Preprint Article Version 1 Preserved in Portico This version is not peer-reviewed

Lowered Antioxidant Defenses and Increased Oxidative Toxicity Are Hallmarks of Deficit Schizophrenia: Neurocognitive and Symptom Correlates

Version 1 : Received: 8 May 2020 / Approved: 9 May 2020 / Online: 9 May 2020 (03:29:18 CEST)

How to cite: Maes, M.; Sirivichayakul, S.; Matsumoto, A.K.; Michelin, A.P.; Semeão, L.D.O.; de Lima Pedrão, J.V.; Moreira, E.G.; Barbosa, D.S.; Carvalho, A.F.; Solmi, M.; Kanchanatawan, B. Lowered Antioxidant Defenses and Increased Oxidative Toxicity Are Hallmarks of Deficit Schizophrenia: Neurocognitive and Symptom Correlates. Preprints 2020, 2020050145 (doi: 10.20944/preprints202005.0145.v1). Maes, M.; Sirivichayakul, S.; Matsumoto, A.K.; Michelin, A.P.; Semeão, L.D.O.; de Lima Pedrão, J.V.; Moreira, E.G.; Barbosa, D.S.; Carvalho, A.F.; Solmi, M.; Kanchanatawan, B. Lowered Antioxidant Defenses and Increased Oxidative Toxicity Are Hallmarks of Deficit Schizophrenia: Neurocognitive and Symptom Correlates. Preprints 2020, 2020050145 (doi: 10.20944/preprints202005.0145.v1).

Abstract

Background: There is now evidence that schizophrenia and deficit schizophrenia are neuro-immune conditions and that oxidative stress toxicity (OSTOX) may play a pathophysiological role. Aims of the study: To compare OSTOX biomarkers and antioxidant (ANTIOX) defenses in deficit versus non-deficit schizophrenia. Methods: We examined lipid hydroperoxides (LOOH), malondialdehyde (MDA), advanced oxidation protein products (AOPP), sulfhydryl (-SH) groups, paraoxonase 1 (PON1) activity and PON1 Q192R genotypes, total radical-trapping antioxidant parameter (TRAP) as well as immune biomarkers in patients with deficit (n=40) and non-deficit (n=40) schizophrenia and healthy controls (n=40). Results: Deficit schizophrenia is characterized by significantly increased levels of AOPP and lowered -SH, and PON1 activity, while no changes in the OSTOX/ANTIOX biomarkers were found in non-deficit schizophrenia. An increased OSTOX/ANTIOX ratio was significantly associated with deficit versus non-deficit schizophrenia (Odds ratio=3.15, p<0.001). Partial least squares analysis showed that 47.6% of the variance in a latent vector extracted from psychosis, excitation, hostility, mannerism, negative symptoms, psychomotor retardation, formal thought disorders, and neurocognitive test scores was explained by LOOH+AOPP, PON1 genotype + activity, CCL11, tumor necrosis factor (TNF)-α, IgA responses to neurotoxic tryptophan catabolites (TRYCATs), whereas -SH groups and IgM responses to MDA showed indirect effects mediated by OSTOX and neuro-immune biomarkers. Discussion: Our findings indicate that with increasing overall severity of schizophrenia, neuro-immune and neuro-oxidative (especially protein oxidation indicating chlorinative stress) toxicities become more prominent and together with lowered antioxidant defenses and impairments in innate immunity-associated resilience against neurotoxic processes shape a distinct nosological entity, namely deficit schizophrenia.

Subject Areas

oxidative stress; antioxidants; biomarkers; deficit schizophrenia; inflammation; cytokines; neuro-immune

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