scholarly journals High-Sugar Diet Disrupts Hypothalamic but Not Cerebral Cortex Redox Homeostasis

Nutrients ◽  
2020 ◽  
Vol 12 (10) ◽  
pp. 3181
Author(s):  
Ewa Żebrowska ◽  
Adrian Chabowski ◽  
Anna Zalewska ◽  
Mateusz Maciejczyk
Keyword(s):  
Cerebral Cortex ◽  
Oxidative Damage ◽  
Redox Homeostasis ◽  
Protein Glycation ◽  
Antioxidant Defenses ◽  
Antioxidant Systems ◽  
Enzymatic Antioxidants ◽  
High Sugar ◽  
Central Plasma ◽  
The Brain

Despite several reports on the relationship between metabolic and neurodegenerative diseases, the effect of a high-sugar diet (HSD) on brain function is still unknown. Given the crucial role of oxidative stress in the pathogenesis of these disorders, this study was the first to compare the effect of an HSD on the activity of prooxidative enzymes, enzymatic and non-enzymatic antioxidants, and protein oxidative damage in the brain structures regulating energy metabolism (hypothalamus) and cognitive functions (cerebral cortex). Male Wistar rats were randomly divided into two groups (n = 10)—control diet (CD) and high-sugar diet (HSD)—for 8 weeks. We showed a decrease in glutathione peroxidase and superoxide dismutase activity and an increase in catalase activity in the hypothalamus of HSD rats compared to controls. The activity of xanthine oxidase and NADPH oxidase and the contents of oxidation (protein carbonyls), glycoxidation (dityrosine, kynurenine and N-formylkynurenine) and protein glycation products (advanced glycation end products and Amadori products) were significantly higher only in the hypothalamus of the study group. The HSD was also responsible for the disruption of antioxidant systems and oxidative damage to blood proteins, but we did not show any correlation between systemic redox homeostasis and the brain levels. In summary, HSD is responsible for disorders of enzymatic antioxidant defenses only at the central (plasma/serum) and hypothalamic levels but does not affect the cerebral cortex. The hypothalamus is much more sensitive to oxidative damage caused by an HSD than the cerebral cortex.

Acute administration of 5-oxoproline induces oxidative damage to lipids and proteins and impairs antioxidant defenses in cerebral cortex and cerebellum of young rats

2010 ◽  
Vol 25 (2) ◽  
pp. 145-154 ◽  
Author(s):  
Carolina Didonet Pederzolli ◽  
Caroline Paula Mescka ◽  
Bernardo Remuzzi Zandoná ◽  
Daniella de Moura Coelho ◽  
Ângela Malysz Sgaravatti ◽  
...  
Keyword(s):  
Cerebral Cortex ◽  
Oxidative Damage ◽  
Antioxidant Defenses ◽  
Acute Administration ◽  
Young Rats

scholarly journals Age Associated Oxidative Damage in Lymphocytes

2010 ◽  
Vol 3 (4) ◽  
pp. 275-282 ◽  
Author(s):  
Nandeslu Gautam ◽  
Subhasis Das ◽  
Santanu Kar Mahapatra ◽  
Subhankari Prasad Chakraborty ◽  
Pratip Kumar Kundu ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Oxidative Damage ◽  
Antioxidant Status ◽  
Antioxidant Defenses ◽  
Protein Damage ◽  
Protein Carbonyls ◽  
Elderly Subjects ◽  
Antioxidant Systems ◽  
Healthy Individuals ◽  
Blood Samples

Lymphocytes are an important immunological cell and have been played a significant role in acquired immune system; hence, may play in pivotal role in immunosenescence. Oxidative stress has been reported to increase in elderly subjects, possibly arising from an uncontrolled production of free radicals with aging and decreased antioxidant defenses. This study was aimed to evaluate the level of lipid-protein damage and antioxidant status in lymphocytes of healthy individuals to correlate between oxidative damage with the aging process. Twenty healthy individuals of each age group (11–20; 21–30; 31–40; 41–50; and 51–60 years) were selected randomly. Blood samples were drawn by medical practitioner and lymphocytes were isolated from blood samples. Malondialdehyde (MDA), protein carbonyls (PC) level were evaluated to determine the lipid and protein damage in lymphocytes. Superoxide dismutase (SOD), catalase (CAT), glutathione and glutathione dependent enzymes were estimated to evaluate the antioxidant status in the lymphocytes. Increased MDA and PC levels strongly support the increased oxidative damage in elderly subject than young subjects. The results indicated that, balance of oxidant and antioxidant systems in lymphocytes shifts in favor of accelerated oxidative damage during aging. Thus oxidative stress in lymphocytes may particular interest in aging and may play important role in immunosenescence.

