RESUMO
Quercetin (QR) is part of a subclass of flavonoids called flavonols. We aimed to investigate the effect of QR on malondialdehyde (MDA), advanced oxidation protein products (AOPPs), and glutathione peroxidase (GSH-Px) activity in the liver of diabetic rats. We compared four groups of male adult Wistar albino rats: a control group, an untreated diabetic group, diabetic groups treated with QR, and QR group. Diabetes was induced by a single injection of streptozotocin (STZ) (50 mg/kg). Animals were kept in standard condition. On the 31st day of the study, the liver tissue was removed for biochemical parameters and histopathological evaluations. In an untreated diabetic group, liver MDA and AOPP levels were significantly higher than all groups. QR treatment significantly decreased the increased MDA, AOPP levels, and increased the decreased GSH-Px enzyme activity in liver tissues. The QR-treated rats in the diabetic group showed an improved histological appearance. Lesser vesicular vacuolization and fibrotic areas were observed in the QR-treated diabetic group than in the diabetic group. The STZ-induced liver injury is associated with oxidative stress, and coadministration of QR may reduce this damage effectively in a rat model. Our results are also supported by morphological improvement in liver tissue. Therefore, we think QR may be effective in treating hyperglycemia and oxidative damage in diabetes.
Assuntos
Antioxidantes/farmacologia , Diabetes Mellitus Experimental/metabolismo , Peroxidação de Lipídeos/efeitos dos fármacos , Fígado/efeitos dos fármacos , Estresse Oxidativo/efeitos dos fármacos , Carbonilação Proteica/efeitos dos fármacos , Quercetina/farmacologia , Animais , Antioxidantes/metabolismo , Antioxidantes/uso terapêutico , Diabetes Mellitus Experimental/tratamento farmacológico , Diabetes Mellitus Experimental/patologia , Fígado/metabolismo , Masculino , Malondialdeído , Extratos Vegetais/farmacologia , Extratos Vegetais/uso terapêutico , Quercetina/uso terapêutico , Ratos WistarRESUMO
There is a widespread use of 2.4â¯GHz electromagnetic radiation emitting devices especially in communication and education. Recent studies show the adverse effects of electromagnetic fields (EMF) such as oxidative stress, cellular damage and apoptosis on tissues. Selenium (Se) has an antioxidant properties by inhibiting oxidative damage being within the structure of antioxidant enzymes like glutathione peroxidase (GSH-Px) and it has also regulatory function for cell cycle and apoptosis. The aim of this study was to investigate the effect of Se on 2.4â¯GHz frequency EMF exposed human embryonic kidney cells (HEK293) by means of alterations in apoptotic and oxidative stress parameters. Our study was planned as control, EMF, 100â¯nM Seâ¯+â¯EMF, 200â¯nM Seâ¯+â¯EMF groups. EMF groups were exposed to 2.4â¯GHz EMF for 1â¯h, element groups were incubated with two different doses of Se added cell culture medium for 48â¯h before EMF exposure. MDA levels were significantly higher whereas SOD and GSH-Px activities were significantly lower in EMF compared to control. 100 and 200â¯nM Seâ¯+â¯EMF application decreased MDA levels, increased SOD and GSH-Px activities than EMF. Apoptosis and caspase-3 were statistically significantly higher but bcl-2 was lower in EMF than control. Apoptosis and caspase-3 were lower in 100 and 200â¯nM Seâ¯+â¯EMF, although bcl-2 were higher than EMF. In conclusion, Se has protective effects against 2.4â¯GHz EMF-induced oxidative stress by reducing lipid peroxidation, regulating SOD and GSH-Px activity. Also, Se has inhibitory effect on 2.4â¯GHz EMF induced apoptosis by increasing the expression of anti-apoptotic protein bcl-2 and suppressing apoptosis regulatory protein caspase-3.
Assuntos
Campos Eletromagnéticos/efeitos adversos , Estresse Oxidativo/efeitos dos fármacos , Estresse Oxidativo/efeitos da radiação , Selênio/farmacologia , Antioxidantes/metabolismo , Apoptose/efeitos dos fármacos , Apoptose/efeitos da radiação , Glutationa Peroxidase/metabolismo , Células HEK293 , Humanos , Peroxidação de Lipídeos/efeitos dos fármacos , Peroxidação de Lipídeos/efeitos da radiação , Malondialdeído/metabolismo , Oxirredução/efeitos dos fármacos , Oxirredução/efeitos da radiaçãoRESUMO
BACKGROUND: Hyperbaric oxygen (HBO) therapy may improve cholestasis, increase hepatic regeneration, and decrease oxidative stress in liver. In this study, we aimed to investigate the effects of HBO therapy on hepatic oxidative stress parameters, such as total thiol groups (T-SH), protein carbonyl (PCO), and total antioxidant capacity (TAC) as well as the predictive value of the noninvasive biochemical marker, sialic acid (SA), and prolidase activity in bile duct ligation (BDL)-induced oxidative damage and fibrosis in rats. METHODS: We divided 32 adult male Sprague Dawley rats into four groups: sham, sham + HBO, BDL, and BDL + HBO; each group contained eight animals. We placed the sham + HBO and BDL + HBO groups in an experimental hyperbaric chamber, in which we administered pure oxygen at 2.5 atmospheres for 90 min on 14 consecutive days. RESULTS: The application of BDL significantly increased PCO levels and prolidase activity, and decreased T-SH and TAC levels. HBO significantly decreased PCO levels and prolidase activity and increased T-SH and TAC levels in the liver tissues. There was no significant difference in sialic acid levels between any groups. CONCLUSIONS: These results indicate that HBO therapy has hepatoprotective effects on BDL-induced injury by decreasing PCO and prolidase activity and increasing antioxidant activities. We therefore suggest that HBO therapy may be useful after BDL-induced injury.
