Lipid peroxidation (LP) in brain regions of developing rats induced by chronic low-level thallium administration

In man, manganese neurointoxication is characterised in the early phase by bizarre behavior reminiscent of that observed in schizophrenia. During chronic manganese intoxication the neuropsychiatric symptoms manifested earlier disappear and are followed by a permanent neurological phase typified by extrapyramidal symptoms similar to those of Parkinson's disease. Study of manganese intoxication in animals may provide important clues towards elucidation of the biochemical defect underlying neuropsychiatric as well as extrapyramidal diseases. Investigations in our laboratory suggest that neurotoxicity of manganese is an exaggeration of function in normal neuronal homeostasis. Manganese neurointoxication in neonatal rats resulted in significant depression of lipid peroxidation in several rat brain regions examined. In the striatum, lipid peroxidative activity was abolished, an effect which may be related to alteration in neurotransmitters often observed in the striatum of manganese-treated rats. The chronic, extrapyramidal stage of manganism, may ensue when excess Mn2+ is oxidised to higher valency forms where it can potentiate the autoxidation of catecholamines, like dopamine, resulting in concomitant formation of free radicals and cytotoxic quinones. This latter effect may arise preferentially in the substantia nigra, where neuromelanin is formed nonenzymatically by autoxidation of dopamine.

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Expression Analysis of 4-Hydroxynonenal Modified Proteins in Schizophrenia Brain; Relevance to Involvement in Redox Dysregulation

Current Proteomics ◽

10.2174/1570164618666210121151004 ◽

2021 ◽

Vol 18 ◽

Author(s):

Sobia Manzoor ◽

Ayesha Khan ◽

Beena Hasan ◽

Shamim Mushtaq ◽

Nikhat Ahmed

Keyword(s):

Oxidative Stress ◽

Lipid Peroxidation ◽

Thiobarbituric Acid ◽

Brain Regions ◽

Protein Adducts ◽

Antioxidant Systems ◽

Control Group ◽

Tbars Level ◽

Elevated Expression ◽

Modified Proteins

Background: Oxidative damage contributes to the pathophysiology of schizophrenia (SZ). Redox imbalance may lead to increased lipid peroxidation, which produces toxic aldehydes like 4-hydroxynonenal (4-HNE) ultimately leading to oxidative stress. Conversely, implications of oxidative stress points towards an alteration in HNE-protein adducts and activities of enzymatic and antioxidant systems in schizophrenia. Objectives: Present study focuses on identification of HNE-protein adducts and its related molecular consequences in schizophrenia pathology due to oxidative stress, particularly lipid peroxidation. Material and Methods: Oxyblotting was performed on seven autopsied brain samples each from cortex and hippocampus region of schizophrenia patients and their respective normal healthy controls. Additionally, thiobarbituric acid substances (TBARS), reduced glutathione (GSH) levels and catalase (CAT) activities associated with oxidative stress, were also estimated. Results: Obtained results indicates substantially higher levels of oxidative stress in schizophrenia patients than healthy control group represented by elevated expression of HNE-protein adducts. Interestingly, hippocampus region of schizophrenia brain shows increased HNE protein adducts compared to cortex. An increase in catalase activity (4.8876 ± 1.7123) whereas decrease in antioxidant GSH levels (0.213 ± 0.015µmol/ml) have been observed in SZ brain. Elevated TBARS level (0.3801 ± 0.0532ug/ml) were obtained in brain regions SZ patients compared with their controls that reflects an increased lipid peroxidation (LPO). Conclusion: Conclusion: We propose the role of HNE modified proteins possibly associated with the pathology of schizophrenia. Our data revealed increase lipid peroxidation as a consequence of increased TBARS production. Furthermore, altered cellular antioxidants pathways related to GSH and CAT also highlight the involvement of oxidative stress in schizophrenia pathology.