scholarly journals Neurochemical evidence that phytanic acid induces oxidative damage and reduces the antioxidant defenses in cerebellum and cerebral cortex of rats

Life Sciences ◽  
2010 ◽  
Vol 87 (9-10) ◽  
pp. 275-280 ◽  
Author(s):  
Guilhian Leipnitz ◽  
Alexandre U. Amaral ◽  
Ângela Zanatta ◽  
Bianca Seminotti ◽  
Carolina G. Fernandes ◽  
...  
Keyword(s):  
Cerebral Cortex ◽  
Oxidative Damage ◽  
Phytanic Acid ◽  
Antioxidant Defenses

Effect of CDA-II, Urinary Preparation on Lipofuscin, Lipid Peroxidation and Antioxidant Systems in Young and Middle-Aged Rat Brain

2001 ◽  
Vol 29 (01) ◽  
pp. 91-99 ◽  
Author(s):  
Wen-Chuan Lin ◽  
Yueh-Wern Wu ◽  
Tung-Yuan Lai ◽  
Ming-Cheng Liau
Keyword(s):  
Lipid Peroxidation ◽  
Oxidative Damage ◽  
Rat Brain ◽  
Antioxidant Systems ◽  
Scavenging Activity ◽  
Aged Rats ◽  
Middle Aged ◽  
Cda Ii ◽  
Endogenous Antioxidants ◽  
The Brain

The levels of lipofuscin and lipid peroxidation reflect the degree of free radical-induced oxidative damage in the brain. We examined the effects of CDA-ll, a preparation of human urine, on lipofuscin and lipid peroxidation in the brain of young (3.5 months) and middle-aged rats (17 months). The rats were given CDA-ll orally at dosages of 0.3 or 1.0 g/kg daily for 8 weeks. CDA-ll significantly suppressed the contents of lipofuscin and lipid peroxidation in both young and middle-aged rats. CDA-ll also elevated the activity of superoxide dismutase, and the amounts of glutathione and ascorbic acid in the middle-aged rats, but not in the young ones. Our results suggest that the protection against oxidative damage by CDA-ll in the young rat brain may be due to its scavenging activity against free radicals. In the middle-aged rats, in addition to the scavenging activity, the levels of endogenous antioxidants were also enhanced by the CDA-ll treatment.

Evidence that 3-hydroxy-3-methylglutaric acid promotes lipid and protein oxidative damage and reduces the nonenzymatic antioxidant defenses in rat cerebral cortex

2008 ◽  
Vol 86 (3) ◽  
pp. 683-693 ◽  
Author(s):  
Guilhian Leipnitz ◽  
Bianca Seminotti ◽  
Josué Haubrich ◽  
Manuela B. Dalcin ◽  
Karina B. Dalcin ◽  
...  
Keyword(s):  
Cerebral Cortex ◽  
Oxidative Damage ◽  
Rat Cerebral Cortex ◽  
Antioxidant Defenses

Acute lysine overload provokes protein oxidative damage and reduction of antioxidant defenses in the brain of infant glutaryl-CoA dehydrogenase deficient mice: A role for oxidative stress in GA I neuropathology

2014 ◽  
Vol 344 (1-2) ◽  
pp. 105-113 ◽  
Author(s):  
Bianca Seminotti ◽  
Rafael Teixeira Ribeiro ◽  
Alexandre Umpierrez Amaral ◽  
Mateus Struecker da Rosa ◽  
Carolina Coffi Pereira ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Oxidative Damage ◽  
Antioxidant Defenses ◽  
The Brain ◽  
Deficient Mice

scholarly journals DHA and Its Elaborated Modulation of Antioxidant Defenses of the Brain: Implications in Aging and AD Neurodegeneration

