The objective of this study was to investigate the antioxidant and hepatoprotective effect of the chronic use of conventional (CGJ) or organic (OGJ) grape juice from the Bordeaux variety grape on oxidative stress and cytoarchitecture in the liver of rats supplemented with a high-fat diet (HFD) for three months. The results demonstrated that HFD induced an increase in thiobarbituric acid-reactive substances (TBARS), catalase (CAT) activity and 2′,7′-dihydrodichlorofluorescein (DCFH) oxidation and a decrease in sulfhydryl content and superoxide dismutase (SOD) and glutathione peroxidase (GPx) activities. HFD also induced hepatocellular degeneration and steatosis. These alterations were prevented by CGJ and OGJ, where OGJ was more effective. Therefore, it was concluded that HFD induced oxidative stress and liver damage and that the chronic use of grape juice was able to prevent these alterations.

Selenium (Se) is an essential mineral for mammals. It is a nutrient related to the complex metabolic and enzymatic functions. Although Se has important physiological functions in the cells, organic compounds of Se can be extremely toxic, and may affect the central nervous system. This study aims to investigate the effect of the chronic treatment with the vinyl chalcogenide 3-methyl-1-phenyl-2-(phenylseleno)oct-2-en-1-one on some parameters of oxidative stress in the brain of rats. Animals received the vinyl chalcogenide (125, 250 or 500 μg/kg body weight) intraperitoneally once a day during 30 days. The cerebral cortex, the hippocampus, and the cerebellum were dissected and homogenized in KCl. Afterward, thiobarbituric acid reactive substances (TBARS), carbonyl, sulfhydryl, catalase (CAT), superoxide dismutase (SOD) and glutathione peroxidase (GPx) activities were measured in the brain. Results showed that the organoselenium enhanced TBARS in the cerebral cortex of rats but the compound was not able to change carbonyl levels. Furthermore, the organoselenium reduced thiol groups measured by the sulfhydryl assay in all tissues studied. The activity of the antioxidant enzyme CAT was increased by the organochalcogen in the cerebral cortex and in the cerebellum, and the activity of SOD was increased in the hippocampus. On the other hand, the activity of the antioxidant enzyme GPx was reduced in all brain structures. Our findings indicate that this organoselenium compound induces oxidative stress in different brain regions of rats, corroborating to the fact that this tissue is a potential target for organochalcogen action.

No abstract

Histidinemia is an inherited metabolic disorder biochemically characterized by high concentrations of histidine in biological fluids. Usually affected patients are asymptomatic although some individuals have mental retardation and speech disorders. Considering the high prevalence of histidinemia and the scarce information on the effects of maternal histidinemia on their progeny, we investigated various parameters of oxidative stress in brain cortex and hippocampus of the offspring from female rats that received histidine (0.5 mg/g of body weight) in the course of pregnancy and lactation. At 21 days of age we found a significant increase of thiobarbituric acid reactive substances (TBARS), 2',7'-dihydrodichlorofluorescein oxidation, superoxide dismutase (SOD) activity, catalase (CAT) activity, total sulfhydryls and glutathione (GSH) content in cerebral cortex and hippocampus. We also verified that at 60 days of age, GSH, SOD and total sulfhydryls returned to normal levels in brain cortex, while the other parameters decreased in the same structure. In the hippocampus, at 60 days of age GSH returned to normal levels, CAT persisted elevated and the other parameters decreased. These results indicate that histidine administration to female rats can induce oxidative stress in the brain from the offspring, which partially recovers 40 days after breastfeeding stopped.

β-Alanine is a β-amino acid derivative of the degradation of pyrimidine uracil and precursor of the oxidative substrate acetyl-coenzyme A (acetyl-CoA). The accumulation of β-alanine occurs in β-alaninemia, an inborn error of metabolism. Patients with β-alaninemia may develop neurological abnormalities whose mechanisms are far from being understood. In this study we evaluated the effects of β-alanine administration on some parameters of oxidative stress and on creatine kinase, pyruvate kinase, and adenylate kinase in cerebral cortex and cerebellum of 21-day-old rats. The animals received three peritoneal injections of β-alanine (0.3 mg /g of body weight) and the controls received the same volume (10 μL/g of body weight) of saline solution (NaCl 0.85 %) at 3 h intervals. CSF levels of β-alanine increased five times, achieving 80 μM in the rats receiving the amino acid. The results of β-alanine administration in the parameters of oxidative stress were similar in both tissues studied: reduction of superoxide dismutase activity, increased oxidation of 2',7'-dihydrodichlorofluorescein, total content of sulfhydryl and catalase activity. However, the results of the phosphoryltransfer network enzymes were similar in all enzymes, but different in the tissues studied: the β-alanine administration was able to inhibit the enzyme pyruvate kinase, cytosolic creatine kinase, and adenylate kinase activities in cerebral cortex, and increase in cerebellum. In case this also occurs in the patients, these results suggest that oxidative stress and alteration of the phosphoryltransfer network may be involved in the pathophysiology of β-alaninemia. Moreover, the ingestion of β-alanine to improve muscular performance deserves more attention in respect to possible side-effects.

The objective of this study was to evaluate the effect of organic and conventional grape juices consumption on the behavior of rats and their neuroprotective effect on the activity of brain energy metabolism enzymes in different brain areas of adult rats on the experimental model of hepatic encephalopathy. Male Wistar rats (90-days-old) were treated once a day with conventional or organic white grape juice by gavage for 14 days (7 μL/g). On the 15th day the rats received carbon tetrachloride (CCl4) in a single dose of 3.0 mL/kg. Cerebral cortex, hippocampus and cerebellum were dissected to measure the activity of creatine kinase (CK) and pyruvate kinase (PK). No changes in feeding behavior were observed after the treatment with the grapes juices. However, there was an increase in grooming behavior in the open field test provoked by both juices. CCl4 inhibited CK activity in cerebral cortex and hippocampus of the rats and CCl4 also reduced PK activity in all brain structures studied. Furthermore, both white grape juices prevented the decrease in the activity of CK and PK. Therefore, we can suggest that organic and conventional white grape juices could restore the activity of enzymes with a central role in brain energy metabolism.

No abstract

O estresse oxidativo tem sido apontado como um ator importante na patogênese de várias doenças, incluindo doenças neurodegenerativas. A Doença de Alzheimer é uma desordem neurodegenerativa relacionada à idade, que é reconhecida como a forma mais comum de demência. Neste artigo, o objetivo foi revisar a participação de estresse oxidativo na Doença de Alzheimer. A Doença de Alzheimer é caracterizada histopatologicamente pela presença de placas amilóides extracelulares, emaranhados neurofibrilares intracelulares, a presença de oligômeros do peptídeo -amiloide e a perda de sinapse. Além disso, o cérebro e o sistema nervoso são mais propensos ao estresse oxidativo e o dano oxidativo influencia nas doenças neurodegenerativas. Entretanto, o aumento do dano oxidativo, disfunção mitocondrial, acúmulo de agregados de proteínas oxidadas, inflamação e defeitos nas proteínas constituem patologias complexas interligadas que levam à morte celular de neurônios. Mutações no ácido desoxirribonucleico mitocondrial e estresse oxidativo contribuem para o envelhecimento, afetando diferentes sistemas de sinalização da célula, bem como conectividade neuronal, podendo levar à morte celular, sendo o maior fator de risco para doenças neurodegenerativas, como na Doença de Alzheimer.