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Thallium Induced Changes in Behavioral Patterns: Correlation With Altered Lipid Peroxidation and Lysosomal Enzyme Activity in Brain Regions of Male Rats

Toxicology and Industrial Health ◽

10.1177/074823378500100109 ◽

1985 ◽

Vol 1 (1) ◽

pp. 81-98 ◽

Cited By ~ 15

Author(s):

David R. Brown ◽

Barbara G. Callahan ◽

Mark A. Cleaves ◽

Robert A. Schatz

Keyword(s):

Lipid Peroxidation ◽

Lysosomal Enzyme ◽

Brain Regions ◽

Male Rats ◽

Patterns Of Behavior ◽

Low Levels ◽

Behavioral Sequelae ◽

Human Poisoning ◽

And Function ◽

Induced Changes

The effects of exposures to low levels of heavy metals is a complex and serious problem. Thallium is a metal which produces behavioral sequelae in human poisoning and is potentially hazardous with low level exposures. A test battery is presented which utilizes biochemical and behavioral testing to assess the effects of low levels of thallium on central nervous system chemistry and function in rats. The doses of thallium used (4 and 8 mg/kg) produced no overt signs of behavioral toxicity but did produce dose-related increases in lipid peroxidation and activation of the lysosomal enzyme beta-galactosidase in selected brain regions. At these dose levels, thallium also selectively altered the patterns of behavior. The study suggests that the target regions of thallium in the brain include the cortex, the cerebellum and the brainstem. The dose-response relationships, found for certain pairs of behavioral acts, were correlated with biochemical changes in one or more brain regions.

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Maternal Dietary Docosahexaenoic Acid Alters Lipid Peroxidation Products and (n-3)/(n-6) Fatty Acid Balance in Offspring Mice

Metabolites ◽

10.3390/metabo9030040 ◽

2019 ◽

Vol 9 (3) ◽

pp. 40 ◽

Cited By ~ 9

Author(s):

Bo Yang ◽

Runting Li ◽

Taeseon Woo ◽

Jimmy Browning ◽

Hailong Song ◽

...

Keyword(s):

Lipid Peroxidation ◽

Docosahexaenoic Acid ◽

Maternal Diet ◽

Brain Regions ◽

Diet Group ◽

Mammalian Brain ◽

Enzymatic Reactions ◽

Functional Changes ◽

Lipid Peroxidation Products ◽

Brain Functions

The abundance of docosahexaenoic acid (DHA) in the mammalian brain has generated substantial interest in the search for its roles in regulating brain functions. Our recent study with a gene/stress mouse model provided evidence to support the ability for the maternal supplement of DHA to alleviate autism-associated behavior in the offspring. DHA and arachidonic acid (ARA) are substrates of enzymatic and non-enzymatic reactions, and lipid peroxidation results in the production of 4-hydroxyhexenal (4-HHE) and 4-hydroxynonenal (4-HNE), respectively. In this study, we examine whether a maternal DHA-supplemented diet alters fatty acids (FAs), as well as lipid peroxidation products in the pup brain, heart and plasma by a targeted metabolite approach. Pups in the maternal DHA-supplemented diet group showed an increase in DHA and a concomitant decrease in ARA in all brain regions examined. However, significant increases in 4-HHE, and not 4-HNE, were found mainly in the cerebral cortex and hippocampus. Analysis of heart and plasma showed large increases in DHA and 4-HHE, but a significant decrease in 4-HNE levels only in plasma. Taken together, the DHA-supplemented maternal diet alters the (n-3)/(n-6) FA ratio, and increases 4-HHE levels in pup brain, heart and plasma. These effects may contribute to the beneficial effects of DHA on neurodevelopment, as well as functional changes in other body organs.

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Defensive role of silibinin against arsenic induced oxidative stress mediated dyslipidemia and neurotoxicity in rats

International Journal of Pharmacology and Toxicology ◽

10.14419/ijpt.v4i1.5803 ◽

2016 ◽

Vol 4 (1) ◽

pp. 78 ◽

Cited By ~ 2

Author(s):

Muthumani Muthu ◽

Sumedha Naroem Chanu ◽

Shagirtha Kalist ◽

Milton Prabu

Keyword(s):