Antioxidants ◽  
2021 ◽  
Vol 10 (6) ◽  
pp. 907
Author(s):  
Mario Díaz ◽  
Fátima Mesa-Herrera ◽  
Raquel Marín
Keyword(s):  
Nerve Cell ◽  
Cell Biology ◽  
Normal Aging ◽  
Brain Parenchyma ◽  
Synaptic Function ◽  
Antioxidant Defenses ◽  
Antioxidant Systems ◽  
Antioxidant Function ◽  
Modulation Of Gene Expression ◽  
The Brain

DHA (docosahexaenoic acid) is perhaps the most pleiotropic molecule in nerve cell biology. This long-chain highly unsaturated fatty acid has evolved to accomplish essential functions ranging from structural components allowing fast events in nerve cell membrane physiology to regulation of neurogenesis and synaptic function. Strikingly, the plethora of DHA effects has to take place within the hostile pro-oxidant environment of the brain parenchyma, which might suggest a molecular suicide. In order to circumvent this paradox, different molecular strategies have evolved during the evolution of brain cells to preserve DHA and to minimize the deleterious effects of its oxidation. In this context, DHA has emerged as a member of the “indirect antioxidants” family, the redox effects of which are not due to direct redox interactions with reactive species, but to modulation of gene expression within thioredoxin and glutathione antioxidant systems and related pathways. Weakening or deregulation of these self-protecting defenses orchestrated by DHA is associated with normal aging but also, more worryingly, with the development of neurodegenerative diseases. In the present review, we elaborate on the essential functions of DHA in the brain, including its role as indirect antioxidant, the selenium connection for proper antioxidant function and their changes during normal aging and in Alzheimer’s disease.

Glucuronyl 3-sulfate occurs exclusively on distal unmyelinated terminals of selected sensory neurons in the peripheral nervous system

1995 ◽  
Vol 53 ◽  
pp. 958-959
Author(s):  
S.S. Spicer ◽  
B.A. Schulte
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Cerebral Cortex ◽  
Peripheral Nervous System ◽  
Sensory Neurons ◽  
Sensory Nerves ◽  
Tissue Antigens ◽  
The Central Nervous System ◽  
The Brain ◽  
Leu 7

Generation of monoclonal antibodies (MAbs) against tissue antigens has yielded several (VC1.1, HNK- 1, L2, 4F4 and anti-leu 7) which recognize the unique sugar epitope, glucuronyl 3-sulfate (Glc A3- SO4). In the central nervous system, these MAbs have demonstrated Glc A3-SO4 at the surface of neurons in the cerebral cortex, the cerebellum, the retina and other widespread regions of the brain.Here we describe the distribution of Glc A3-SO4 in the peripheral nervous system as determined by immunostaining with a MAb (VC 1.1) developed against antigen in the cat visual cortex. Outside the central nervous system, immunoreactivity was observed only in peripheral terminals of selected sensory nerves conducting transduction signals for touch, hearing, balance and taste. On the glassy membrane of the sinus hair in murine nasal skin, just deep to the ringwurt, VC 1.1 delineated an intensely stained, plaque-like area (Fig. 1). This previously unrecognized structure of the nasal vibrissae presumably serves as a tactile end organ and to our knowledge is not demonstrable by means other than its selective immunopositivity with VC1.1 and its appearance as a densely fibrillar area in H&E stained sections.

Neurotransmitter systems of female mouse brain during growth of malignant melanoma modeled on the background of chronic pain

2018 ◽  
pp. 49-55
Author(s):  
О.И. Кит ◽  
И.М. Котиева ◽  
Е.М. Франциянц ◽  
И.В. Каплиева ◽  
Л.К. Трепитаки ◽  
...  
Keyword(s):  
Chronic Pain ◽  
Cerebral Cortex ◽  
Malignant Melanoma ◽  
Sciatic Nerve ◽  
Female Mouse ◽  
Combined Effects ◽  
Malignant Growth ◽  
Course Of Disease ◽  
The Brain ◽  
Melanoma Growth