Assuntos
Antioxidantes/metabolismo , Colestase/terapia , Dipeptidases/metabolismo , Oxigenoterapia Hiperbárica , Fígado/patologia , Animais , Biomarcadores/análise , Colestase/etiologia , Colestase/patologia , Ducto Colédoco/cirurgia , Dipeptidases/sangue , Modelos Animais de Doenças , Humanos , Ligadura , Fígado/metabolismo , Masculino , Ácido N-Acetilneuramínico/análise , Estresse Oxidativo , Oxigênio/uso terapêutico , Valor Preditivo dos Testes , Ratos , Ratos Sprague-Dawley , EspectrofotometriaRESUMO
OBJECTIVES: Current evidence suggests that the beneficial vascular effects of statins are not limited to the statins' lipid-lowering properties; these drugs can also improve vascular endothelial cell function. Nω-nitro-l-arginine methyl ester (L-NAME) is a potent synthetic nitric oxide inhibitor, and long-term oral L-NAME treatment is used to induce vascular lesions in experimental animal models. METHODS: We determined the effects of statins on protein carbonyl (PCO), lipid hydroperoxides (LHP), oxidized low-density lipoproteins (ox-LDL) and antioxidants such as paraoxonase 1 (PON1) and total thiols (T-SH) in long-term L-NAME-treated rats. Adult male Wistar rats were divided into three groups, namely, control, L-NAME-treated (1 mg/mL in drinking water for three weeks), and atorvastatin plus L-NAME-treated (4 mg/kg/day atorvastatin for 1 week during the third week of L-NAME treatment) groups. RESULTS: In the L-NAME group, the ox-LDL, LHP and PCO were higher and the PON1 and T-SH were lower than the concentrations observed for the controls. When compared with the L-NAME group, the L-NAME plus atorvastatin group had significantly lower ox-LDL and LHP and higher PON1 activities. Additionally, the elevated total cholesterol (TC) and low-density lipoprotein-C (LDL-C) in the L-NAME group were decreased by atorvastatin administration. TC and LDL-C were positively correlated with ox-LDL and LHP and negatively correlated with PON1 in all groups. High-density lipoprotein-C (HDL-C) was negatively correlated with ox-LDL. CONCLUSION: PON1 prevents LDL oxidation and inactivates LDL-derived oxidized phospholipids; its activity showed a pronounced decrease in the L-NAME treatment group and was increased in the atorvastatin group. Based on our findings, we concluded that the atorvastatin had HDL-related antioxidant activity as well as lipid-lowering properties.
Assuntos
Ácidos Heptanoicos/farmacologia , Inibidores de Hidroximetilglutaril-CoA Redutases/farmacologia , Hipertensão/tratamento farmacológico , Estresse Oxidativo/efeitos dos fármacos , Pirróis/farmacologia , Animais , Arildialquilfosfatase/metabolismo , Atorvastatina , Avaliação Pré-Clínica de Medicamentos , Hipertensão/sangue , Hipertensão/induzido quimicamente , Peroxidação de Lipídeos , Lipídeos/sangue , Masculino , NG-Nitroarginina Metil Éster , Carbonilação Proteica , Ratos , Ratos Wistar , Compostos de Sulfidrila/sangueRESUMO
The effects of hyperthyroidism on oxidative DNA damage in liver tissue and modification by vitamin C supplementation were investigated in rats. Animals were rendered hyperthyroid by administration of L-thyroxine (0.4 mg/100 g food) for 25 d. In the plasma samples, T(3), T(4), and thyroid-stimulating hormone (TSH) were measured by radioimmunoassay and ascorbate spectrophotometrically. Oxidative damage to hepatic nuclear DNA was determined by measuring deoxy-guanosine (dG) and 8-oxodG by high-performance liquid chromatography with diode array detector electrochemical detection (HPLC-DAD-ECD). In hyperthyroidism, 8-oxodG/(10(5) dG) levels were significantly higher and plasma vitamin C levels lower than in control rats. The results of this experimental study show that oxidative damage to hepatic nuclear DNA increases in the hyperthyroid state and that vitamin C was not effective in preventing this damage.