Active ribosomal genes, translational homeostasis and oxidative stress in the pathogenesis of schizophrenia and autism

Porokhovnik, Lev N.; Passekov, Vladimir P.; Gorbachevskaya, N. L.; Sorokin, Alexander; Вейко, Н. Н.; Lyapunova, N. A.

doi:10.1097/ypg.0000000000000076

Cited by 25 publications

(17 citation statements)

References 62 publications

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“…For instance, insulin release that is stimulated by glucose production in β-cells has been linked to H 2 O 2 regulatory action [ 57 ]. Recent mathematical modeling described the OS dynamics to be of oscillatory nature [ 58 ] and tissue depending [ 59 ], which may explain the inconsistency of experimental data related to antioxidant enzymes measurements. Alternatively, focusing on stable OS markers such as MDA may reflect more reliable information on OS damage under long-term dynamics.…”

Section: Discussionmentioning

confidence: 99%

In Vitro and In Vivo Antioxidant and Anti-Hyperglycemic Activities of Moroccan Oat Cultivars

Marmouzi

Karym²,

Saïdi³

et al. 2017

Antioxidants

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Improvement of oat lines via introgression is an important process for food biochemical functionality. This work aims to evaluate the protective effect of phenolic compounds from hybrid Oat line (F11-5) and its parent (Amlal) on hyperglycemia-induced oxidative stress and to establish the possible mechanisms of antidiabetic activity by digestive enzyme inhibition. Eight phenolic acids were quantified in our samples including ferulic, p-hydroxybenzoic, caffeic, salicylic, syringic, sinapic, p-coumaric and chlorogenic acids. The Oat extract (2000 mg/kg) ameliorated the glucose tolerance, decreased Fasting Blood Glucose (FBG) and oxidative stress markers, including Superoxide dismutase (SOD), Catalase (CAT), Glutathione peroxidase (GPx), Glutathione (GSH) and Malondialdehyde (MDA) in rat liver and kidney. Furthermore, Metformin and Oat intake prevented anxiety, hypercholesterolemia and atherosclerosis in diabetic rats. In vivo anti-hyperglycemic effect of Oat extracts has been confirmed by their inhibitory activities on α-amylase (723.91 μg/mL and 1027.14 μg/mL) and α-glucosidase (1548.12 μg/mL & 1803.52 μg/mL) enzymes by mean of a mixed inhibition.

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Section: Discussionmentioning

confidence: 99%

In Vitro and In Vivo Antioxidant and Anti-Hyperglycemic Activities of Moroccan Oat Cultivars

Marmouzi

Karym²,

Saïdi³

et al. 2017

Antioxidants

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“…ALS (amyotrophic lateral sclerosis), schizophrenia, mitochondrial disorders, hypertension and diabetes [1][2][3][4][5][6][7][8][9][10][11][12][13]. Dickens et al [14] reported that MD in vitro enhances intracellular ROS production leading to endogenous OS in endothelial cells, and Garcia et al [15] showed that Mg 2+ supplementation reduces ROS formation in mitochondria.…”

Section: Introductionmentioning

confidence: 99%

PARK7/DJ-1 dysregulation by oxidative stress leads to magnesium deficiency: implications in degenerative and chronic diseases

et al. 2015

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Disturbed magnesium (Mg(2+)) homoeostasis and increased levels of OS (oxidative stress) are associated with poor clinical outcomes in patients suffering from neurodegenerative, cardiovascular and metabolic diseases. Data from clinical and animal studies suggest that MD (Mg(2+) deficiency) is correlated with increased production of ROS (reactive oxygen species) in cells, but a straightforward causal relationship (including molecular mechanisms) between the two conditions is lacking. The multifactorial protein PARK7/DJ-1 is a major antioxidant protein, playing a key role in cellular redox homoeostasis, and is a positive regulator of AR (androgen receptor)-dependent transcription. SLC41A1 (solute carrier family 41 member 1), the gene encoding a ubiquitous cellular Mg(2+)E (Mg(2+)efflux) system, has been shown to be regulated by activated AR. We hypothesize that overexpression/up-regulation of PARK7/DJ-1, attributable to OS and related activation of AR, is an important event regulating the expression of SLC41A1 and consequently, modulating the Mg(2+)E capacity. This would involve changes in the transcriptional activity of PARK7/DJ-1, AR and SLC41A1, which may serve as biomarkers of intracellular MD and may have clinical relevance. Imipramine, in use as an antidepressant, has been shown to reduce the Mg(2+)E activity of SLC41A1 and OS. We therefore hypothesize further that administration of imipramine or related drugs will be beneficial in MD- and OS-associated diseases, especially when combined with Mg(2+) supplementation. If proved true, the OS-responsive functional axis, PARK7/DJ-1-AR-SLC41A1, may be a putative mechanism underlying intracellular MD secondary to OS caused by pro-oxidative stimuli, including extracellular MD. Furthermore, it will advance our understanding of the link between OS and MD.

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“…Given that high oxidation activity must be balanced with antioxidant activity in the brain, it is an organ prone to oxidation-related damage [ 6 , 7 , 8 ]. Such OS is a potential factor in brain deterioration and loss of gray matter, which lead to issues with cognition and daily functioning [ 9 , 10 , 11 , 12 ]; furthermore, OS has been associated with a plethora of psychiatric disorders [ 13 , 14 , 15 , 16 , 17 ]. One such disorder, schizophrenia is characterized by emotional, cognitive, and behavioral disturbances, as well as inaccurate perceptions of reality and high mortality and morbidity [ 18 , 19 , 20 , 21 , 22 ].…”

Section: Introductionmentioning

confidence: 99%

Regulation of Reactive Oxygen Species-Mediated Damage in the Pathogenesis of Schizophrenia

Madireddy

2020

Brain Sciences

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The biochemical integrity of the brain is paramount to the function of the central nervous system, and oxidative stress is a key contributor to cerebral biochemical impairment. Oxidative stress, which occurs when an imbalance arises between the production of reactive oxygen species (ROS) and the efficacy of the antioxidant defense mechanism, is believed to play a role in the pathophysiology of various brain disorders. One such disorder, schizophrenia, not only causes lifelong disability but also induces severe emotional distress; however, because of its onset in early adolescence or adulthood and its progressive development, consuming natural antioxidant products may help regulate the pathogenesis of schizophrenia. Therefore, elucidating the functions of ROS and dietary antioxidants in the pathogenesis of schizophrenia could help formulate improved therapeutic strategies for its prevention and treatment. This review focuses specifically on the roles of ROS and oxidative damage in the pathophysiology of schizophrenia, as well as the effects of nutrition, antipsychotic use, cognitive therapies, and quality of life on patients with schizophrenia. By improving our understanding of the effects of various nutrients on schizophrenia, it may become possible to develop nutritional strategies and supplements to treat the disorder, alleviate its symptoms, and facilitate long-term recovery.

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Active ribosomal genes, translational homeostasis and oxidative stress in the pathogenesis of schizophrenia and autism

Cited by 25 publications

References 62 publications

In Vitro and In Vivo Antioxidant and Anti-Hyperglycemic Activities of Moroccan Oat Cultivars

In Vitro and In Vivo Antioxidant and Anti-Hyperglycemic Activities of Moroccan Oat Cultivars

PARK7/DJ-1 dysregulation by oxidative stress leads to magnesium deficiency: implications in degenerative and chronic diseases

Regulation of Reactive Oxygen Species-Mediated Damage in the Pathogenesis of Schizophrenia

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