Известно, что биогенные амины (БА) участвуют в злокачественном росте, их уровень изменяется в ЦНС при болевом воздействии, однако исследований о сочетанном влиянии хронической боли (ХБ) и онкопатологии на динамику БА в головном мозге не проводилось. Цель: изучить особенности баланса БА в коре головного мозга в динамике роста меланомы, воспроизведенной на фоне ХБ. Материалы и методы. Работа выполнена на 64 мышах-самках, весом 21-22 г. Животным основной группы меланому В16/F10 перевивали под кожу спины через 2 недели после перевязки седалищных нервов. Группой сравнения служили мыши с меланомой без боли. Уровни БА: адреналина, норадреналина, дофамина (ДА), серотонина (5-НТ), гистамина, а также 5-ОИУК определяли методом иммуноферментного анализа. Результаты. У мышей с ХБ уменьшается содержание большинства БА, однако уровень ДА не изменяется. Метаболизм 5-НТ происходит с участием МАО. Развитие меланомы сопровождается увеличением содержания ДА и 5-НТ, тогда как МАО - ингибируется. Направленность сдвигов БА при развитии меланомы на фоне ХБ оказалась практически такой же, как и без неё. В то же время ХБ ограничивает накопление 5-НТ в коре мозга при меланоме, что сопровождается более агрессивным её течением. Выводы. ХБ ограничивает включение стресс-лимитирующих механизмов в головном мозге при развитии меланомы у мышей, что приводит к более агрессивному течению злокачественного процесса. Biogenic amines (BA) are known to be involved in malignant growth, and their CNS levels change in pain; however, there are no studies of combined effects of chronic pain (CP) and cancer on BA dynamics in the brain. Aim: To study features of BA balance in the cerebral cortex during melanoma growth associated with CP. Material and methods. The study included 64 female mice weighing 21-22 g. In the main groups, B16/F10 melanoma was transplanted under the skin of the back two weeks following sciatic nerve ligation. Mice with melanoma without pain were used as the control. Concentrations of BA: adrenaline, noradrenaline, dopamine (DA), serotonin (5-HT), histamine and 5-HIAA were measured with ELISA. Results. Concentrations of BAs decreased in mice with CP although DA levels did not change. 5-HT metabolism involved MAO. The development of melanoma was accompanied by increases in DA and 5-HT whereas MAO was inhibited. The direction of BA changes during the development of melanoma was the same with and without CP. At the same time, CP with melanoma limited accumulation of 5-HT in the cerebral cortex, which resulted in even more aggressive course of cancer. Conclusion. CP restricted the activation of cerebral stress-limiting mechanisms during the development of melanoma in mice, which resulted in a more aggressive course of disease.

Involvement of Heme Oxygenase-1 in Neuropsychiatric and Neurodegenerative Diseases

2018 ◽  
Vol 24 (20) ◽  
pp. 2283-2302 ◽  
Author(s):  
Vivian B. Neis ◽  
Priscila B. Rosa ◽  
Morgana Moretti ◽  
Ana Lucia S. Rodrigues
Keyword(s):  
Neurodegenerative Diseases ◽  
Heme Oxygenase ◽  
Therapeutic Potential ◽  
Redox Homeostasis ◽  
Antioxidant Defenses ◽  
Heme Oxygenase 1 ◽  
Physiological Conditions ◽  
And Oxidative Stress ◽  
Defensive Mechanism

Heme oxygenase (HO) family catalyzes the conversion of heme into free iron, carbon monoxide and biliverdin. It possesses two well-characterized isoforms: HO-1 and HO-2. Under brain physiological conditions, the expression of HO-2 is constitutive, abundant and ubiquitous, whereas HO-1 mRNA and protein are restricted to small populations of neurons and neuroglia. HO-1 is an inducible enzyme that has been shown to participate as an essential defensive mechanism for neurons exposed to oxidant challenges, being related to antioxidant defenses in certain neuropathological conditions. Considering that neurodegenerative diseases (Alzheimer’s Disease (AD), Parkinson’s Disease (PD) and Multiple Sclerosis (MS)) and neuropsychiatric disorders (depression, anxiety, Bipolar Disorder (BD) and schizophrenia) are associated with increased inflammatory markers, impaired redox homeostasis and oxidative stress, conditions that may be associated with alterations in HO-levels/activity, the purpose of this review is to present evidence on the possible role of HO-1 in these Central Nervous System (CNS) diseases. In addition, the possible therapeutic potential of targeting brain HO-1 is explored in this review.

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