Chronic exposure to TiO micro- and nano particles: A biochemical and histopathological experimental study.

The aim of this work was to analyze the effects of long-term exposure to titanium dioxide (TiO) micro- (MPs) and nanoparticles (NPs) (six and 12 months) on the biochemical and histopathological response of target organs using a murine model. Male Wistar rats were intraperitoneally injected with a suspension of TiO NPs (5 nm; TiO-NP5 group) or MPs (45 μm; TiO-NP5 group); the control group was injected with saline solution. Six and 12 months post-injection, titanium (Ti) concentration in plasma and target organs was determined spectrometrically (ICP-MS).

Air pollution induces morpho-functional, biochemical and biomechanical vascular dysfunction in undernourished rats.

Air pollution (gases and particulate matter -PM) and child undernutrition are globally recognized stressors with significant consequences. PM and its components breach the respiratory alveolar-capillary barrier, entering the vasculature transporting not only harmful particles and its mediators but, altering vascular paracrine and autocrine functions. The aim of this study was to investigate the effects of Residual Oil Fly Ash (ROFA), on the vasculature of young animals with nutritional growth retardation (NGR).

Decreased immune response in undernourished rats after air pollution exposure.

Children are highly vulnerable subpopulation to malnutrition and air pollution. We investigate, in a rat nutritional growth retardation (NGR) model, the impact of Residual Oil Fly Ash (ROFA) on the lung immune response using in vitro and ex vivo methods. In vitro: Alveolar macrophages (AM) were isolated from Control (C) and NGR animals, cultured and treated with ROFA (1-100 µg/ml) for 24 h.

Exfoliated oral mucosa cells as bioindicators of short- and long-term systemic titanium contamination.

Background: Humans are exposed to exogenous sources of titanium-containing particles that can enter the body mainly by inhalation, ingestion, or dermal absorption. Given the widespread use of biomaterials in medicine, the surface of a titanium (Ti) biomedical device is a potential endogenous source of Ti ions and/or Ti-containing particles, such as TiO micro-(MPs) and nano-particles (NPs), resulting from biotribocorrosion processes. Ti ions or Ti-containing particles may deposit in epithelial cells of the oral mucosa, and the latter may therefore serve as bioindicators of short and long-term systemic Ti contamination.

A Biocompatible Ultrananocrystalline Diamond (UNCD) Coating for a New Generation of Dental Implants.

Implant therapy using osseointegratable titanium (Ti) dental implants has revolutionized clinical dental practice and has shown a high rate of success. However, because a metallic implant is in contact with body tissues and fluids in vivo, ions/particles can be released into the biological milieu as a result of corrosion or biotribocorrosion. Ultrananocrystalline diamond (UNCD) coatings possess a synergistic combination of mechanical, tribological, and chemical properties, which makes UNCD highly biocompatible.

Systemic effect of TiO micro- and nanoparticles after acute exposure in a murine model.

The surface of a biomedical implant can be a potential endogenous source of release of microparticles (MPs) and nanoparticles (NPs) into the biological environment. In addition, titanium particles from exogenous sources can enter the body through inhalation, ingestion, or dermal contact. The aim of this work was to evaluate the biological response of the lung, liver, and kidneys to acute exposure to titanium dioxide (TiO ).

Rationale for the use of sphingosine analogues in COVID-19 patients.

Despite the recent announcement of promising drug candidates to treat COVID-19, there is currently no effective antiviral drug or vaccine. There is strong evidence that acute lung injury/acute respiratory distress syndrome (ALI/ARDS), likely triggered by a cytokine storm, is responsible for the severity of disease seen in COVID-19 patients. In support of this hypothesis, pilot studies using IL-6 receptor inhibitors such as tocilizumab have shown promising results.

NADPH oxidase and mitochondria are relevant sources of superoxide anion in the oxinflammatory response of macrophages exposed to airborne particulate matter.

Exposure to ambient air particulate matter (PM) is associated with increased cardiorespiratory morbidity and mortality. In this context, alveolar macrophages exhibit proinflammatory and oxidative responses as a result of the clearance of particles, thus contributing to lung injury. However, the mechanisms linking these pathways are not completely clarified.

