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1.
Brain Res Bull ; 180: 1-11, 2022 03.
Artículo en Inglés | MEDLINE | ID: mdl-34954227

RESUMEN

Sports-related concussions are particularly common during adolescence, and there is insufficient knowledge about how recurrent concussions in this phase of life alter the metabolism of essential structures for memory in adulthood. In this sense, our experimental data revealed that seven recurrent concussions (RC) in 35-day-old rats decreased short-term and long-term memory in the object recognition test (ORT) 30 days after injury. The RC protocol did not alter motor and anxious behavior and the immunoreactivity of brain-derived neurotrophic factor (BDNF) in the cerebral cortex. Recurrent concussions induced the inflammatory/oxidative stress characterized here by increased glial fibrillary acidic protein (GFAP), interleukin 1ß (IL 1ß), 4-hydroxynonenal (4 HNE), protein carbonyl immunoreactivity, and 2',7'-dichlorofluorescein diacetate oxidation (DCFH) levels and lower total antioxidant capacity (TAC). Inhibited Na+,K+-ATPase activity (specifically isoform α2/3) followed by Km (Michaelis-Menten constant) for increased ATP levels and decreased immunodetection of alpha subunit of this enzyme, suggesting that cognitive impairment after RC is caused by the inability of surviving neurons to maintain ionic gradients in selected targets to inflammatory/oxidative damage, such as Na,K-ATPase activity.


Asunto(s)
Conmoción Encefálica , Disfunción Cognitiva , Hipocampo , Trastornos de la Memoria , Enfermedades Neuroinflamatorias , Estrés Oxidativo/fisiología , ATPasa Intercambiadora de Sodio-Potasio/metabolismo , Memoria Espacial/fisiología , Factores de Edad , Animales , Conmoción Encefálica/complicaciones , Conmoción Encefálica/inmunología , Conmoción Encefálica/metabolismo , Conmoción Encefálica/fisiopatología , Disfunción Cognitiva/etiología , Disfunción Cognitiva/inmunología , Disfunción Cognitiva/metabolismo , Disfunción Cognitiva/fisiopatología , Modelos Animales de Enfermedad , Hipocampo/inmunología , Hipocampo/metabolismo , Hipocampo/fisiopatología , Masculino , Trastornos de la Memoria/etiología , Trastornos de la Memoria/inmunología , Trastornos de la Memoria/metabolismo , Trastornos de la Memoria/fisiopatología , Enfermedades Neuroinflamatorias/etiología , Enfermedades Neuroinflamatorias/inmunología , Enfermedades Neuroinflamatorias/metabolismo , Enfermedades Neuroinflamatorias/fisiopatología , Ratas , Ratas Wistar
2.
J Fish Dis ; 41(3): 469-474, 2018 Mar.
Artículo en Inglés | MEDLINE | ID: mdl-29193157

RESUMEN

Several studies have been demonstrated that phosphotransfer network, through the adenylate kinase (AK) and pyruvate kinase (PK) activities, allows for new perspectives leading to understanding of disease conditions associated with disturbances in energy metabolism, metabolic monitoring and signalling. In this sense, the aim of this study was to evaluate whether experimental infection by Aeromonas caviae alters hepatic AK and PK activities of silver catfish Rhamdia quelen. Hepatic AK and PK activities decreased in infected animals compared to uninfected animals, as well as the hepatic adenosine triphosphate (ATP) levels. Also, a severe hepatic damage was observed in the infected animals due to the presence of dilation and congestion of vessels, degeneration of hepatocytes and loss of liver parenchyma architecture and sinusoidal structure. Therefore, we have demonstrated, for the first time, that experimental infection by A. caviae inhibits key enzymes linked to the communication between sites of ATP generation and ATP utilization. Moreover, the absence of a reciprocal compensatory mechanism between these enzymes contributes directly to hepatic damage and for a severe energetic imbalance, which may contribute to disease pathophysiology.


Asunto(s)
Aeromonas caviae/fisiología , Bagres , Enfermedades de los Peces/enzimología , Proteínas de Peces/genética , Infecciones por Bacterias Gramnegativas/veterinaria , Hígado/enzimología , Adenilato Quinasa/genética , Adenilato Quinasa/metabolismo , Animales , Metabolismo Energético , Enfermedades de los Peces/virología , Proteínas de Peces/metabolismo , Infecciones por Bacterias Gramnegativas/enzimología , Infecciones por Bacterias Gramnegativas/virología , Hígado/virología , Piruvato Quinasa/genética , Piruvato Quinasa/metabolismo
3.
J Fish Dis ; 41(1): 27-32, 2018 Jan.
Artículo en Inglés | MEDLINE | ID: mdl-28699699

