes and prefrontal cortex cells. Nanoplastics from polyethylene, propylene, polyvinyl chloride and polyethylene terephthalate have been investigated in very few studies and it is currently not possible to draw conclusion about their genotoxic hazard. In summary, there is some evidence suggesting that PS particles may be genotoxic in mammalian cells.There is concern about human exposure to nanoplastics from intentional use or degradation of plastics in the environment. This review assesses genotoxic effects of nanoplastics, defined as particles with a primary size of less than 1000 nm. The majority of results on genotoxicity come from studies on polystyrene (PS) particles in mammalian cell cultures. Most studies have measured DNA strand breaks (standard comet assay), oxidatively damaged DNA (Fpg-modified comet assay) and micronuclei. Twenty-nine out of 60 results have shown statistically significant genotoxic effects by PS exposure in cell cultures. A statistical analysis indicates that especially modified PS particles are genotoxic (odds ratio = 8.6, 95 % CI: 1.6, 46) and immune cells seems to be more sensitive to genotoxicity than other cell types such as epithelial cells (odds ratio = 8.0, 95 % CI: 1.6, 39). On the contrary, there is not a clear association between statistically significant effects in genotoxicity tests and the primary size of PS particles, (i.e. smaller versus larger than 100 nm) or between the type of genotoxic endpoint (i.e. repairable versus permanent DNA lesions). Three studies of PS particle exposure in animals have shown increased level of DNA strand breaks in leukocytes and prefrontal cortex cells. Nanoplastics from polyethylene, propylene, polyvinyl chloride and polyethylene terephthalate have been investigated in very few studies and it is currently not possible to draw conclusion about their genotoxic hazard. In summary, there is some evidence suggesting that PS particles may be genotoxic in mammalian cells.</p
Aminated polystyrene and DNA strand breaks in A549, Caco-2, THP-1 and U937 human cell lines
No full textPlastic is used extensively worldwide. However, plastic particles that are less than 1000 nm (i.e. nanoplastics) may be hazardous to human cells. Nanoplastics might be manufactured intentionally or be formed in the environment by degradation of larger plastic items. Ingestion and inhalation are the two most common routes of human exposure to nanoplastics, indicating that epithelial cells have direct exposure. However, immune cells will also interact with particles during tissue inflammation. An assessment of published studies suggests that polystyrene (PS) particles generate higher levels of DNA damage in immune cells compared to epithelial cells, although it has not been formally studied under the same experimental condition. To investigate this, we assessed cytotoxicity, oxidative stress and DNA strand breaks in lung epithelial (A549) cells, intestinal epithelial (Caco-2) cells, and two monocytes (THP-1 and U937) after exposure to amine-functionalized polystyrene particles (PS-NH2) with declared particle size of 240 nm. No cytotoxicity or intracellular reactive oxygen species production were found at concentrations up to 200 µg/mL. Exposure to PS-NH2 was associated with glutathione depletion in A549 cells. However, there was no increase in the level of DNA strand breaks, measured by the comet assay, in any of the cell lines under standard assay conditions. Diethyl maleate treatment was used to render cells susceptible to oxidative stress. By itself, diethyl maleate treatment led to approximately 50 % glutathione depletion and increased DNA strand breaks, but additional DNA damage was not observed in cells by PS-NH2 exposure in A549, Caco-2, THP-1 and U937 cells.Plastic is used extensively worldwide. However, plastic particles that are less than 1000 nm (i.e. nanoplastics) may be hazardous to human cells. Nanoplastics might be manufactured intentionally or be formed in the environment by degradation of larger plastic items. Ingestion and inhalation are the two most common routes of human exposure to nanoplastics, indicating that epithelial cells have direct exposure. However, immune cells will also interact with particles during tissue inflammation. An assessment of published studies suggests that polystyrene (PS) particles generate higher levels of DNA damage in immune cells compared to epithelial cells, although it has not been formally studied under the same experimental condition. To investigate this, we assessed cytotoxicity, oxidative stress and DNA strand breaks in lung epithelial (A549) cells, intestinal epithelial (Caco-2) cells, and two monocytes (THP-1 and U937) after exposure to amine-functionalized polystyrene particles (PSNH2) with declared particle size of 240 nm. No cytotoxicity or intracellular reactive oxygen species production were found at concentrations up to 200 mu g/mL. Exposure to PS-NH2 was associated with glutathione depletion in A549 cells. However, there was no increase in the level of DNA strand breaks, measured by the comet assay, in any of the cell lines under standard assay conditions. Diethyl maleate treatment was used to render cells susceptible to oxidative stress. By itself, diethyl maleate treatment led to approximately 50 % glutathione depletion and increased DNA strand breaks, but additional DNA damage was not observed in cells by PS-NH2 exposure in A549, Caco-2, THP-1 and U937 cells
