Sandra Regina Castro Soares

Air pollution and antibodies against modified lipoproteins are associated with atherosclerosis and vascular remodeling in hyperlipemic mice

We analyzed the impact of chronic exposure to urban air pollution on the development of atherosclerosis. Hyperlipemic mice (LDLR(-/-)) were submitted to a high fat diet and air pollution for four months. We measured the susceptibility of LDL to oxidative modifications (TBARS), the presence of anti-oxLDL and an apoB-derived peptide (apoB-D) in blood and the degree of atherosclerosis in the aortic arch. Air pollution increased the susceptibility of LDL to oxidation as well as anti-oxLDL and anti-apo-B levels. These levels were even higher than in mice submitted to a high fat diet and non-polluted air. The lipid content of the atherosclerotic plaques in the aorta was increased in groups with a high cholesterol diet independently of the air quality. However, the thickness of the arterial wall was greater in mice fed a high lipid diet with polluted air. Thus, we conclude that urban air pollution exacerbates the susceptibility of LDL to oxidation, atherogenesis and vascular remodeling in hyperlipemic mice and that an immune response accompanies this process.

Influence of medium-chain triglyceride-based lipid emulsion on rat polymorphonuclear cell functions

Intravenous lipid emulsions are used as energy and essential fatty acids sources. There are controversial reports postulating in vitro and in vivo inhibitory effects of long-chain triglycerides (LCT) upon the blood polymorphonuclear leukocytes (PMNL) functions. In the present study the in vivo and in vitro effects of LCT and a physical mixture of medium- and long-chain triglycerides (MCT/LCT) emulsions were investigated on select PMNL functions, i.e., chemotaxis, phagocytosis, and bacterial killing. Blood from 20 rats was incubated with LCT, MCT, MCT/LCT, and saline, respectively. MCT-containing emulsions exhibited an inhibitory effect on all PMNL functions investigated, whereas LCT exerted an effect on the phagocytic index only. The administration of a parenteral supply of LCT, MCT/LCT, and saline for 30 h followed by saline infusion for 14 h in discontinuous mode did not influence any of the investigated PMNL functions. Similarly, continuous infusion over 44 h at increasing infusion rates up to 1.5 mL/h did not affect the PMNL functions. The obvious difference between in vitro and in vivo response of the PMNL model emphasizes the necessity for continuous monitoring of in vivo conditions. Appropriate interpretation of the data requires continuous circumspection and consideration of trials in a clinical setting.

Urban air pollution induces micronuclei in peripheral erythrocytes of mice in vivo.

In this study, we explored the role of chronic exposure to urban air pollution in causing DNA damage (micronuclei frequency in peripheral erythrocytes) in rodents in vivo. Mice (n=20) were exposed to the urban atmosphere of São Paulo for 120 days (February to June 1999) and compared to animals (n=20) maintained in the countryside (Atibaia) for the same period. Daily levels of inhalable particles (PM10), CO, NO(2), and SO(2), were available for São Paulo. Occasional measurements of CO and O(3) were made in Atibaia, showing negligible levels of pollution in the area. The frequency of micronuclei (repeated-measures ANOVA) increased with aging, the highest values obtained for the 90th day of experiment (P<0.001). The exposure to urban air pollution elicited a significant (P=0.016) increase of micronuclei frequency, with no significant interaction with time of study. Associations (Spearmans correlation) between pollution levels of the week that precede blood sampling and micronuclei counts were observed in São Paulo. The associations between micronuclei counts and air pollution were particularly strong for pollutants associated with automotive emissions, such as CO (P=0.037), NO(2) (P<0.001), and PM10 (P<0.001). Our results support the concept that urban levels of air pollution may cause somatic mutations.

X-ray induced degradation of poly(vinylidene fluoride) films

Abstract The X-ray induced degradation of poly(vinylidene fluoride) (PDVF) films has been investigated by IR, X-ray diffraction, UV/visible and differential scanning calorimetry (DSC) techniques. The IR spectra show a significant decrease in intensity of bands characteristic of crystalline regions, namely a moderate decrease in intensity of bands corresponding to the α form and a small decrease in intensity of bands of the β form. The X-ray results show an increase in crystallinity after the first 3 h of irradiation; at longer exposure times, there is a decrease in crystallinity, the α form being preferentially attacked relative to the β form, as shown by IR spectra. The loss of crystallinity under X-ray irradiation was demonstrated by DSC measurements. The appearance of a new IR band at 1714 cm −1 , whose intensity increases with X-ray exposure time, is evidence of the formation of conjugated double bonds by dehydrofluorination. The UV/visible spectra show several absorption bands associated with diene, triene and tetraene, the diene band being dominant. The DSC thermograms show changes in the shape of the curve and the appearance of new melting peaks at lower temperatures with increasing exposure time. The reactions taking place in PVDF films irradiated in vacuum by X-rays are thus apparently similar to those in films irradiated by γ-rays or electron beams and films subjected to high-energy ion implantation.

Cell death mechanisms in Leishmania amazonensis triggered by methylene blue-mediated antiparasitic photodynamic therapy

Antiparasitic photodynamic therapy (ApPDT) is an emerging approach to manage cutaneous leishmaniasis (CL) since no side effects, contraindications and parasite resistance have been reported. In addition, methylene blue (MB) is a suitable photosensitizer to mediate ApPDT on CL. In this study we aimed to look for the best parameters to eradicate Leishmania amazonensis and investigated the cell death pathways involved in MB-mediated ApPDT. MB uptake by parasites was determined using different MB concentrations (50, 100, 250 and 500 μM) and incubation times (10, 30 and 60 min). L. amazonensis promastigotes were cultured and submitted to ApPDT using different concentrations of MB (50, 100 and 250 μM) combined to a red LED emitting at 645 ± 10 nm. The pre-irradiation time was 10 min. Two optical powers (100 mW and 250 mW) were tested and cells were exposed to 60 and 300 s of MB-mediated ApPDT delivering energies of 6, 15, 30 and 75 J and fluences of 21.2, 53.1, 106.2 and 265.4 J/cm2, respectively. Following ApPDT, cells were prepared for flow cytometry and transmission electron microscopy to unravel the mechanisms of cell death. Our results showed the lowest MB concentration (50 μM) and the lowest optical power (100 mW) promoted the highest percentage of cell decrease. ApPDT caused alterations on cell membrane permeability as well depolarization of mitochondrial membrane potential. We also observed ultrastructural changes of the parasites such as cell shrinkage, intense vacuolization of the cytoplasm, enlargement of mitochondrion-kinetoplast complex, and small blebs on parasite flagella and cell membrane after MB-mediated ApPDT. Taken together, our findings ratify that ApPDT parameters play a pivotal role in cell susceptibility and suggest that apoptosis is involved in parasite death regardless MB-mediated ApPDT protocol.