Lipid Peroxidation ◽

Antioxidant Properties ◽

Brain Regions ◽

Lipid Profiles ◽

Antioxidant Enzyme Activities ◽

Enzymatic Antioxidants ◽

Ros Production ◽

Protein Carbonyl Content ◽

Defensive Role ◽

The Brain

Arsenic (As) is an environmental toxic metalloid that is present in everywhere such as air, water and soil. Generally, inorganic arsenic has a tendency to be more toxic than organic arsenic. The present study was designed to determine whether oral administration of silibinin (SB), which has been shown to have substantial antioxidant properties, when pre-administered (75 mg/kg body weight) once daily for 4 weeks along with arsenic (5 mg/kg) would prevent arsenic-induced changes in antioxidant defense system, superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GPX),glutathione-S-transferase (GST),glutathione reductase (GR), glucose-6-phosphate dehydrogenase (G6PD), reduced glutathione (GSH), total sulfhydryl groups (TSH) and vitamin C in rat brain regions such as cortex, striatum, cerebellum, hippocampus and brain stem. Our study also examined the effect of SB over arsenic-induced reactive oxygen species (ROS) production and lipid peroxidation level (LPO) and protein carbonyl content (PC) in distinct brain regions of rats. Moreover, As also alters the lipid profiles such as total lipids, phospholipids, cholesterol, cerebrosides and gangliosides in various regions of the brain. Pre-administration of SB restores the altered enzymatic and non-enzymatic antioxidants, lipid profiles and also markedly reduced the ROS, LPO, PC and accumulation of As in various regions of the brain. These results suggested that arsenic-induced deficits in antioxidant enzyme activities and increase in ROS production and lipid peroxidation levels in brain regions can be remarkably prevented by pre-administration of SB.

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Is Oxidative Stress in Mice Brain Regions Diminished by 2-[(2,6-Dichlorobenzylidene)amino]-5,6-dihydro-4H-cyclopenta[b]thiophene-3-carbonitrile?

Oxidative Medicine and Cellular Longevity ◽

10.1155/2013/194192 ◽

2013 ◽

Vol 2013 ◽

pp. 1-8 ◽

Cited By ~ 2

Author(s):

A. C. Fortes ◽

A. A. C. Almeida ◽

G. A. L. Oliveira ◽

P. S. Santos ◽

W. De Lucca Junior ◽

...

Keyword(s):

Oxidative Stress ◽

Lipid Peroxidation ◽

Superoxide Dismutase ◽

Western Blot ◽

Blot Analysis ◽

Western Blot Analysis ◽

Brain Regions ◽

Saline Control ◽

Control Group ◽

Nitrite Content

2-[(2,6-Dichlorobenzylidene)amino]-5,6-dihydro-4H-cyclopenta[b]thiophene-3-carbonitrile, 5TIO1, is a new 2-aminothiophene derivative with promising pharmacological activities. The aim of this study was to evaluate its antioxidant activity in different areas of mice central nervous system. Male Swiss adult mice were intraperitoneally treated with Tween 80 dissolved in 0.9% saline (control group) and 5TIO1 (0.1, 1, and 10 mg kg−1). Brain homogenates—hippocampus, striatum, frontal cortex, and cerebellum—were obtained after 24 h of observation. Superoxide dismutase and catalase activities, lipid peroxidation and nitrite content were measured using spectrophotometrical methods. To clarify the 5TIO1’s mechanism on oxidative stress, western blot analysis of superoxide dismutase and catalase was also performed. 5TIO1 decreased lipid peroxidation and nitrite content in all brain areas and increased the antioxidant enzymatic activities, specially, in cerebellum. The data of Western blot analysis did not demonstrate evidence of the upregulation of these enzymes after the administration of this compound. Our findings strongly support that 5TIO1 can protect the brain against neuronal damages regularly observed during neuropathologies.

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Changes in dietary folate intake differentially affect oxidised lipid and mitochondrial DNA damage in various brain regions of rats in the absence/presence of intracerebroventricularly injected amyloid β-peptide challenge

British Journal Of Nutrition ◽

10.1017/s0007114510005052 ◽

2011 ◽

Vol 105 (9) ◽

pp. 1294-1302 ◽

Cited By ~ 11

Author(s):

Ta-Fu Chen ◽

Ming-Jang Chiu ◽

Chou-Tz Huang ◽

Ming-Chi Tang ◽

Sue-Jane Wang ◽

...

Keyword(s):

