Ana Carla Balthar Bandeira

Oxidative effects on lung inflammatory response in rats exposed to different concentrations of formaldehyde.

The formaldehyde (FA) is a crosslinking agent that reacts with cellular macromolecules such as proteins, nucleic acids and molecules with low molecular weight such as amino acids, and it has been linked to inflammatory processes and oxidative stress. This study aimed to analyze the oxidative effects on pulmonary inflammatory response in Fischer rats exposed to different concentrations of FA. Twenty-eight Fischer rats were divided into 4 groups (N = 7). The control group (CG) was exposed to ambient air and three groups were exposed to different concentrations of FA: 1% (FA1%), 5% (FA5%) and 10% (FA10%). In the Bronchoalveolar Lavage Fluid (BALF), the exposure to a concentration of 10% promoted the increase of inflammatory cells compared to CG. There was also an increase of macrophages and lymphocytes in FA10% and lymphocytes in FA5% compared to CG. The activity of NADPH oxidase in the blood had been higher in FA5% and FA10% compared to CG. The activity of superoxide dismutase enzyme (SOD) had an increase in FA5% and the activity of the catalase enzyme (CAT) showed an increase in FA1% compared to CG. As for the glutathione system, there was an increase in total glutathione (tGSH), reduced glutathione (GSH) and oxidized glutathione (GSSG) in FA5% compared to CG. The reduced/oxidized glutathione ratio (GSH/GSSG) had a decrease in FA5% compared to CG. There was an increase in lipid peroxidation compared to all groups and the protein carbonyl formation in FA10% compared to CG. We also observed an increase in CCL2 and CCL5 chemokines in the treatment groups compared to CG and in serum there was an increase in CCL2, CCL3 and CCL5 compared to CG. Our results point out to the potential of formaldehyde in promoting airway injury by increasing the inflammatory process as well as by the redox imbalance.

Short-term exposure to formaldehyde promotes oxidative damage and inflammation in the trachea and diaphragm muscle of adult rats

Formaldehyde (FA) is an environmental pollutant widely used in industry. Exposure to FA causes irritation of the respiratory mucosa and is associated with inflammation and oxidative stress in the airways. This study aimed at investigating the oxidative effects on the inflammatory response in the trachea and the diaphragm muscle (DM) of rats exposed to different concentrations of formaldehyde. Twenty-eight Fischer male rats were divided into four groups: control group (CG) exposed to the ambient air; and three groups exposed to the following formaldehyde concentrations of 1% (FA1), 5% (FA5) and 10% (FA10), respectively. The exposure occurred for twenty minutes, three times a day for five days. Oxidative stress analyses were performed by carbonyl protein, lipid peroxidation and catalase activity. The assessment of inflammatory cell influx in both organs and the mucus production in the trachea was carried out. There was an increase of lipid peroxidation in the trachea and the DM of FA1 and FA5 groups compared to the CG and FA10. The oxidation of DM proteins increased in FA10 group compared to CG, FA1 and FA5. The catalase enzyme activity in the DM was reduced in FA1, FA5 and FA10 compared to the CG. Meanwhile, there was a reduction in the enzymatic activity of FA10 compared to the CG in the trachea. The morphometric analysis in the DM demonstrated an influx of inflammatory cells in FA10 compared to the CG. In FA10 group, the tracheal epithelium showed metaplasia and ulceration. In addition, the tracheal epithelium showed more mucus deposits in FA5 compared to CG, FA1 and FA10. The results demonstrated that the exposure to formaldehyde at different concentrations in a short period of time promotes oxidative damage and inflammation in the DM and the trachea and causes metaplasia, ulceration and increased mucus at the latter.

Lycopene pretreatment improves hepatotoxicity induced by acetaminophen in C57BL/6 mice.

Acetaminophen (APAP) is an antipyretic and analgesic drug that, in high doses, leads to severe liver injury and potentially death. Oxidative stress is an important event in APAP overdose. Researchers are looking for natural antioxidants with the potential to mitigate the harmful effects of reactive oxygen species in different models. Lycopene has been widely studied for its antioxidant properties. The aim of this study was to evaluate the antioxidant potential of lycopene pretreatment in APAP-induced liver injury in C57BL/6 mice. C57BL/6 male mice were divided into the following groups: control (C); sunflower oil (CO); acetaminophen 500mg/kg (APAP); acetaminophen 500mg/kg+lycopene 10mg/kg (APAP+L10), and acetaminophen 500mg/kg+lycopene 100mg/kg (APAP+L100). Mice were pretreated with lycopene for 14 consecutive days prior to APAP overdose. Analyses of blood serum and livers were performed. Lycopene was able to improve redox imbalance, decrease thiobarbituric acid reactive species level, and increase CAT and GSH levels. In addition, it decreased the IL-1β expression and the activity of MMP-2. This study revealed that preventive lycopene consumption in C57BL/6 mice can attenuate the effects of APAP-induced liver injury. Furthermore, by improving the redox state, and thus indicating its potential antioxidant effect, lycopene was also shown to have an influence on inflammatory events.

