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1.
Food Chem Toxicol ; 69: 38-45, 2014 Jul.
Article in English | MEDLINE | ID: mdl-24694906

ABSTRACT

We evaluated the influence of dietary fats on ultraviolet radiation (UVR)-induced oxidative damage in skin of rats. Animals from two consecutive generations born of dams supplemented with fats during pregnancy and breastfeeding were maintained in the same supplementation: soybean-oil (SO, rich in n-6 FA, control group), fish-oil (FO, rich in n-3 FA) or hydrogenated-vegetable-fat (HVF, rich in TFA). At 90 days of age, half the animals from the 2nd generation were exposed to UVR (0.25 J/cm(2)) 3×/week for 12 weeks. The FO group presented higher incorporation of n-3 FA in dorsal skin, while the HVF group incorporated TFA. Biochemical changes per se were observed in skin of the HVF group: greater generation of reactive oxygen species (ROS), lower mitochondrial integrity and increased Na(+)K(+)-ATPase activity. UVR exposure increased skin wrinkles scores and ROS generation and decreased mitochondrial integrity and reduced-glutathione levels in the HVF group. In FO, UVR exposure was associated with smaller skin thickness and reduced levels of protein-carbonyl, together with increased catalase activity and preserved Na(+)K(+)-ATPase function. In conclusion, while FO may be protective, trans fat may be harmful to skin health by making it more vulnerable to UVR injury and thus more prone to develop photoaging and skin cancer.


Subject(s)
Fish Oils/pharmacology , Skin/radiation effects , Trans Fatty Acids/pharmacology , Ultraviolet Rays/adverse effects , Animals , Antioxidants/metabolism , Dietary Fats/pharmacology , Fatty Acids/analysis , Female , Hydrogenation , Mitochondria/drug effects , Mitochondria/radiation effects , Pregnancy , Protein Carbonylation/drug effects , Protein Carbonylation/radiation effects , Rats, Wistar , Reactive Oxygen Species/metabolism , Skin/drug effects , Skin/metabolism , Skin/pathology , Sodium-Potassium-Exchanging ATPase/metabolism , Soybean Oil/pharmacology , Sunlight/adverse effects
2.
Brain Res ; 1388: 134-40, 2011 May 04.
Article in English | MEDLINE | ID: mdl-21300037

ABSTRACT

Brain damage from neonatal hypoxia-ischemia (HI) plays a major role in neonatal mortality and morbidity. Using the Rice-Vannucci model of HI in rats, we verified that 8 days after HI injury, adenosine deaminase (ADA), N-acetyl-glucosaminidase (NAG) and myeloperoxidase (MPO) activities increased in the left hemisphere hippocampus (HI group); however, the activity of 5'-nucleotidase (5'NT) remained unchanged. In the hematoxylin-eosin analysis (HE), we detected selective and delayed degeneration of hippocampal pyramidal neurons and astroglial reaction accompanied by glial fibrillary acidic protein (GFAP)-positive and vimentin-positive in the immunohistochemistry analysis in the HI group compared with the control group. We observed the selective necrosis of neurons, vascular endothelial proliferation and inflammatory response accompanied by the increase of the key enzyme of adenosine metabolism in the HI group. The increase of ADA activity, despite the 5'NT activity was not altered, indicates the predominance of ADA activity in the postischemic homeostasis of extra cellular adenosine. The presence of leukocytes into the ischemic areas displays the possible importance of the neutrophil-macrophages associated with the increase of MPO and NAG activities 8 days after HI. These findings may contribute to the evaluation of some consequences of the damage caused by neonatal HI.


