Conjugation of acrylamide with glutathione catalysed by glutathione-S-transferases of rat liver and brain

Acrylamide, an α , β unsaturated electrophile and a cumulative neurotoxin, was found to react with glutathione giving rise to an S-conjugate of acrylamide. Glutathione S-transferase of rat liver and brain cytosols (active on both acrylamide and 1-chloro 2,4 dinitrobenzene) emerged as a single major peak on elution from Sephadex G-75. The enzymic conjugation of acrylamide with glutathione increased with protein and was dependent on incubation time and pH of medium. Acrylamide inhibited glutathione-S-transferase activity towards 1-chloro 2,4-dinitro-benzene of both liver and brain cytosol, in a concentration and time dependent manner. Enzyme catalyzed conjugation of acrylamide with glutathione was induced significantly by phenobarbital and t-SO (tans-stilbene oxide). The enzymic conjugation of acrylamide increased two fold from neonatal to adult and then showed a decreasing pattern at subsequent ages

Binding of acrylamide with glutathione-S-transferases

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Nitrite content and antioxidant enzyme levels in the blood of schizophrenia patients

Rationale: Recent studies have suggested augmentation in the inflammatory response as well as involvement of nitric oxide (NO) in mood disorders. Polymorphonuclear leukocytes (PMN), NO and free radicals have been associated with inflammatory response; however, the status of NO in the PMN has not been investigated so far in schizophrenia patients. Objectives: The present study was undertaken to investigate levels of nitrite (a metabolite of NO), malonaldehyde (MDA, lipid peroxidation product) and antioxidant enzymes such as superoxide dismutase (SOD), catalase and glutathione peroxidase (Gpx) in the PMN of schizophrenia patients. Methods: Patients with schizophrenia (n=62) were diagnosed according to DSM-IV and were free of anti-psychotic medications/ECT for at least 3 months. Mean age of the patients was 29.06± 1.17 years, with a male to female ratio of 4:1, and mean duration of illness was 3.7± 0.6 years. The control group consisted of 82 healthy subjects with a mean age of 37.0± 1.26 and a male to female ratio of 5:1. PMN were isolated from the blood. Nitrite, MDA and antioxidant enzymes were estimated by standard biochemical techniques in the PMN of normal healthy controls and schizophrenia patients. Platelet and plasma nitrite levels were also estimated in controls and schizophrenia patients. Results: Nitrite content in the PMN was reduced to 68%, while plasma and platelet nitrite content in schizophrenia patients was not significantly changed in comparison to controls. Malonaldehyde (MDA) content in PMN was significantly augmented in schizophrenia patients but activity of SOD, catalase and Gpx remain unaltered. Conclusion: Results obtained indicate a significant decrease in NO synthesis and an increase in MDA in the PMN of schizophrenia patients, while antioxidant enzyme activities were not altered in the PMN of schizophrenia patients. This suggests that the decrease in PMN NO synthesis by PMN might lead to oxidative stress in schizophrenia patients

Altered platelet monoamine oxidase-B activity in Idiopathic Parkinson's disease

A case-control study was undertaken to investigate the status of platelet monoamine oxidase-B (MAO-B) activity in Indian cases of idiopathic Parkinson's disease. A significant increase in the activity of platelet MAO-B was observed in Parkinson's cases (n = 26) as compared to controls (n = 26). No significant change in the activity of the enzyme was observed while the data was analysed with respect to age, sex and duration of disease. A trend of decrease in platelet MAO-B activity was observed in Parkinson's cases with respect to stage although the change was not significant. No correlation in platelet MAO-B activity was observed with respect to age and sex in the control subjects. Parkinson's cases treated with L-DOPA and MAO-B inhibitor exhibited decreased platelet MAO-B activity as compared to drug naive cases and those treated with L-DOPA alone. Interestingly, Parkinson's cases treated with L-DOPA and amantadine also had lower platelet MAO-B activity as compared to drug naive cases and those treated with L-DOPA alone. Activity of platelet MAO-B in Parkinson's patients was increased in naive cases and those treated with L-DOPA alone or in combination with other drugs compared to controls. The results of the present study indicate that phenotypic activity of platelet MAO-B is high in Indian Parkinson's cases. Further, action mechanism of drugs used in the treatment of Parkinson's disease could be understood by assay of platelet MAO-B activity. It is an interesting observation and may be looked further in large number of cases