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1.
Artigo em Inglês | MEDLINE | ID: mdl-33803962

RESUMO

Plastics are ubiquitous persistent pollutants, forming the most representative material of the Anthropocene. In the environment, they undergo wear and tear (i.e., mechanical fragmentation, and slow photo and thermo-oxidative degradation) forming secondary microplastics (MPs). Further fragmentation of primary and secondary MPs results in nanoplastics (NPs). To assess potential health damage due to human exposure to airborne MPs and NPs, we summarize the evidence collected to date that, however, has almost completely focused on monitoring and the effects of airborne MPs. Only in vivo and in vitro studies have assessed the toxicity of NPs, and a standardized method for their analysis in environmental matrices is still missing. The main sources of indoor and outdoor exposure to these pollutants include synthetic textile fibers, rubber tires, upholstery and household furniture, and landfills. Although both MPs and NPs can reach the alveolar surface, the latter can pass into the bloodstream, overcoming the pulmonary epithelial barrier. Despite the low reactivity, the number of surface area atoms per unit mass is high in MPs and NPs, greatly enhancing the surface area for chemical reactions with bodily fluids and tissue in direct contact. This is proven in polyvinyl chloride (PVC) and flock workers, who are prone to persistent inflammatory stimulation, leading to pulmonary fibrosis or even carcinogenesis.


Assuntos
Poluentes Ambientais , Poluentes Químicos da Água , Humanos , Microplásticos , Plásticos , Cloreto de Polivinila , Poluentes Químicos da Água/análise
2.
Artigo em Inglês | MEDLINE | ID: mdl-34071645

RESUMO

Due to ingestion of contaminated foods, the human gastrointestinal tract is the most likely site of exposure to microplastics (MPs) with gut barrier dysfunction and intestinal inflammation. Aimed to assess the effects induced by MPs with different granulometry (polystyrene (PS) 3 and 10 µm), we performed an in vitro study by using the human intestinal cell line HT29. As a novelty, we assessed the sub-chronic exposure extending the treatment up to 48 days simulating the in vivo situation. In the range of 100-1600 particles mL-1, both the PS suspensions had moderate cytotoxicity after 24 h with percentages of mortality between 6.7 and 21.6 for the 10 µm and 6.1 and 29.6 for the 3 µm PS. Microscopic observation highlighted a more pronounced lysosomal membrane permeabilization in HT29 exposed to PS 3µm. Reactive oxygen species production was higher in cells exposed to PS 10 µm, but sub-chronic exposure highlighted the ability of the cells to partially neutralize this effect. Comet-assay confirmed the temporary oxidative damage that was PS-induced. Overall, considering the very fast turnover of intestinal cells, the increase in cell mortality, equal to 25% and 11% for 3 and 10 µm PS-MPs for each time point, could trigger intestinal disorders due to prolonged exposure.


Assuntos
Microplásticos , Poluentes Químicos da Água , Linhagem Celular , Humanos , Plásticos/toxicidade , Poliestirenos/análise , Espécies Reativas de Oxigênio , Poluentes Químicos da Água/análise
3.
Artigo em Inglês | MEDLINE | ID: mdl-34501585

RESUMO

HIV-positive people showed a high oral prevalence of HPV-DNA and have a greater incidence of head and neck carcinomas compared to general population. We performed a molecular survey evaluating the presence of HPV-DNA in saliva of HIV-positive and HIV-negative subjects in order to quantify the risk represented by HIV-positivity. The sample was made up by 102 subjects: 40 HIV-positive, 32 HIV-negative with sexual risk behaviors (SRB) and 30 HIV-negative without risk factors. DNA was extracted from cellular pellets and HPV detection and genotyping were performed by PCR assays. In the HIV-positive group (of which 58.3% declared SRB) 33.33% of the sample were HPV-positive (33.33% to high-risk genotypes, 25.0% to low-risk genotypes and 41.66% to other genotypes). In the HIV-negative SRB group, HPV-positive subjects were 37.04% (60.0% to high risk genotypes, 20.0% to low risk genotypes, and 20.0% to other genotypes). Finally, in the control group, the HPV-positive subjects were 7.14% (50% to high-risk genotypes and 50% to low-risk genotypes). In the HIV group, concerning the HPV positivity, there was no significant difference between subjects with and without SRBs. In summary, we found a high oral HPV-DNA detection in HIV+ group, showing a strong relationship between HIV and HPV.


Assuntos
Infecções por HIV , Infecções por Papillomavirus , Genótipo , Infecções por HIV/epidemiologia , Humanos , Epidemiologia Molecular , Papillomaviridae/genética , Infecções por Papillomavirus/epidemiologia , Prevalência , Saliva
4.
Environ Toxicol Pharmacol ; 56: 121-128, 2017 Dec.
Artigo em Inglês | MEDLINE | ID: mdl-28910697

RESUMO

Multi walled carbon nanotubes (MWCNTs) activate pathways involved in cytotoxicity, genotoxicity and inflammation. Inhaled MWCNTs are translocated to extra pulmonary organs and their hydrophobicity allows them to cross the blood-brain barrier (BBB). Further exposure of central nervous system (CNS) occurs via olfactory neurons. Using differentiated SH-SY5Y, we studied the neurotoxicity and neuroinflammation of pristine and functionalised MWCNTs. ROS overproduction was dose- and time-dependent (P<0.01) and was related to mitochondrial impairment, DNA damage and decreased viability (P<0.05). Transcript levels of TNFα, IL-1ß and IL-6 increased, as confirmed by an ELISA test. Raman spectra were acquired to assess MWCNT-cells interactions. The almost superimposable pro-oxidant activity of both CNTs could be imputable to excessive lengths with regard to the pristine MWCNTs and to the eroded surface, causing increased reactivity, with regard to functionalised MWCNTs. Considering the ease with which lightweight MWCNTs aerosolize and the increased production, the results underlined the potential onset of neurodegenerative diseases, due to unintentional MWCNT exposure.


Assuntos
Inflamação/genética , Mitocôndrias/efeitos dos fármacos , Nanotubos de Carbono/toxicidade , Espécies Reativas de Oxigênio/metabolismo , Barreira Hematoencefálica , Linhagem Celular , Sobrevivência Celular/efeitos dos fármacos , Dano ao DNA , Relação Dose-Resposta a Droga , Regulação da Expressão Gênica/efeitos dos fármacos , Humanos , Inflamação/metabolismo , Interleucina-1beta/genética , Interleucina-6/genética , Mitocôndrias/genética , Fatores de Tempo , Fator de Necrose Tumoral alfa/genética
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