Redox Dysregulation and Oxidative Stress in Schizophrenia: Nutrigenetics as a Challenge in Psychiatric Disease Prevention

Q., Kim; Conus, Philippe; Cuénod, Michel

doi:10.1159/000324366

Cited by 9 publications

(4 citation statements)

References 181 publications

(205 reference statements)

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“…In addition, the GSH precursor N-acetyl cysteine, given to patients in a clinical trial, improves the negative symptoms (9), the auditory-evoked potentials mismatch negativity, (33) and the neuronal synchronization (12). Together with data on experimental models of GSH deficit that mimicked most morphologic, physiologic, and behavioral anomalies found in the disease (10,11,(52)(53)(54) [for review, see (17,18)], these data suggest that a developmental redox dysregulation constitutes one ''hub'' on which convergence takes place between genetic impairments of GSH synthesis and environmental vulnerability factors known to generate oxidative stress (17).…”

Section: Introductionmentioning

confidence: 87%

Genetic Dysregulation of Glutathione Synthesis Predicts Alteration of Plasma Thiol Redox Status in Schizophrenia

Gysin

Kraftsik

Boulat

et al. 2011

Antioxidants & Redox Signaling

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Genetic studies have shown an association between schizophrenia and a GAG trinucleotide repeat (TNR) polymorphism in the catalytic subunit (GCLC) of the glutamate cysteine ligase (GCL), the key enzyme for glutathione (GSH) synthesis. The present study was aimed at analyzing the influence of a GSH dysregulation of genetic origin on plasma thiols (total cysteine, homocysteine, and cysteine-glycine) and other free amino acid levels as well as fibroblast cultures GSH levels. Plasma thiols levels were also compared between patients and controls. As compared with patients with a low-risk GCLC GAG TNR genotype, patients with a high-risk genotype, having an impaired GSH synthesis, displayed a decrease of fibroblast GSH and plasma total cysteine levels, and an increase of the oxidized form of cysteine (cystine) content. Increased levels of plasma free serine, glutamine, citrulline, and arginine were also observed in the high-risk genotype. Taken together, the high-risk genotypes were associated with a subgroup of schizophrenia characterized by altered plasma thiols and free amino acid levels that reflect a dysregulation of redox control and an increased susceptibility to oxidative stress. This altered pattern potentially contributes to the development of a biomarker profile useful for early diagnosis and monitoring the effectiveness of novel drugs targeting redox dysregulation in schizophrenia.

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Section: Introductionmentioning

confidence: 87%

Genetic Dysregulation of Glutathione Synthesis Predicts Alteration of Plasma Thiol Redox Status in Schizophrenia

Gysin

Kraftsik

Boulat

et al. 2011

Antioxidants & Redox Signaling

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“…Factual evidence says that schizophrenic patients show higher indexes of oxidative stress that may affect the deterioration manifested throughout the disease 11 and may be associated with cognitive deficits in these patients 14 . Modern studies implicated these mechanisms in managing brain pathology, raising the probability that distorted parameters of the basic phenomenon of oxidative stress can lead to the pathogenesis of SCZ and associated abnormalities 15‐17 …”

Section: Introductionmentioning

confidence: 99%

Effect of antioxidant, malondialdehyde, macro‐mineral, and trace element serum concentrations in Bangladeshi patients with schizophrenia: A case‐control study

