scholarly journals Dexamethasone increased the survival rate in Plasmodium berghei-infected mice

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Danilo Reymão Moreira ◽  
Ana Carolina Musa Gonçalves Uberti ◽  
Antonio Rafael Quadros Gomes ◽  
Michelli Erica Souza Ferreira ◽  
Aline da Silva Barbosa ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Survival Rate ◽  
Plasmodium Berghei ◽  
Redox Status ◽  
No Synthase ◽  
Ischemia And Reperfusion ◽  
Inos Inhibition ◽  
The Brain ◽  
Plasmodial Infection ◽  
Stimulation Of

AbstractThe present study aimed to evaluate the effects of dexamethasone on the redox status, parasitemia evolution, and survival rate of Plasmodium berghei-infected mice. Two-hundred and twenty-five mice were infected with Plasmodium berghei and subjected to stimulation or inhibition of NO synthesis. The stimulation of NO synthesis was performed through the administration of L-arginine, while its inhibition was made by the administration of dexamethasone. Inducible NO synthase (iNOS) inhibition by dexamethasone promoted an increase in the survival rate of P. berghei-infected mice, and the data suggested the participation of oxidative stress in the brain as a result of plasmodial infection, as well as the inhibition of brain NO synthesis, which promoted the survival rate of almost 90% of the animals until the 15th day of infection, with possible direct interference of ischemia and reperfusion syndrome, as seen by increased levels of uric acid. Inhibition of brain iNOS by dexamethasone caused a decrease in parasitemia and increased the survival rate of infected animals, suggesting that NO synthesis may stimulate a series of compensatory redox effects that, if overstimulated, may be responsible for the onset of severe forms of malaria.

scholarly journals Inhibition Of Nitric Oxide Synthesis By Dexamethasone Increases Survival Rate In Plasmodium berghei-Infected Mice

2018 ◽  
Author(s):  
Danilo Reymão Moreira ◽  
Ana Carolina MG Uberti ◽  
Antonio Rafael Q Gomes ◽  
Michelli Erica Souza Ferreira ◽  
Rogério Silva Santos ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Survival Rate ◽  
Plasmodium Berghei ◽  
Redox Balance ◽  
Redox Status ◽  
Clinical Severity ◽  
Host Cells ◽  
High Incidence ◽  
Inos Inhibition ◽  
The Relationship

Malaria still presents great epidemiologic importance by its high incidence in the world and potential clinical severity. Plasmodium parasites are highly susceptible to changes in the redox balance and the relationship between the redox state of the parasite and host cells is very complex and involves nitric oxide (NO) synthesis. Thus, the present study is aimed at evaluating the effects of NO synthesis on the redox status, parasitemia evolution and survival rate of Plasmodium berghei-infected mice. Two-hundred and twenty-five mice were infected with Plasmodium berghei and submitted to the stimulation or inhibition of NO synthesis. The stimulation of NO synthesis was performed through the administration of L-arginine, while its inhibition was made by the administration of dexamethasone. Inducible NO synthase (iNOS) inhibition by dexamethasone promoted an increase in the survival rate of P. berghei-infected mice and data suggested the participation of oxidative stress in brain as a result of plasmodial infection, as well as the inhibition of brain NO synthesis, which promoted survival rate of almost 90% of the animals until the 15th day of infection, with possible direct interference of ischemia and reperfusion syndrome, as seen by increased levels of uric acid. Inhibition of iNOS caused a decrease of parasitemia and increased survival rate of infected animals, suggesting that the synthesis of NO may stimulate a series of compensatory redox effects that, if overstimulated, may be responsible for the onset of severe forms of malaria.

scholarly journals Disparate Central and Peripheral Effects of Circulating IGF-1 Deficiency on Tissue Mitochondrial Function

2019 ◽  
Vol 57 (3) ◽  
pp. 1317-1331 ◽  
Author(s):  
Gavin Pharaoh ◽  
Daniel Owen ◽  
Alexander Yeganeh ◽  
Pavithra Premkumar ◽  
Julie Farley ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Cognitive Function ◽  
Spatial Learning ◽  
Mitochondrial Function ◽  
Coupling Efficiency ◽  
Redox Status ◽  
Cellular Aging ◽  
Age Related ◽  
The Brain ◽  
Circulating Levels

