ABSTRACT
Chagas disease and leishmaniasis are neglected tropical diseases caused by the protozoan parasites Trypanosoma cruzi and Leishmania spp., respectively. They are among the most important parasitic diseases, affecting millions of people worldwide, being a considerable global challenge. However, there is no human vaccine available against T. cruzi and Leishmania infections, and their control is based mainly on chemotherapy. Treatments for Chagas disease and leishmaniasis have multiple limitations, mainly due to the high toxicity of the available drugs, long-term treatment protocols, and the occurrence of drug-resistant parasite strains. In the case of Chagas disease, there is still the problem of low cure rates in the chronic stage of the disease. Therefore, new therapeutic agents and novel targets for drug development are urgently needed. Antioxidant defence in Trypanosomatidae is a potential target for chemotherapy because the organisms present a unique mechanism for trypanothione-dependent detoxification of peroxides, which differs from that found in vertebrates. Cellular thiol redox homeostasis is maintained by the biosynthesis and reduction of trypanothione, involving different enzymes that act in concert. This study provides an overview of the antioxidant defence focusing on iron superoxide dismutase A, tryparedoxin peroxidase, and ascorbate peroxidase and how the enzymes play an important role in the defence against oxidative stress and their involvement in drug resistance mechanisms in T. cruzi and Leishmania spp.
ABSTRACT
Aims: The purpose of this study was to evaluate the effect of vitamin E supplementation on oxidant-antioxidant balance in chronic renal failure patients treated by hemodialysis. Study Design: The study utilized a randomized experimental design. The experimental intervention consisted of vitamin E supplementation Place and Duration of Study: 40 patients on hemodialysis (M/W=22/18; 36±12 years) received nutritional councils based on the NKF K/DOQI (National Kidney Foundation- Kidney Disease Outcomes Quality Initiative) guidelines. Patients were randomized into 2 groups:one was used as control and the second group was treated by vitamin E supplementation (100mg/day=146IU/d) during 30 days. Methodology: Pro-oxidant status was assessed by thiobarbituric acid reactive substances, hydroperoxides and carbonyls analysis. Antioxidant defence was performed by the analysis of Superoxide dismutase, Catalase, Glutathione reductase activities and Vitamin E amounts. Results: At 30 days of supplementation, in treated patients compared to controls, levels of triacylglycerols and total cholesterol were unchanged. Hydroperoxides concentrations were decreased (p<0.001) while thiobarbituric acid reactive substances concentrations were unchanged. Carbonyls levels were decreased (p<0.001). High concentrations of vitamin E were noted in treated group (p<0.01). Similar superoxide dismutase activity was noted. However, an increase in vitamin E concentrations, catalase and glutathione reductase activities were observed in treated group (p<0.01). Conclusion: In conclusion, in hemodialysis patients, vitamin E supplementation was without effect on lipid profile. However, vitamin E exerts a protective effect on cardiovascular diseases by decreasing radical attack of biological molecules and increasing antioxidant defense.
ABSTRACT
Present study is conducted to evaluate the response of bean (Dolichos lablab cv . pusa early prolific) plants to supplemental UV-B (sUV-B: 280-315 nm: 7.2 kJ m-2 d-1) radiation. UV-B caused alteration in biomass translocation pattern with more retention of biomass in below ground parts leading to an increment in root shoot ratio. Specific leaf area (SLA) which is the measure of leaf thinness, increased in plants under sUV-B exposure by 95.7 and 82.3% after 15 and 30 days after germination. Photosynthetic machinery of bean plants was the potential target of UV-B as photosynthetic rate was decreased by 88.6 % at 30 days after germination. sUV-B lead to the formation of reactive oxygen species thus generating oxidative stress. Stimulation of antioxidant defense system (enzymatic and non-enzymatic) was observed due to sUV-B radiation. Phenolic content decreased (34.7 and 18.6%) but protein showed varied response, increased initially (34%) thereafter declined (10.2%) under sUV-B radiation.