RESUMEN

It has been recognized that the cholinergic and adenosinergic systems have an essential role in immune and inflammatory responses during bacterial fish pathogens, such as the enzymes acetylcholinesterase (AChE) and adenosine deaminase (ADA), which are responsible for catalysis of the anti-inflammatory molecules acetylcholine (ACh) and adenosine (Ado) respectively. Thus, the aim of this study was to investigate the involvement of the cholinergic and adenosinergic systems on the immune response and inflammatory process in gills of experimentally infected Rhamdia quelen with Streptococcus agalactiae. Acetylcholinesterase activity decreased, while ACh levels increased in gills of infected animals compared to uninfected animals. On the other hand, a significant increase in ADA activity with a concomitant decrease in Ado levels was observed in infected animals compared to uninfected animals. Based on this evidence, we concluded that infection by S. agalactiae in silver catfish alters the cholinergic and adenosinergic systems, suggesting the involvement of AChE and ADA activities on immune and inflammatory responses, regulating the ACh and Ado levels. In summary, the downregulation of AChE activity exerts an anti-inflammatory profile in an attempt to reduce or prevent the tissue damage, while the upregulation of ADA activity exerts a pro-inflammatory profile, contributing to disease pathophysiology.


Asunto(s)
Enfermedades de los Peces/microbiología , Branquias/inmunología , Infecciones Estreptocócicas/veterinaria , Streptococcus agalactiae/inmunología , Acetilcolinesterasa/análisis , Adenosina Desaminasa/análisis , Animales , Bagres , Enfermedades de los Peces/inmunología , Branquias/enzimología , Branquias/microbiología , Inflamación/inmunología , Inflamación/microbiología , Infecciones Estreptocócicas/inmunología
4.
Andrologia ; 48(1): 51-8, 2016 Feb.
Artículo en Inglés | MEDLINE | ID: mdl-25892208

RESUMEN

Polychlorinated biphenyls (PCBs) are a group of environmental contaminants widely reported to cause gonadal toxicity in both humans and animals. This study investigated the amelioratory role of quercetin in PCBs-induced DNA damage in male Wistar rats. Polychlorinated biphenyls were administered intraperitoneally at a dose of 2 mg kg(-1) alone or in combination with quercetin (orally) at 50 mg kg(-1) for 25 days. Quercetin modulation of PCBs-induced gonadal toxicity was evaluated using selected oxidative stress indices, comet assay, measurement of DNA concentration and histology of the testes. Administration of PCBs alone caused a significant (P < 0.05) depletion in the total thiol level in testes of treated rats. Conversely, the levels of reactive oxygen species (ROS) and thiobarbituric acid reactive substances (TBARS) production were markedly elevated in testes of PCBs-treated rats compared with control. Further, PCBs exposure produced statistically significant increases in DNA tail migration, degraded double-stranded DNA (dsDNA) concentration and histological alterations of testes of the treated rats compared to control. Quercetin cotreatment significantly improved the testicular antioxidant status, decreased DNA fragmentation and restored the testicular histology, thus demonstrating the protective effect of quercetin in PCBs-treated rats.


Asunto(s)
Antioxidantes/farmacología , Daño del ADN/efectos de los fármacos , Contaminantes Ambientales/toxicidad , Estrés Oxidativo/efectos de los fármacos , Bifenilos Policlorados/toxicidad , Quercetina/farmacología , Testículo/efectos de los fármacos , Animales , Masculino , Ratas , Ratas Wistar , Especies Reactivas de Oxígeno/metabolismo , Testículo/metabolismo , Sustancias Reactivas al Ácido Tiobarbitúrico/metabolismo
5.
Mol Cell Endocrinol ; 314(1): 84-9, 2010 Jan 15.
Artículo en Inglés | MEDLINE | ID: mdl-19666082

RESUMEN

It now appears that obesity is associated with a low-grade inflammation of white adipose tissue resulting from chronic activation of the innate immune system as interleukin-1 beta (IL-1). Previous investigations have described a positive association between IL-1 beta +3953 (C>T) gene polymorphism (rs 1143634) and obesity, suggesting functional effects on fat mass, fat metabolism and body mass. However, it is necessary to determine if these results occur in other populations and if they are influenced by sex and age. Therefore, we performed a case-control study using 880 Caucasian subjects (59.7+/-11.9 years old) from the Brazilian Aging Research Program (non-overweight=283, overweight=334, obese=263) previously investigated in genetic studies, in whom we analyzed the IL-1 beta +3953C/T polymorphism. We observed higher T allele (CT/TT) frequency in non-overweight than overweight and obese groups. The odds ratio showed 1.340 (95% CI: 1.119-1.605) times more chance of the obese group being CC carriers compared to non-overweight group independent of sex and age. This study corroborates the idea that the IL-1 system is linked to the development of obesity.


Asunto(s)
Interleucina-1beta/genética , Obesidad/fisiopatología , Polimorfismo de Nucleótido Simple , Tejido Adiposo/metabolismo , Adolescente , Adulto , Anciano , Índice de Masa Corporal , Brasil , Estudios de Casos y Controles , Femenino , Frecuencia de los Genes , Genotipo , Humanos , Interleucina-1beta/metabolismo , Masculino , Persona de Mediana Edad , Oportunidad Relativa , Adulto Joven
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