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Biomedical subjects

R D Reddy

Publications and source records attributed to R D Reddy.

5 recordsLinked to original sources
PubMed2001

Oxidative damage and schizophrenia: an overview of the evidence and its therapeutic implications.

Free radicals are highly reactive chemical species generated during normal metabolic processes. which in excess can lead to membrane damage. Elaborate antioxidant defence systems exist to protect against oxidative stress. There is accumulating evidence of altered antioxidant capacity in schizophrenia. Membrane dysfunction can be secondary to free radical-mediated pathology, and may contribute to specific aspects of schizophrenic symptomatology and complications of its treatment. Specifically, free radical-mediated abnormalities may contribute to the development of a number of clinically significant consequences, including prominent negative symptoms, tardive dyskinesia, neurological 'soft' signs and parkinsonian symptoms. Our previous results showing altered membrane dynamics and antioxidant enzyme activities in schizophrenia, and findings from other investigators, are consistent with the notion of free radical-mediated neurotoxicity in schizophrenia. These findings provide a theoretical basis from which the development of novel therapeutic strategies such as fatty acid and antioxidant supplementation can occur in the future.

Antipsychotic Agents↗
PubMed2000

Membrane phospholipid abnormalities in postmortem brains from schizophrenic patients.

Previous studies in schizophrenia have shown alterations in membrane phospholipids and polyunsaturated fatty acids. However, these studies have primarily examined peripheral (non-neuronal) cell types. The purpose of the present study was to examine whether the membrane deficits seen in peripheral tissues are also observed in the brain. The caudate was the primary region of interest for this study. Using high-pressure liquid chromatography in conjunction with an evaporative light-scattering detector, we first measured the level of various membrane phospholipids (PL) in schizophrenic (n=11) and control groups with (n=7) and without (n=14) other mental disorders. Polyunsaturated fatty acids (PUFAs) were then determined by capillary gas chromatography. Within groups, there are no significant correlations between membrane PL levels and other collection and demographic parameters including age, postmortem interval, storage time and brain weight. Significantly lower amounts of phosphatidylcholine and phosphatidylethanolamine were found in postmortem brain tissue from schizophrenic patients than in those from control groups, even after accounting for potential confounds. In addition, strong reductions of total PUFAs and saturated fatty acids were found in schizophrenic brains, relative to control brains. Specifically, the reduced PUFAs were largely attributable to decreases in arachidonic acid (AA) and, to a lesser extent, its precursors, linoleic and eicosadienoic acids. There are no significant differences between the control groups with and without other mental disorders. The present findings suggest that deficits identified in peripheral membranes may also be present in the brain from schizophrenic patients. Such a deficit in membrane AA may contribute to the many biological, physiological, and clinical phenomena observed in schizophrenia.

Arachidonic Acid↗
PubMed1999

Human plasma glutathione peroxidase and symptom severity in schizophrenia.

BACKGROUND: Previous studies have shown impaired antioxidant defense system in schizophrenia, including alterations in glutathione peroxidase (GSH-Px) activity in erythrocytes. There exists a related enzyme, human plasma GSH-Px (hpGSH-Px), that has not been previously examined in schizophrenia. METHODS: An enzyme-linked immunoassay was used to determine hpGSH-Px levels in male schizophrenic patients (n = 39), using a within-subject, on-off haloperidol (HD) treatment design, compared with age- and gender-matched normal control subjects (n = 37). RESULTS: hpGSH-Px was not significantly different between normal control subjects and patients, consistent with our previous findings in erythrocyte GSH-Px. There were no significant treatment effects. hpGSH-Px was significantly and positively correlated with psychosis rating scores in patients both on and off HD treatment. CONCLUSIONS: Although not different from normal controls, hpGSH-Px levels in patients may reflect oxidative stress associated with greater psychosis severity. The present findings thus suggest that schizophrenic patients, without obvious increase of endogenous antioxidant enzymes (e.g., hpGSH-Px), may be at risk for oxidative damage.

Adult↗
PubMed1996

Free radical pathology in schizophrenia: a review.

There is evidence that free radicals are involved in membrane pathology, and may play a role in schizophrenia. Free radicals are reactive chemical species generated during normal metabolic processes, and, in excess, can damage lipids, proteins, and DNA. Regions of high oxygen consumption, lipid content, and transition metals are at particular risk. Hence, neuronal membranes are uniquely vulnerable to radical-mediated damage. Elaborate antioxidant defense systems exist to protect against oxidative stress. In schizophrenia there is evidence for dysregulation of free radical metabolism, as detected by abnormal activities of critical antioxidant enzymes and other indices of lipid peroxidation in plasma, red blood cells, and cerebrospinal fluid. Such abnormalities have been associated with tardive dyskinesia, negative symptoms, neurological signs, poor premorbid function, and CT scan abnormalities. Studies to date have generally been exploratory. Further elucidation of the role of free radicals and antioxidants in schizophrenia and its treatment will require systematic investigation.

Cell Membrane↗