Subject(s)
Hippocampus/enzymology , Hippocampus/pathology , Hypoxia-Ischemia, Brain/metabolism , Hypoxia-Ischemia, Brain/pathology , Animals , Animals, Newborn , Astrocytes/metabolism , Astrocytes/pathology , Hexosaminidases/metabolism , Hippocampus/injuries , Hypoxia-Ischemia, Brain/immunology , Immunohistochemistry , Inflammation/metabolism , Inflammation/pathology , Male , Neurons/metabolism , Neurons/pathology , Peroxidase/metabolism , Rats , Rats, Wistar
3.
Int J Dev Neurosci ; 27(8): 857-62, 2009 Dec.
Article in English | MEDLINE | ID: mdl-19559780

ABSTRACT

Hypoxia ischemia (HI) is a common cause of damage in the fetal and neonatal brain. Lifelong disabilities such as cerebral palsy, epilepsy, behavioral and learning disorders are some of the consequences of brain injury acquired in the perinatal periods. Inflammation and formation of free radicals appear to play key roles in neonatal HI. The aim of this study was to describe the chronological sequence of adenosine deaminase (ADA) activity, the oxidative damage changes and astrocyte response using the classic model of neonatal HI. We observed an increase in the activity of ADA and lipid peroxidation in the cerebral cortex 8 days after neonatal HI. This was accompanied by a GFAP-positive, and the degree of brain damage was determined histochemically by hematoxylin-eosin (HE). Taking into account the important anti-inflammatory role of adenosine, ADA may provide an efficient means for scavenging cell-surrounding adenosine and play an important part in subsequent events of neonatal HI in association with GFAP reactive gliosis. The present investigation showed that neonatal HI causes the increase of free radicals and significant damage in the cerebral cortex. The increase in ADA activity may reflect the activation of the immune system caused by HI because the morphological analysis exhibited a lymphocytic infiltration.


Subject(s)
Adenosine Deaminase/metabolism , Astrocytes/metabolism , Cerebral Cortex/cytology , Cerebral Cortex/metabolism , Hypoxia-Ischemia, Brain/metabolism , Lipid Peroxidation , Animals , Animals, Newborn , Astrocytes/cytology , Cerebral Cortex/pathology , Cerebral Cortex/physiopathology , Humans , Hypoxia-Ischemia, Brain/complications , Hypoxia-Ischemia, Brain/pathology , Hypoxia-Ischemia, Brain/physiopathology , Infant , Infant, Newborn , Oxidative Stress , Rats , Rats, Wistar
4.
Inhal Toxicol ; 21(11): 906-12, 2009 Sep.
Article in English | MEDLINE | ID: mdl-19459774

ABSTRACT

Cigarette smoke is a complex mixture of various toxic substances that are capable of initiating oxidative damage and promoting blood platelet alterations. In this study, we investigated the activities of the ectoenzymes NTPDase (ectonucleoside triphosphate diphosphohydrolase, CD39) and 5'-nucleotidase (CD73) in platelets as well as adenosine deaminase (ADA) in the plasma of rats exposed to aged and diluted sidestream smoke during 4 weeks. The rats were divided into two groups: I (control) and II (exposed to smoke). After the exposure period, blood was collected and the platelets and plasma were separated for enzymatic assay. The results demonstrated that NTPDase (with ATP as substrate) and 5'-nucleotidase (AMP as substrate) activities were significantly higher in group II (p < 0.05) as compared to group I, while no significant difference was observed for NTPDase with ADP as substrate. The ADA activity was significantly reduced in group II (p < 0.05) as compared with group I. Platelet aggregation was significantly increased in group II (p < 0.05) as compared with group I. We suggest that these alterations in the activity of enzymes from the purinergic system are associated with an increase in platelet aggregation. However, our study has demonstrated that the organism tries to compensate for this enhanced aggregation by increasing hydrolysis of AMP and reducing hydrolysis of adenosine, a potent inhibitor of aggregation and an important modulator of vascular tone.


Subject(s)
Adenosine Deaminase/metabolism , Adenosine Triphosphatases/metabolism , Tobacco Smoke Pollution/adverse effects , 5'-Nucleotidase/blood , Adenosine/blood , Animals , Blood Gas Analysis , Blood Platelets/enzymology , Carboxyhemoglobin/metabolism , Hydrogen-Ion Concentration , Lung/enzymology , Lung/pathology , Male , Platelet Aggregation/drug effects , Pulmonary Fibrosis/chemically induced , Pulmonary Fibrosis/pathology , Rats , Rats, Wistar , Nicotiana/chemistry
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