AbstractAge-related decline in circulating levels of insulin-like growth factor (IGF)-1 is associated with reduced cognitive function, neuronal aging, and neurodegeneration. Decreased mitochondrial function along with increased reactive oxygen species (ROS) and accumulation of damaged macromolecules are hallmarks of cellular aging. Based on numerous studies indicating pleiotropic effects of IGF-1 during aging, we compared the central and peripheral effects of circulating IGF-1 deficiency on tissue mitochondrial function using an inducible liver IGF-1 knockout (LID). Circulating levels of IGF-1 (~ 75%) were depleted in adult male Igf1f/f mice via AAV-mediated knockdown of hepatic IGF-1 at 5 months of age. Cognitive function was evaluated at 18 months using the radial arm water maze and glucose and insulin tolerance assessed. Mitochondrial function was analyzed in hippocampus, muscle, and visceral fat tissues using high-resolution respirometry O2K as well as redox status and oxidative stress in the cortex. Peripherally, IGF-1 deficiency did not significantly impact muscle mass or mitochondrial function. Aged LID mice were insulin resistant and exhibited ~ 60% less adipose tissue but increased fat mitochondrial respiration (20%). The effects on fat metabolism were attributed to increases in growth hormone. Centrally, IGF-1 deficiency impaired hippocampal-dependent spatial acquisition as well as reversal learning in male mice. Hippocampal mitochondrial OXPHOS coupling efficiency and cortex ATP levels (~ 50%) were decreased and hippocampal oxidative stress (protein carbonylation and F2-isoprostanes) was increased. These data suggest that IGF-1 is critical for regulating mitochondrial function, redox status, and spatial learning in the central nervous system but has limited impact on peripheral (liver and muscle) metabolism with age. Therefore, IGF-1 deficiency with age may increase sensitivity to damage in the brain and propensity for cognitive deficits. Targeting mitochondrial function in the brain may be an avenue for therapy of age-related impairment of cognitive function. Regulation of mitochondrial function and redox status by IGF-1 is essential to maintain brain function and coordinate hippocampal-dependent spatial learning. While a decline in IGF-1 in the periphery may be beneficial to avert cancer progression, diminished central IGF-1 signaling may mediate, in part, age-related cognitive dysfunction and cognitive pathologies potentially by decreasing mitochondrial function.

scholarly journals Alteration on redox status in saliva of microcephaly children

2021 ◽  
Vol 10 (7) ◽  
pp. e40010716796
Author(s):  
Thayane Miranda Alves ◽  
Cintia Megid Barbieri ◽  
Marco Aurelio Gomes ◽  
Heitor Ceolin Araujo ◽  
Nathália de Oliveira Visquette ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Neurological Disorders ◽  
Redox Balance ◽  
Redox Status ◽  
Antioxidant Defenses ◽  
Frap Assay ◽  
Reducing Ability ◽  
Anticonvulsant Medication ◽  
Total Antioxidant ◽  
The Brain

Microcephaly is described as a reduction of the head circumference, due to the premature fusion of the bones of the skull, preventing the brain from growing normally and reaching its maximum development. This condition may result in neurological disorders, phonation and chewing dysfunction, dysphagia and risk of malnutrition. This alteration contributes to oral hygiene impairment, and continuous uses of the antipsychotic and anticonvulsant medication. Thus, the purpose of this study was to evaluate if microcephaly modified redox balance in saliva. Our hypothesis is that in the microcephalic patient's salivary oxidative stress is lower because of the increase in antioxidant defenses. The study included 13 patients with microcephaly (microcephalic group – MC) and 12 patients without neurological disorders (normocephalic group – NC), from zero to ten years old, no edentulous. Saliva was collected using a cotton wool swab, placing it on the child's mouth floor. After centrifugation, supernatants were fractionated and stored at -80 °C for analyses. Lipid oxidative was evaluated by TBARS methods, total antioxidant capacity by the ferric reducing ability (FRAP) assay, uric acid (UA) was quantified by modified Trinder reaction, and superoxide dismutase activity (SOD) by inhibition of the pyrogallol auto-oxidation. Total protein was measured using the method of Lowry.  Compared to NC group, TBARS was significantly lower in MC group, while FRAP, UA and SOD were higher. Our hypothesis was confirmed. MC patients have lower salivary oxidative stress, due to increased oxidant defenses.

Oxidative Stress and Neurodegeneration

2019 ◽  
pp. 24-47 ◽  
Author(s):  
Newman Osafo ◽  
David Darko Obiri ◽  
Kwabena Owusu Danquah ◽  
Oduro Kofi Yeboah ◽  
Aaron Opoku Antwi ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Spinal Cord ◽  
Nervous System ◽  
Transcription Factor ◽  
Growth Factor ◽  
Inhibitory Effect ◽  
Factor I ◽  
Forkhead Box ◽  
The Brain ◽  
Stimulation Of

Neurons are the building units of the nervous system and are therefore critical units for the health of the brain and the spinal cord. This is necessitated by their inability to be either replaced or reproduced once lost. Their losses are implicated in a number of conditions which have been elaborated in this chapter. Oxidative stress has been strongly implicated in neurodegeneration through blockade of neuroprotection by a number of mechanisms including inhibitory effect on insulin-like growth factor I (IGF-1) via stimulation of the transcription factor, Forkhead box O3 (FOXO3). This chapter elaborates on these two phenomena which cannot be decoupled.