Changes in extrapulmonary organs and serum enzyme biomarkers after chronic exposure to Buenos Aires air pollution.

Urban air pollution is a serious environmental problem in developing countries worldwide, and health is a pressing issue in the megacities in Latin America. Buenos Aires is a megacity with an estimated moderate Air Quality Index ranging from 42 to 74 μg/m. Exposure to Urban Air Particles from Buenos Aires (UAP-BA) induces morphological and physiological respiratory alterations; nevertheless, no studies on extrapulmonary organs have been performed.

Monitoring human genotoxicity risk associated to urban and industrial Buenos Aires air pollution exposure.

The quality of life in large megacities is directly affected by its air quality. In urban environments, suspended particles from anthropogenic origin is one of the main air contaminants identified as highly genotoxic, mutagenic, or carcinogenic. Atmospheric monitoring is therefore imperative, and bioassays to detect the effects of genotoxic agents give usually excellent results.

Hazardous effects of urban air particulate matter acute exposure on lung and extrapulmonary organs in mice.

Air particulate matter (PM) can lead to extrapulmonary adverse reactions in organs such as liver and heart either by particle translocation from the lung to the systemic circulation or by the release of lung mediators. Young BALB/c mice were intranasal instilled with 1mg/BW of Urban Air Particles from Buenos Aires or Residual Oil Fly Ash. Histopathology, oxidative metabolism and inflammation on lungs and extrapulmonary organs and the systemic response were evaluated.

Neurotoxicity mediated by oxidative stress caused by titanium dioxide nanoparticles in human neuroblastoma (SH-SY5Y) cells.

Background: Titanium is widely used in biomedicine. Due to biotribocorrosion, titanium dioxide (TiO) nanoparticles (NPs) can be released from the titanium implant surface, enter the systemic circulation, and migrate to various organs and tissues including the brain. A previous study showed that 5 nm TiO NPs reached the highest concentration in the brain.

Chronic exposure to urban air pollution from Buenos Aires: the ocular mucosa as an early biomarker.

Air pollution represents a major health problem in megacities, bringing about 8 million deaths every year. The aim of the study was to evaluate in vivo the ocular and respiratory mucosa biological response after chronic exposure to urban air particles from Buenos Aires (UAP-BA). BALB/c mice were exposed to UAP-BA or filtered air for 1, 6, 9, and 12 months.

Oxidative stress response to air particle pollution in a rat nutritional growth retardation model.

Air pollution consisting of gases and particulate matter-(PM) represents a health problem in cities worldwide. However, air pollution does not impact equally all individuals, as children appear to be more vulnerable subpopulations. Air pollution and malnutrition are two distinct factors that have been associated with oxidative damage.

Evaluation of metabolic reactivity in macrophages from mice with chronic sodium arsenite intake and experimental carcinogenesis.

 Arsenic is carcinogenic to human beings, and environmental exposure to arsenic is a public health issue that affects large populations around the world. Thus, studies are needed to determine the mode of action of arsenic and to prevent harmful effects that arise from arsenic intake. In particular, knowledge of the effects of arsenic exposure in individuals who are undergoing a carcinogenesis process is lacking.

Volcanic ash from Puyehue-Cordón Caulle Volcanic Complex and Calbuco promote a differential response of pro-inflammatory and oxidative stress mediators on human conjunctival epithelial cells.

Volcanic ash could pose a hazard to the ocular surface as it is constantly exposed to environmental particles. We exposed conjunctival cells to Puyehue-Cordón Caulle volcanic complex (PCCVC) or Calbuco ash particles and evaluated proliferation, viability, apoptosis, MUC1 expression, pro-inflammatory cytokines, and oxidative stress markers. Ash particles from these volcanoes vary in size, composition, and morphology.

Titanium Nanoparticle Size Influences Trace Concentration Levels in Skin Appendages.