The antioxidant and anti-inflammatory properties of lycopene in mice lungs exposed to cigarette smoke

Lycopene is a carotenoid with known antioxidant and anti-inflammatory properties. We aimed to evaluate the in vitro and in vivo effects of lycopene on reducing the redox imbalance and inflammation induced by cigarette smoke (CS). For the in vitro study, J774A.1 (macrophages) cells were incubated in the presence of 0.5, 1.0, 2.0, 4.0, 8.0, 10.0 and 25 μM of lycopene for 3, 6 and 24 h or in the presence of 0.1%, 0.25%, 0.5%, 0.625%, 1.25%, 2.25%, 5% and 10% cigarette smoke extract (CSE) for 3, 6 and 24 h to assess cell viability and measurement of intracellular reactive oxygen species (ROS). For the in vivo study, 40 mice were divided into 5 groups: a control exposed to ambient air (CG), a vehicle-control group that received 200 μl of sunflower oil by orogastric gavage, a group exposed to CS and two groups administered lycopene (diluted in sunflower oil) at doses of either 25 or 50 mg/kg/day prior to exposure to CS (LY25+CS and LY50+CS). The total treatment time lasted 5 days. A cell viability decrease was observed at 10- and 25-μM concentrations of lycopene in 3, 6 and 24 h compared with CG. There was an increase of ROS production in 24 h in CS compared with CG. Lycopene concentrations of 1 μM and 2 μM were able to reduce the production of ROS in 24 h compared with CS. In the bronchoalveolar lavage fluid, the total number of leukocytes increased in the CS group compared with the control groups (CG). Administration with lycopene at the highest dose suppressed this CS-induced increase in leukocytes. Lipid peroxidation and DNA damage increased in the CS group compared with that in the controls, and this increase was suppressed by lycopene at the highest dose. In contrast, superoxide dismutase activity decreased in the CS group compared with that in the controls. Catalase activity also increased in the CS group compared with that in both control groups, and this increase was suppressed in LY25+CS and LY50+CS. There was an increase in the levels of tumor necrosis factor-α, interferon-γ and interleukin-10 after exposure to CS, and these effects were suppressed by both doses of lycopene. These data elucidate the role of lycopene as an antioxidant and anti-inflammatory agent in these two models of short-term exposure to CS.

The administration of a high refined carbohydrate diet promoted an increase in pulmonary inflammation and oxidative stress in mice exposed to cigarette smoke

This study aimed to evaluate the effects of a high refined carbohydrate diet and pulmonary inflammatory response in C57BL/6 mice exposed to cigarette smoke (CS). Twenty-four male mice were divided into four groups: control group (CG), which received a standard diet; cigarette smoke group (CSG), which was exposed to CS; a high refined carbohydrate diet group (RG), which received a high refined carbohydrate diet; and a high refined carbohydrates diet and cigarette smoke group (RCSG), which received a high refined carbohydrate diet and was exposed to CS. The animals were monitored for food intake and body weight gain for 12 weeks. After this period, the CSG and RCSG were exposed to CS for five consecutive days. At the end of the experimental protocol, all animals were euthanized for subsequent analyses. There was an increase of inflammatory cells in the bronchoalveolar lavage fluid (BALF) of CSG compared to CG and RCSG compared to CG, CSG, and RG. In addition, in the BALF, there was an increase of tumor necrosis factor alpha in RCSG compared to CG, CSG, and RG; interferon gamma increase in RCSG compared to the CSG; and increase in interleukin-10 in RCSG compared to CG and RG. Lipid peroxidation increased in RCSG compared to CG, CSG, and RG. Furthermore, the oxidation of proteins increased in CSG compared to CG. The analysis of oxidative stress showed an increase in superoxide dismutase in RCSG compared to CG, CSG, and RG and an increase in the catalase activity in RCSG compared with CG. In addition, there was a decrease in the glutathione reduced/glutathione total ratio of CSG, RG, and RCSG compared to CG. Therefore, the administration of a high refined carbohydrate diet promoted an increase in pulmonary inflammation and oxidative stress in mice exposed to CS.