ABSTRACT
La Ciclosporina A (CyA) es un inmunosupresor que presenta efectos adversos como la hepatotoxicidad. Se estudió el efecto de CyA sobre el sistema de defensa antioxidante (SDA), su relación con la lipoperoxidación y la función hepática. Ratas machos wistar de 200-260 g de peso fueron tratadas durante 7 días (agudo) y 120 días (crónico) con dosis orales de CyA de 5 y 20 mg/kg/ día. Se estudió el SDA midiendo el contenido hepático total de glutatión (GSH), glutatión peroxidasa (GPx) y catalasa (CAT); el perfil de funcionamiento hepático (PFH) se realizó determinando aspartato aminotransferasa (AST), alanín aminotransferasa (ALT) y bilirrubina total (Bt) y para la lipoperoxidación se midieron las sustancias reactivas al ácido tiobarbitúrico (SRAT). Los resultados fueron confirmados con estudios histológicos. El tratamiento agudo con 20 mg/kg/día de CyA mostró aumento significativo de SRAT (30,51±1,97 nmol/g), pérdida de GSH (2,47±0,06 µmol/g), incremento significativo de GPx (663,25±1,88 mU/mg) y CAT (290,65±3,31 mU/mg). El tratamiento crónico con 5 mg/kg/día de CyA mostró disminución tiempo-dependiente del SDA con disminución de GSH (3,19±0,05 µmol/g), GPx (569,6±2,67 mU/mg) y CAT (223,3±2,78 mU/mg), sin cambios en SRAT. Los resultados del tratamiento crónico y agudo con 20 mg/kg/día de CyA son coincidentes y sólo en esta dosis se observaron alteraciones de la histo-arquitectura del parénquima hepático. Se concluye que dosis de 20 mg/kg/día de CyA en tratamiento agudo y crónico provocan lipoperoxidación con compromiso del SDA y alteración del hepatocito; dosis de 5 mg/kg/día de CyA en tratamiento crónico producen deterioro reversible del SDA sin lipoperoxidación. La inmunosupresión aplicada en clínica con dosis de 3 a 8 mg/kg/día produciría disminución del SDA sin cambios en la histo-arquitectura del parénquima hepático.
Cyclosporin A (CyA), an immunosuppressive agent, exerts adverse effects such as hepatotoxicity. The effect of CyA on the Antioxidant Defence System(ADS), its relation to lipoperoxidation, and liver function were studied. Assays were performed on male wistar rats weighing 200-260 g during acute (7 days) and chronic (120 days) treatment with oral doses of CyA of 5 and 20 mg/kg/day. ADS was studied in rat liver homogenate by measuring the liver content of total glutathion (GSH), glutathion peroxidase(GPx) and catalase (CAT); the Liver Profile Test (LPT) was measured by determining aspartate amino transferase (AST), alanin amino transferase (ALT) and total bilirubin (TB), and lipoperoxidation by determining thiobarbituric acid reactive substances (TRAS). The results were confirmed by histological studies. In the acute treatment, 20 mg/kg/day with CyA, a significant increase in TRAS (30.51±1.97 nmol/g), a loss of GSH (2.47±0.06 µmol/g) and a significant increase in GPx (663.25±1.88 mU/mg) and CAT (290.65±3.31 mU/mg) were observed. In the chronic treatment, 5 mg/kg/day with CyA, a time-dependent decrease in the ADS with a diminution in GSH (3.19±0.05 µmol/g), GPx (569.6±2.67 mU/mg) and CAT (223.3±2.78 mU/mg) were observed, with no changes in TRAS. The results for the chronic and acute treatment with 20 mg/kg/day of CyA are coincident, only this dose causing alterations in liver parenchyma histoarchitecture. CyA doses of 20 mg/kg/day during acute and chronic treatment cause lipoperoxidation with ADS involvement and hepatocyte alteration. CyA doses of 5 mg/kg/day during chronic treatment cause deterioration in the ADS with no lipoperoxidation, hepatotoxicity being reversible. Immunosuppression in human patients with 3 to 8 mg/kg/day doses, would cause a decrease in the ADS with no structural or functional changes in the hepatocyte.