Acute phase response following pulmonary exposure to soluble and insoluble metal oxide nanomaterials in mice
No full textBackground: Acute phase response (APR) is characterized by a change in concentration of different proteins, including C-reactive protein and serum amyloid A (SAA) that can be linked to both exposure to metal oxide nanomaterials and risk of cardiovascular diseases. In this study, we intratracheally exposed mice to ZnO, CuO, Al2O3, SnO2 and TiO2 and carbon black (Printex 90) nanomaterials with a wide range in phagolysosomal solubility. We subsequently assessed neutrophil numbers, protein and lactate dehydrogenase activity in bronchoalveolar lavage fluid, Saa3 and Saa1 mRNA levels in lung and liver tissue, respectively, and SAA3 and SAA1/2 in plasma. Endpoints were analyzed 1 and 28 days after exposure, including histopathology of lung and liver tissues. Results: All nanomaterials induced pulmonary inflammation after 1 day, and exposure to ZnO, CuO, SnO2, TiO2 and Printex 90 increased Saa3 mRNA levels in lungs and Saa1 mRNA levels in liver. Additionally, CuO, SnO2, TiO2 and Printex 90 increased plasma levels of SAA3 and SAA1/2. Acute phase response was predicted by deposited surface area for insoluble metal oxides, 1 and 28 days post-exposure. Conclusion: Soluble and insoluble metal oxides induced dose-dependent APR with different time dependency. Neutrophil influx, Saa3 mRNA levels in lung tissue and plasma SAA3 levels correlated across all studied nanomaterials, suggesting that these endpoints can be used as biomarkers of acute phase response and cardiovascular disease risk following exposure to soluble and insoluble particles.</p
Effects of alcohol consumption on the allergen-specific immune response in mice
No full textThere is evidence that chronic alcohol consumption impairs the T-helper 1 (Th1) lymphocyte-regulated cell-mediated immune response possibly favoring a Th2 deviation of the immune response. Moreover, a few epidemiological studies have linked alcohol consumption to allergen-specific IgE sensitization
Nanoplastics from ground polyethylene terephthalate food containers:Genotoxicity in human lung epithelial A549 cells
No full textThe ubiquitous pollution of plastic particles in most environmental matrices leads to concern about any potential adverse effects on human health. Most studies on the toxicological effect of nanoplastics has focused on standard particles of polystyrene. In reality humans are exposed to a large variety of different types and sizes of plastic material via oral intake and inhalation. In this study, we investigated the effect of polyethylene terephthalate (PET) nanoplastic particles from ground food containers from a supermarket. The aim was to investigate a possible link between exposure to PET nanoplastics and genotoxic response in a cell model of the human airway epithelial (A549) cells. Further, we investigated the combined effect of PET and chemicals known to alter the cellular redox state, as a model of partially compromised antioxidant defense system. DNA damage was assessed by the alkaline comet assay. The ground PET nanoplastics have a mean hydrodynamic diameter of 136 nm in water. The results showed that PET exposure led to increased reactive oxygen species production (approximately 30 % increase compared to unexposed cells). In addition, exposure to PET nanoplastic increased the level of DNA strand breaks (net increase = 0.10 lesions/106 base pair, 95 % confidence interval: 0.01, 0.18 lesions/106 base pair). Pre- or post-exposure to hydrogen peroxide or buthionine sulfoximine did not lead to a higher level of DNA damage. Overall, the study shows that exposure to PET nanoplastics increases both intracellular reactive oxygen production and DNA damage in A549 cells
Synergistic Effects of Zinc Oxide Nanoparticles and Fatty Acids on Toxicity to Caco-2 Cells
No full textFatty acids exposure may increase sensitivity of intestinal epithelial cells to cytotoxic effects of zinc oxide (ZnO) nanoparticles (NPs). This study evaluated the synergistic effects of ZnO NPs and palmitic acid (PA) or free fatty acids (FFAs) mixture (oleic/PA 2:1) on toxicity to human colon epithelial (Caco-2) cells. The ZnO NPs exposure concentration dependently induced cytotoxicity to Caco-2 cells showing as reduced proliferation and activity measured by 3 different assays. PA exposure induced cytotoxicity, and coexposure to ZnO NPs and PA showed the largest cytotoxic effects. The presence of FFAs mixture did not affect the ZnO NPs-induced cytotoxicity. Filtration of freshly prepared suspension of NPs through a 0.45-µm pore size membrane significantly reduced the cytotoxicity, indicating a role of concentration or size of particles in cytotoxic effects. The ZnO NPs and PA coexposure induced production of mitochondrial reactive oxygen species (mROS) but not intracellular ROS production, whereas FFAs mixture exposure did not induce mROS and inhibited intracellular ROS. Both ZnO NPs and fatty acids (PA and FFAs mixture) promoted lysosomal destabilization, which was not correlated with cytotoxicity. These results indicated that PA can enhance ZnO NPs-induced cytotoxicity probably by the augmentation of mROS production, whereas FFAs mixture did not affect ROS production. Synergistic effects between ZnO NPs and fatty acids may be important when considering NPs toxicity via oral exposure.</p
- …