Acromial Morphometric Analysis Using Imaging Software

El objetivo de este estudio fue medir con precision la morfologia acromial para describir los patrones anatomicos de sus subtipos y llevar a cabo un estudio de la literatura sobre las relaciones entre los subtipos morfologicos y las enfermedades relacionadas. Tomamos fotografias de la escapula del Instituto de Anatomia de la Universidad Sombra Severino, y se analizaron las imagenes con el Software Image-J®. El angulo acromial medio fue de 139,23 ± 2,781°, no habiendo diferencias significativas entre los lados derecho e izquierdo. De observo una correlacion positiva entre el angulo acromial y el angulo de la columna vertebral de la escapula. La correlacion mencionada anteriormente, juega un papel importante en los trastornos de la inflamacion del hombro, especialmente el sindrome, lo cual refuerza la importancia de los estudios de la morfologia acromial.

The exposure to formaldehyde causes renal dysfunction, inflammation and redox imbalance in rats

Twenty-eight Fischer male rats were divided into four groups: control group (CG), exposed to the ambient air, and groups exposed to formaldehyde (FA) at concentrations of 1% (FA1%), 5% (FA5%) and 10% (FA10%). Kidney function was assessed by dosage of uric acid, creatinine and urea. Morphometry was performed on the thickness of the lumen of Bowmans capsule and diameter of the lumen of the renal tubules. We evaluated the redox imbalance through the catalase and superoxide dismutase activity as well as oxidative damage by lipid peroxidation. Inflammatory chemokines CCL2, CCL3 and CCL5 were analyzed by enzyme immunoassays. There was an increase in the concentration of urea in FA10% compared with CG and FA1%. The levels of creatinine, renal lumen and lipid peroxidation increased in all FA-treated groups compared with CG. The concentration of uric acid in FA10% was lower compared with all other groups. There was an increase in the space of Bowmans capsule in FA5% and FA10% compared with CG and FA1%. However, the superoxide dismutase activity was higher in FA5% compared with other groups while CCL5 was higher in FA1% compared with CG. The exposure to formaldehyde in a short period of time leads to changes in the kidney function, inflammation and morphology, as well as promoted the increase of superoxide dismutase activity and oxidative damage.

The Effects of the Combination of a Refined Carbohydrate Diet and Exposure to Hyperoxia in Mice

Obesity is a multifactorial disease with genetic, social, and environmental influences. This study aims at analyzing the effects of the combination of a refined carbohydrate diet and exposure to hyperoxia on the pulmonary oxidative and inflammatory response in mice. Twenty-four mice were divided into four groups: control group (CG), hyperoxia group (HG), refined carbohydrate diet group (RCDG), and refined carbohydrate diet + hyperoxia group (RCDHG). The experimental diet was composed of 10% sugar, 45% standard diet, and 45% sweet condensed milk. For 24 hours, the HG and RCDHG were exposed to hyperoxia and the CG and RCDG to ambient air. After the exposures were completed, the animals were euthanized, and blood, bronchoalveolar lavage fluid, and lungs were collected for analyses. The HG showed higher levels of interferon-γ in adipose tissue as compared to other groups and higher levels of interleukin-10 and tumor necrosis factor-α compared to the CG and RCDHG. SOD and CAT activities in the pulmonary parenchyma decreased in the RCDHG as compared to the CG. There was an increase of lipid peroxidation in the HG, RCDG, and RCDHG as compared to the CG. A refined carbohydrate diet combined with hyperoxia promoted inflammation and redox imbalance in adult mice.

Protótipo de ventilação mecânica espontânea e artificial.

Current essay focuses on research with regard to pregnancy. Pregnancy brings about huge physical and psychological transformations in the female with a great variety of emotional oscillations, such as fear, anxiety, insecurity, doubts, happiness and others, which, because of the prevailing imbalance, contribute towards the start of post-partum depression symptoms. Scientific registers focusing on PPD prevention methods already demonstrate the use of psycho-social, psycho-pharmacological and hormonal strategies even though no single isolated intervention is sufficiently efficacious in the development of the disease. A review of the literature, based on on-line access to abstracts from databases, is provided. The psychotherapeutic approach is of fundamental importance in treatment, coupled to family support and follow-up.