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. Preprints2020, 2020050145. https://doi.org/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. https://doi.org/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. Preprints2020, 2020050145. https://doi.org/10.20944/preprints202005.0145.v1
APA Style
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. (2020). Lowered Antioxidant Defenses and Increased Oxidative Toxicity Are Hallmarks of Deficit Schizophrenia: Neurocognitive and Symptom Correlates. Preprints. https://doi.org/10.20944/preprints202005.0145.v1
Chicago/Turabian Style
Maes, M., Marco Solmi and Buranee Kanchanatawan. 2020 "Lowered Antioxidant Defenses and Increased Oxidative Toxicity Are Hallmarks of Deficit Schizophrenia: Neurocognitive and Symptom Correlates" Preprints. https://doi.org/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.
Medicine and Pharmacology, Psychiatry and Mental Health
Copyright:
This is an open access article distributed under the Creative Commons Attribution License which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.