Lipid Peroxidation ◽

Dna Damage ◽

Folic Acid ◽

Neuronal Death ◽

Brain Regions ◽

Folate Intake ◽

Amyloid Β Peptide ◽

Aβ Peptide ◽

Dietary Folate ◽

Dietary Folate Intake

Accumulating evidence suggests that changes in dietary folate intake may modulate the risks of Alzheimer's disease (AD) through as yet unknown mechanisms. The aims of the present study were to investigate how dietary folate affects the brain folate distribution, levels of oxidised lipid and DNA damage in the absence/presence of β-amyloid(25–35)(Aβ) peptide challenge, a pathogenic hallmark of AD. Male Wistar rats were assigned to diets with folic acid at 0 (folate deprivation; FD), 8 (moderate folate; MF) and 8 mg folic acid/kg diet+0·003 % in drinking-water (folate supplementation; FS) for 4 weeks. A single injection of Aβ peptide (1 mg/ml) or the vehicle solution was intracerebroventricularly (icv) administrated to rats a week before killing. Brain folate, a marker of oxidative injury, and neuronal death were assayed. In the absence of an Aβ injection, FD rats showed reduced folate levels, and increased 2-thiobarbituric acid-reactive substances and a mitochondrial (mt)DNA 4834 bp large deletion (mtDNA4834deletion) in the hippocampus compared with the counterpart brains of control rats (P < 0·05). A single icv injection of Aβ peptide potentiated lipid peroxidation in the medulla of FD rats, which was ameliorated by feeding FD rats with the MF and FS diets (P < 0·05). Feeding the FS diet to Aβ-injected rats enriched brain folate levels and reduced mtDNA4834deletion in the hippocampal and medullary regions compared with corresponding tissues of Aβ+FD rats (P < 0·05). Aβ+FS rats had reduced rates of neuronal death in the frontal cortex compared with Aβ+FD rats (P < 0·05). Taken together, our data revealed that folate deprivation differentially depleted brain folate levels, and increased lipid peroxidation and mtDNA4834deletions, particularly, in the hippocampus. Upon Aβ challenge, the FS diet may protect various brain regions against lipid peroxidation, mitochondrial genotoxicity and neural death associated with folate deprivation.

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Centella asiatica and Its Fractions Reduces Lipid Peroxidation Induced by Quinolinic Acid and Sodium Nitroprusside in Rat Brain Regions

Neurochemical Research ◽

10.1007/s11064-015-1582-5 ◽

2015 ◽

Vol 40 (6) ◽

pp. 1197-1210 ◽

Cited By ~ 9

Author(s):

Naiani Ferreira Marques ◽

Sílvio Terra Stefanello ◽

Amanda L. F. Froeder ◽

Alcindo Busanello ◽

Aline Augusti Boligon ◽

...

Keyword(s):

Lipid Peroxidation ◽

Sodium Nitroprusside ◽

Rat Brain ◽

Quinolinic Acid ◽

Centella Asiatica ◽

Brain Regions ◽

Rat Brain Regions

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Melatonin reduces kainate‐induced lipid peroxidation in homogenates of different brain regions

The FASEB Journal ◽

10.1096/fasebj.9.12.7672513 ◽

1995 ◽

Vol 9 (12) ◽

pp. 1205-1210 ◽

Cited By ~ 118

Author(s):

Daniela Melchiorri ◽

Russel J. Reiter ◽

Ewa Sewerynek ◽

Li Dun Chen ◽

Giuseppe Nistic

Keyword(s):

Lipid Peroxidation ◽

Brain Regions

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FFA and OFA encode distinct types of face identity information

10.1101/2020.05.12.090878 ◽

2020 ◽

Cited By ~ 1

Author(s):

Maria Tsantani ◽

Nikolaus Kriegeskorte ◽

Katherine Storrs ◽

Adrian Lloyd Williams ◽

Carolyn McGettigan ◽

...

Keyword(s):

Brain Activity ◽

Activity Patterns ◽

Brain Regions ◽

Image Encoding ◽

Low Level ◽

Social Traits ◽

Face Area ◽

Face Similarity ◽

And Gender ◽

High Level

AbstractFaces of different people elicit distinct functional MRI (fMRI) patterns in several face-selective brain regions. Here we used representational similarity analysis to investigate what type of identity-distinguishing information is encoded in three face-selective regions: fusiform face area (FFA), occipital face area (OFA), and posterior superior temporal sulcus (pSTS). We used fMRI to measure brain activity patterns elicited by naturalistic videos of famous face identities, and compared their representational distances in each region with models of the differences between identities. Models included low-level to high-level image-computable properties and complex human-rated properties. We found that the FFA representation reflected perceived face similarity, social traits, and gender, and was well accounted for by the OpenFace model (deep neural network, trained to cluster faces by identity). The OFA encoded low-level image-based properties (pixel-wise and Gabor-jet dissimilarities). Our results suggest that, although FFA and OFA can both discriminate between identities, the FFA representation is further removed from the image, encoding higher-level perceptual and social face information.

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