As a result of biotribocorrosion, the surface of a titanium (Ti) biomedical device can be a potential source of systemic contamination with Ti nanoparticles (NPs). Although NPs can be chemically similar, differences in particle size may lead to different biological responses. The aim of this experimental study was to determine Ti trace levels in skin appendages and plasma and explore the influence of NP size on trace levels using a murine model.

Active caspase-3 expression levels as bioindicator of individual radiosensitivity.

Several molecules and events involved in cell response to radiation-induced damage have been investigated towards a personalized radiotherapy. Considering the importance of active caspase-3 in the proteolytic cascade that ensures radiation-induced apoptosis execution, this research was designed to evaluate the expression levels of this protein as a bioindicator of individual radiosensitivity. Peripheral blood samples of 10 healthy individuals were gamma-irradiated (cobalt-60 source) with 1, 2 and 4 Gy (control: non-irradiated samples), and active caspase-3 expression levels were measured in lymphocytes, by flow cytometry, ex vivo and after different times of in vitro incubation (24, 48 and 72 hours).

Biokinetics and tissue response to ultrananocrystalline diamond nanoparticles employed as coating for biomedical devices.

Although Ultrananocrystalline diamond (UNCD) has been proposed as a coating material for titanium biomedical implants, the biological effects and toxicity of UNCD particles that could eventually detach have not been studied to date. The biokinetics and biological effects of UNCD compared to titanium dioxide (TiO ) nanoparticles was evaluated in vivo using Wistar rats (n = 30) i.p.

Acute exposure to air pollution particulate matter aggravates experimental myocardial infarction in mice by potentiating cytokine secretion from lung macrophages.

Clinical, but not experimental evidence has suggested that air pollution particulate matter (PM) aggravates myocardial infarction (MI). Here, we aimed to describe mechanisms and consequences of PM exposure in an experimental model of MI. C57BL/6J mice were challenged with a PM surrogate (Residual Oil Fly Ash, ROFA) by intranasal installation before MI was induced by permanent ligation of the left anterior descending coronary artery.

Selective TNF-α targeting with infliximab attenuates impaired oxygen metabolism and contractile function induced by an acute exposure to air particulate matter.

Inflammation plays a central role in the onset and progression of cardiovascular diseases associated with the exposure to air pollution particulate matter (PM). The aim of this work was to analyze the cardioprotective effect of selective TNF-α targeting with a blocking anti-TNF-α antibody (infliximab) in an in vivo mice model of acute exposure to residual oil fly ash (ROFA). Female Swiss mice received an intraperitoneal injection of infliximab (10 mg/kg body wt) or saline solution, and were intranasally instilled with a ROFA suspension (1 mg/kg body wt).

Acute exposure to Buenos Aires air particles (UAP-BA) induces local and systemic inflammatory response in middle-aged mice: A time course study.

Exposure to air particulate matter (PM) is associated with increased cardiovascular morbimortality. However, PM doesn't affect equally to all people, being the old cohort the most susceptible and studied. We hypothesized that another specific life phase, the middle-aged subpopulation, may be negatively affected.

In vivo short-term exposure to residual oil fly ash impairs pulmonary innate immune response against environmental mycobacterium infection.

Epidemiological studies have shown that pollution derived from industrial and vehicular transportation induces adverse health effects causing broad ambient respiratory diseases. Therefore, air pollution should be taken into account when microbial diseases are evaluated. Environmental mycobacteria (EM) are opportunist pathogens that can affect a variety of immune compromised patients, which impacts significantly on human morbidity and mortality.

mRNA of cytokines in bone marrow and bone biomarkers in response to propranolol in a nutritional growth retardation model.

Background: The aim of this study was to assess mRNA of IL-6, TNFα and IL-10 cytokines in bone marrow, possible mediators involved in altered bone remodeling with detrimental consequences on bone quality in NGR (Nutritional growth retardation) rats.

Methods: Weanling male Wistar rats were assigned either to control (C) or experimental group (NGR) (n=20 each). C and NGR groups were assigned to 2 groups according to receiving saline solution (SS) or propranolol hydrochloride (P): C, C+P (CP), NGR or NGR+P (NGRP).