Peroxisomes, oxidative stress, and inflammation

Terlecky, Stanley R.; Terlecky, Laura J.; Giordano, Courtney R.

doi:10.4331/wjbc.v3.i5.93

Cited by 77 publications

(75 citation statements)

References 21 publications

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“…And the converse is trueelevated oxidative stress triggers inflammation, whereas redox balance inhibits the cellular response. Thus, oxidative stress and inflammation may be seen as both causes and consequences of cellular pathology in many disorders [27], probably in degenarative diseases such as schizophrenia.…”

Section: Discussionmentioning

confidence: 99%

Increased Oxidant Stress and Inflammation in Patients with Chronic Schizophrenia

Yeğin¹,

Ay²,

Aydın³

et al. 2012

IJCM

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Background: Several lines of evidence, including postmortem studies, suggest increased oxidative stress and inflammation in patients with schizophrenia. Alteration of oxidative stress markers has been reported in schizoprenia studies, but with inconsistent results. Oxidized low-density lipoproteins (oxLDL) have been reported to be capable of eliciting neurocytotoxicity. On the other hand, paraoxonase (PON1), an arylesterase(ARE), plays a role in protection against oxidative modifications of LDL and is considered to be one of the antioxidant enzymes. There are no studies showing the changes in oxidative stress and inflammation together, nor the activities of PON1 and ARE in schizophrenic patients. In this study, we examined PON1, ARE activities and oxidative/anti-oxidative markers in patients with chronic schizophrenia and healthy controls. Methods: We recruited 30 male chronic schizophrenic patients and 30 male healthy control subjects and examined C-reactive protein(CRP), fibrinogen, PON1, ARE and plasma total antioxidant status (TAS) and total oxidant status (TOS), oxidative stress index(OSI) in both groups. Schizophrenia symptoms were assessed using the positive and negative syndrome scale (PANSS). The related routine lipid profile parameters including HDL were also examined. Results: Patients had significantly higher CRP, fibrinogen, TOS and OSI levels; but the patients and control subjects did not differ on activities of the antioxidant enzymes PON1 and ARE. Interestingly, there were not any group differences in the lipid profile parameters except the triglyceride levels, that increased significantly in the patient group. Conclusions: In the present study, reporting the ARE activities besides the PON1 activities in schizophrenic patients for the first time, we showed that PON1 and ARE enzyme activities were not statistically different in patients with chronic schizophrenia. This study provides additional evidence of increased oxidative stress and inflammation in chronic schizophrenia, but no alterations in the antioxidant status were observed. Our results suggest that other mechanisms than the high density lipoprotein(HDL)-disfunctionality, namely decreases in PON1 or ARE enzyme activities, are more important in oxidative or antioxidative pathophysiological processes in schizophrenia.

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Section: Discussionmentioning

confidence: 99%

Increased Oxidant Stress and Inflammation in Patients with Chronic Schizophrenia

Yeğin¹,

Ay²,

Aydın³

et al. 2012

IJCM

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“…TD significantly increases pro-inflammatory cytokines, chemokines, interferons, as well as many transcription factors known to control inflammatory gene expression are upregulated in TD animals [33]. The neuroinflammation may alter mitochondrial membrane potential and thus its function, resulting in an increase in ROS [84]. Reversely, oxidative stress can also induce neuroinflammation.…”

Section: Mechanisms Underlying Td-mediated Neurodegenerationmentioning

confidence: 99%

Thiamine Deficiency and Neurodegeneration: the Interplay Among Oxidative Stress, Endoplasmic Reticulum Stress, and Autophagy

2016

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Thiamine (Vitamin B1) is an essential nutrient and indispensable for normal growth and development of the organism due to its multilateral participation in key biochemical and physiological processes. Humans must obtain thiamine from their diet since it is synthesized only in bacteria, fungi and plants. Thiamine deficiency (TD) can result from inadequate intake, increased requirement, excessive deletion and chronic alcohol consumption. TD affects multiple organ systems, including the cardiovascular, muscular, gastrointestinal, and central and peripheral nervous systems. In the brain, TD causes a cascade of events including mild impairment of oxidative metabolism, neuroinflammation and neurodegeneration, which are commonly observed in neurodegenerative diseases, such as Alzheimer’s disease (AD), Parkinson’s disease (PD) and Huntington’s disease (HD). Thiamine metabolites may serve as promising biomarkers for neurodegenerative diseases and thiamine supplementations exhibit therapeutic potential for patients of some neurodegenerative diseases. Experimental TD has been used to model aging-related neurodegenerative diseases. However, to date, the cellular and molecular mechanisms underlying TD-induced neurodegeneration are not clear. Recent research evidence indicates that TD causes oxidative stress, endoplasmic reticulum (ER) stress and autophagy in the brain, which are known to contribute to the pathogenesis of various neurodegenerative diseases. In this review, we discuss the role of oxidative stress, ER stress and autophagy in TD-mediated neurodegeneration. We propose that it is the interplay of oxidative stress, ER stress and autophagy that contributes to TD-mediated neurodegeneration.

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“…Inflammation provokes an increase of reactive oxygen species and anti-inflammatory responses suppress the oxidative stress. The vice versa is also true (15). Similarly, it is established that glucocorticoids generate a pro-oxidative state and deteriorate the antioxidant defense, while the oxidative stress results in the hyperactivity of HPA axis (16).…”

Section: Introductionmentioning

confidence: 95%

Antidepressant‐like effects of quercetin in diabetic rats are independent of hypothalamic–pituitary–adrenal axis

Demir

Gergerlioğlu

Öz

2015

Acta Neuropsychiatr.

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Peroxisomes, oxidative stress, and inflammation

Cited by 77 publications

References 21 publications

Increased Oxidant Stress and Inflammation in Patients with Chronic Schizophrenia

Increased Oxidant Stress and Inflammation in Patients with Chronic Schizophrenia

Thiamine Deficiency and Neurodegeneration: the Interplay Among Oxidative Stress, Endoplasmic Reticulum Stress, and Autophagy

Antidepressant‐like effects of quercetin in diabetic rats are independent of hypothalamic–pituitary–adrenal axis

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