Oxidative stress in blood platelets from schizophrenic patients

Abstract

Oxidative stress in blood platelets is observed in various diseases, including neuropsychiatric disorders. The aim of our study was to evaluate oxidative stress in blood platelets from patients with schizophrenic disorders by measuring the activity of the platelet antioxidative enzyme, superoxide dismutase (SOD), concomitant with the level of thiobarbituric acid reactive species (TBARS). In blood platelets obtained from schizophrenic patients (with paranoid schizophrenia according to DSM-IV criteria) and from healthy volunteers the level of reactive oxygen species was also measured via chemiluminescence. In resting blood platelets from schizophrenic patients the chemiluminescence was higher than in platelets from control subjects (P < 0.05), but in thrombin-activated platelets an increase (about 53%) of chemiluminescence was observed, however this increase was lower than in thrombin-stimulated platelets from healthy subjects (101.5%). The results indicate that in platelets from schizophrenic patients generation of reactive oxygen species is enhanced. Moreover, we observed that SOD activity in blood platelets from schizophrenic patients was significantly lower than in control platelets and that a correlation exists between increased lipid peroxidation and inhibition of the activity of this antioxidative enzyme in schizophrenic platelets.

Oxidative/Nitrative Modifications of Plasma Proteins and Thiols from Patients with Schizophrenia

“…Homocysteine may act as an antagonist at the glycine site of the NMDA receptor (in the presence of normal or low glycine levels) or it may act as an agonist at the glutamate site of this receptor (when glycine levels are increased) [35] . Homocysteine may also enhance oxidative stress [35,37] ; our earlier [3,5] and present results ( fig. 1-3 ) and the results of Yao et al [38] suggest that schizophrenia is characterized by abnormal oxidative stress.…”

“…A cell membrane dysfunction caused by lipid peroxidation can be secondary to a free radical-mediated pathology and may contribute to specific aspects of schizophrenic symptomatology and complications of its treatment. Our earlier studies by using different specific biomarkers of oxidative stress, including activity of the platelet antioxidative enzyme, superoxide dismutase, revealed that in blood platelets from schizophrenic patients oxidative stress occurs [3] . We found that suppressed superoxide dismutase activity in blood platelets from schizophrenic patients is associated with enhanced ROS generation and lipid peroxidation when compared with healthy controls [3] .…”

“…Our earlier studies by using different specific biomarkers of oxidative stress, including activity of the platelet antioxidative enzyme, superoxide dismutase, revealed that in blood platelets from schizophrenic patients oxidative stress occurs [3] . We found that suppressed superoxide dismutase activity in blood platelets from schizophrenic patients is associated with enhanced ROS generation and lipid peroxidation when compared with healthy controls [3] . We also observed that the level of isoprostanes (indicators of oxidative stress) in schizophrenic patients in the acute period of psychosis is extremely high compared with control group [5] , and our results indicate that in schizophrenic patients increased production of isoprostanes reflects oxidative stress and oxidative damage of lipids.…”

“…In schizophrenic patients dysregulation of reactive oxygen species (ROS) metabolism, as detected by abnormal activities of critical antioxidant enzymes and other indicators such as lipid peroxidation in plasma, red blood cells, blood platelets and cerebrospinal fluid, is observed [1][2][3] . Such abnormalities have been associated with tardive dyskinesia, negative symptoms, neurological signs and poor premorbid function.…”

Oxidative stress in psychiatric disorders: evidence base and therapeutic implications

“…TBARS are lowmolecular-weight substances, consisting largely of malondialdehyde (MDA), which are formed from the decomposition of unstable lipid peroxidation products and react with thiobarbituric acid to form fluorescent adducts (Fukunaga et al, 1998). TBARS have been reported to be elevated in the plasma Dietrich-Muszalska and Olas, 2007 ;Kuloglu et al, 2002c ;Mahadik et al, 1998;Ranjekar et al, 2003;Zhang et al, 2006a), erythrocytes (Altuntas et al, 2000;Herken et al, 2001), leucocytes (Srivastava et al, 2001) and platelets (Dietrich-Muszalska et al, 2005) of schizophrenia patients, in conjunction with abnormalities in antioxidant levels, and depleted essential polyunsaturated fatty acids, which are especially prone to lipid peroxidation (Arvindakshan et al, 2003b;Khan et al, 2002). Data on CSF levels of TBARS in schizophrenia are limited, but one small study has been published, reporting reduced levels in a group of actively psychotic patients compared with controls (Skinner et al, 2005).…”