Influence of hydrogen peroxide induced oxidative stress on survival rate of early chick embryo development

2016 ◽  
Vol 5 (06) ◽  
pp. 4603 ◽  
Author(s):  
Jaywant Tanaji Jadhav* ◽  
Suryakant Kengar
Keyword(s):  
Oxidative Stress ◽  
Hydrogen Peroxide ◽  
Survival Rate ◽  
Chick Embryo ◽  
Embryo Development ◽  
Redox Status ◽  
Ros Generation ◽  
Chick Embryos ◽  
Normal Morphology ◽  
Stress Influences

Reactive oxygen species (ROS) induced oxidative stress influences embryonic growth and development. Hydrogen peroxide (H2O2) is a major source of ROS generation that induces oxidative stress by altering redox status. In present study, direct effect of H2O2 generated oxidative stress on survival rate and associated toxicity in chick embryo was studied during early development. Chick embryos at 96 hrs of incubation were treated with single doses of 2.5μg, 5.0μg, 10μg, 50μg, 100μg, 300μg and 500μg H2O2 concentrations per embryo. The toxic effects recorded after 144 hrs of development. The results showed that treatments of 2.5 and 5.0μg H2O2 doses did not affect survival rate and embryo development. 10μg and 50μg H2O2 doses treatment exhibited slightly reduced survival rate without affecting normal morphology. Administration of 100 and 300μg H2O2 doses caused predominant decrease in the survival rate in comparison with the normal and PBS treated control embryos with deformities such as growth retardation, defected brain, limbs and vascular development with hemorrhage. Treatment of 500μg H2O2 exhibited no survival of embryos. These results indicated that post-omphalomesentric stages of early chick embryos are more susceptible to elevated level of H2O2 induced oxidative stress leading to significant reduction in survival rate with associated deformities. These results are discussed with probable reasons.

scholarly journals Naringin Supplementation during Pregnancy Induces Sex and Region-Specific Alterations in the Offspring’s Brain Redox Status

2021 ◽  
Vol 18 (9) ◽  
pp. 4805
Author(s):  
Bernardo Gindri dos Santos ◽  
Caroline Peres Klein ◽  
Mariana Scortegagna Crestani ◽  
Rafael Moura Maurmann ◽  
Régis Mateus Hözer ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Prefrontal Cortex ◽  
Wistar Rats ◽  
Redox Status ◽  
Disease Models ◽  
Dependent Manner ◽  
Beneficial Effects ◽  
Sensitive Periods ◽  
The Brain

Research has shown the beneficial effects of naringin supplementation to adult rodents, which can ameliorate oxidative stress in disease models. However, evidence has demonstrated that polyphenol supplementation induced detrimental effects when consumed during sensitive periods of development, such as pregnancy. Therefore, we investigated the effect of maternal naringin supplementation during pregnancy on the offspring’s cerebral redox status. Pregnant Wistar rats were divided into control and naringin groups and supplemented from gestational day 15 to gestational day 21. On postnatal days 1, 7, and 21, offspring were euthanized, and the prefrontal cortex, hippocampus, striatum, and cerebellum dissected. On postnatal day 1, maternal naringin supplementation positively modulated the pups’ brain redox status. On postnatal day 7, a pro-oxidative milieu was observed in the offspring’s striatum and cerebellum in a sex-dependent manner, even though the prefrontal cortex and hippocampus were not negatively affected. Besides, the alterations observed on postnatal day 7 did not persist up to weaning. Our findings demonstrated that the effect induced by naringin supplementation in the brain redox status differed according to the period of development in which naringin was consumed since the beneficial effects usually found in the adult rodents became detrimental when the supplementation was applied during pregnancy.

Chemical Stimulation of the Brain Makes Stimulating Reading

1975 ◽  
Vol 20 (12) ◽  
pp. 923-924
Author(s):  
MADGE E. SCHEIBEL ◽  
ARNOLD B. SCHEIBEL
Keyword(s):  
Chemical Stimulation ◽  
The Brain ◽  
Stimulation Of

SOME ASPECTS OF MECHANISM OF SUCCINAMIDES INFLUENCE ON METABOLIC HOMEOSTASIS OF THE ORGANISM

2018 ◽  
pp. 27-31
Author(s):  
I. A. Palagina
Keyword(s):  
Nitric Oxide ◽  
Biological Activity ◽  
Antioxidant System ◽  
No Synthase ◽  
Antioxidant Potential ◽  
Metabolic Homeostasis ◽  
Energetic Metabolism ◽  
Complex Action ◽  
Energy Processes ◽  
Stimulation Of

Succinate containing compounds possess many types of biological activity and are used for the development of drugs with the target and complex action. This paper is devoted to some aspects of the mechanism of succinamides’ action in a dose of 100 mg/kg. We studied the influence of the compound with antidiabetic properties, -phenylethylamide of 2-oxysuccinanyl acid ( -PhEA-OSAA), and its metabolites such as 2-hydroxyphenylsuccinamide (2-HPhSA) and β-phenylethylsuccinamide ( -PhESA) on the marker indicators of energetic metabolism (EM), antioxidant system (AOS) and nitric oxide (NO) metabolism in subacute experiment on rats. Studies have shown that the action of -FEA-OSAKA on metabolic homeostasis is realized through stimulation of EM, reduction of intensity of NO-synthase metabolism and weakening of the AOS. The nature of the action of -FES and 2-GFS, taking into account the indicators of the state of homeostasis, largely coincides with β-FEA-OSAKA. It was found that the key links in the mechanism of toxic action of succinamides are the effect on antioxidant potential, NO metabolism and energy processes.

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