Uddin

Sultana

Uddin

et al. 2021

Health Science Reports

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Background Schizophrenia (SCZ) is an incurable neuropsychiatric disorder generally described by impaired social behavior and altered recognition of reality. For the first time, this study explored serum levels of antioxidants (vitamin A, E, and C), malondialdehyde (MDA), macro‐minerals (calcium, potassium, and sodium), and trace elements (zinc, iron, and selenium) in Bangladeshi patients with SCZ and thereby, discovering any pathophysiological correlation. Methods This case‐controlled study evaluated 63 patients with SCZ as cases and 63 healthy individuals as controls. Vitamin A and E levels were defined by RP‐HPLC. MDA and vitamin C levels were measured by using UV spectrophotometry, and macro and trace elements by atomic absorption spectroscopy. Results This study found significantly ( P ≤ 0.05) elevated MDA levels and decreased levels of antioxidants—vitamin A, C, and E and significantly ( P ≤ 0.05) diminished levels of macro and trace elements in cases in contrast to the controls. Serum levels of zinc (Zn), selenium (Se), iron (Fe), potassium (K), calcium (Ca), and sodium (Na) were determined to be 0.33 ± 0.008, 0.0252 ± 0.00060, 0.24 ± 0.01, 64.18 ± 2.72, 36.88 ± 2.56, and 2657.5 ± 53.32 mg/L, respectively, in cases, whereas 0.79 ± 0.03, 0.0650 ± 0.00355,0.78 ± 0.03, 168.01 ± 2.85, 86.43 ± 2.55, and 3200.8 ± 29.96 mg/L, respectively, were determined in controls. Pearson's correlation analysis revealed a negative correlation between Zn and Na, Zn and K, Zn and Ca, Zn and Fe, Zn and Se, Fe and Na, and Fe and Se in patients. Conclusions The findings connect that the pathogenesis of SCZ may have a correlation with altered levels of antioxidants, MDA, macro‐minerals, and trace elements.

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“…Meta‐analyses suggest that maternal infection during pregnancy increases the risk of these disorders in offspring 3,4 . Importantly, there are accumulating interests in the early prevention by anti‐inflammatory compounds 5‐7 . However, there are no anti‐inflammatory compounds that can be used in the early intervention for pregnant women with MIA.…”

Section: Introductionmentioning

confidence: 99%

“…3,4 Importantly, there are accumulating interests in the early prevention by anti-inflammatory compounds. [5][6][7] However, there are no anti-inflammatory compounds that can be used in the early intervention for pregnant women with MIA.…”

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confidence: 99%

Dietary intake of glucoraphanin during pregnancy and lactation prevents the behavioral abnormalities in the offspring after maternal immune activation

Fujita

Ishima

et al. 2020

Neuropsychopharm Rep

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Aim Epidemiological data suggest that maternal immune activation (MIA) plays a role in the etiology of neuropsychiatric disorders including autism spectrum disorder (ASD) and schizophrenia. However, there is no prophylactic nutrition that can prevent the onset of neurodevelopmental disorders in offspring after MIA. The aim of this study was undertaken to examine whether dietary intake of glucoraphanin (GF: the precursor of a natural anti‐inflammatory compound sulforaphane) can prevent the onset of behavioral abnormalities in offspring after MIA. Methods One percent of GF food pellet or normal food pellet was given into female mice during pregnancy and lactation (from E5 to P21). Saline (5 mL/kg/d) or poly(I:C) (5 mg/kg/d) was injected into pregnant mice from E12 to E17. Behavioral tests and immunohistochemistry of parvalbumin (PV) were performed in male offspring. Results Dietary intake of GF during pregnancy and lactation prevented cognitive deficits and social interaction deficits in the juvenile offspring after MIA. Furthermore, dietary intake of GF during pregnancy and lactation prevented cognitive deficits in the adult offspring after MIA. Moreover, dietary intake of GF prevented the reduction of PV immunoreactivity in the medial prefrontal cortex of adult offspring after MIA. Conclusion These data suggest that dietary intake of GF during pregnancy and lactation could prevent behavioral abnormalities in offspring after MIA.

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Redox Dysregulation and Oxidative Stress in Schizophrenia: Nutrigenetics as a Challenge in Psychiatric Disease Prevention

Cited by 9 publications

References 181 publications

Genetic Dysregulation of Glutathione Synthesis Predicts Alteration of Plasma Thiol Redox Status in Schizophrenia

Genetic Dysregulation of Glutathione Synthesis Predicts Alteration of Plasma Thiol Redox Status in Schizophrenia

Effect of antioxidant, malondialdehyde, macro‐mineral, and trace element serum concentrations in Bangladeshi patients with schizophrenia: A case‐control study

Dietary intake of glucoraphanin during pregnancy and lactation prevents the behavioral abnormalities in the offspring after maternal immune activation

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