scholarly journals Low Doses of Imidacloprid Induce Oxidative Stress and Neural Cell Disruption in Earthworm Eisenia fetida

2021 ◽  
Vol 84 ◽  
pp. 1-11
Author(s):  
Artem Huslystyi ◽  
Victor Nedzvetsky ◽  
Serhii Yermolenko ◽  
Viktor Gasso ◽  
Vladyslav Petrushevskyi ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Nervous System ◽  
Molecular Mechanisms ◽  
Neuron Specific Enolase ◽  
Stress Generation ◽  
Low Doses ◽  
Neuronal Marker ◽  
Dose Dependent Decrease ◽  
Species Production ◽  
Dose Dependent

Imidacloprid is a widely used pesticide that belongs to the class of neonicotinoids. There is a piece of rising evidence that neonicotinoids exert cytotoxic effects in non-target organisms including vertebrate species such as mammals. Nevertheless, dose-limiting toxicity and molecular mechanisms of neonicotinoids' deleterious effects are still poorly understood. In accord to imidacloprid fate in the environment, the most of used pesticide is absorbed in the soil. Therefore, earthworms, which are prevailing soil organisms, could be considered as a target of neonicotinoids toxicity. The earthworm’s simple nervous system is a prospective model for neurotoxicological studies. We exposed earthworms to imidacloprid in a paper contact test with a doses range of 0.1‑0.4 µg/cm2 for 14 days. In the present work, we studied the imidacloprid effect on oxidative stress generation and neuronal marker neuron-specific enolase (NSE) expression. The exposure to imidacloprid induced a dose-dependent decrease in NSE. Both reactive oxygen species production and lipid peroxidation level were upregulated as well. Observed NSE decline suggests imidacloprid-caused disturbance in earthworm neuron cells. Obtained data have shown that relatively low doses of imidacloprid are potent to induce cytotoxicity in neurons. Furthermore, neurotoxicity could be recognized as one of an individual scenario of the general imidacloprid toxicity. Thus, presented results suggest the cytotoxicity of imidacloprid low doses in non-target organisms and hypothesize that NSE downregulation could be estimated as a biomarker of neonicotinoid cytotoxicity in a nervous system of non-insect species.

Cardiovascular effects of microinjection of low doses of serotonin into the NTS of unanesthetized rats

1997 ◽  
Vol 272 (4) ◽  
pp. R1135-R1142 ◽  
Author(s):  
J. C. Callera ◽  
L. G. Bonagamba ◽  
C. Sevoz ◽  
R. Laguzzi ◽  
B. H. Machado
Keyword(s):  
Cardiovascular Effects ◽  
Cardiovascular Responses ◽  
Cardiovascular Reflexes ◽  
Low Doses ◽  
Reflex Bradycardia ◽  
Baseline Values ◽  
Dose Dependent Decrease ◽  
Baroreceptor Activation ◽  
Dose Dependent

In the present study, we analyzed in conscious rats the effects of microinjections of serotonin (5-HT; pmol range) into the nucleus of the solitary tract (NTS) on basal mean arterial pressure (MAP) and heart rate (HR) and also on the reflex bradycardia induced by the activation of the baro- and chemoreflex evaluated 1 min after 5-HT microinjection into the NTS. The data show that unilateral microinjection of 5-HT in the picomolar range into the NTS of unanesthetized rats produced a dose-dependent decrease in MAP and HR, which was blocked by previous microinjection of ketanserin (250 pmol/50 nl) into the NTS. The changes in MAP and HR induced by 5-HT were of very short duration, with a return to baseline values a few seconds later. The cardiovascular responses to baro- or chemoreflex activation 1 min after 5-HT microinjection into the NTS did not differ from the control, indicating that low doses of 5-HT produced no effect on the cardiovascular reflexes tested at that time. The present data show that, as also observed in anesthetized rats, the microinjection of picomolar doses of 5-HT into the NTS elicits the typical cardiovascular responses to baroreceptor activation. These effects, hypotension and bradycardia, seem to be mediated by 5-HT2 receptors because both were blocked by a selective 5-HT2 receptor antagonist. However, since microinjection of 5-HT (1 pmol) into the NTS produced no changes in the cardiovascular responses to the baro- and chemoreflex activated 1 min later, the role of 5-HT2 receptors in the processing of the cardiovascular afferent messages in the NTS remains to be elucidated.

Interaction of propranolol and phentolamine with ethanol in the rat

1976 ◽  
Vol 54 (4) ◽  
pp. 622-625 ◽  
Author(s):  
D. Frankel ◽  
H. Kalant ◽  
J. M. Khanna ◽  
A. E. LeBlanc
Keyword(s):  
Nervous System ◽  
Dependent Manner ◽  
Low Doses ◽  
Adrenergic Mechanism ◽  
Adrenergic Nervous System ◽  
Ethanol Effect ◽  
Dose Dependent ◽  
Higher Doses

The possible role of the adrenergic nervous system in the intoxicant effects of ethanol was examined in studies of the interaction of propranolol and phentolamine with ethanol. Propranolol tended to increase the effect of lower doses of ethanol in a dose-dependent manner. However, the effect of higher doses of ethanol (over 2.0 g/kg) tended to be diminished by low doses of propranolol, whereas higher doses of propranolol were ineffective or actually increased the ethanol effect. Phentolamine tended to decrease the effect of the lower ethanol doses. These findings are inconsistent with any simple adrenergic mechanism in the mediation of the intoxicant effect of ethanol.

scholarly journals Effects of Low-Dose versus High-Doseγ-Tocotrienol on the Bone Cells Exposed to the Hydrogen Peroxide-Induced Oxidative Stress and Apoptosis

2012 ◽  
Vol 2012 ◽  
pp. 1-10 ◽  
Author(s):  
Nizar Abd Manan ◽  
Norazlina Mohamed ◽  
Ahmad Nazrun Shuid
Keyword(s):  
Oxidative Stress ◽  
Hydrogen Peroxide ◽  
Antioxidant Enzymes ◽  
Low Dose ◽  
Bone Cells ◽  
Dependent Manner ◽  
Low Doses ◽  
Antioxidant Enzymes Activities ◽  
High Doses ◽  
Dose Dependent

Oxidative stress and apoptosis can disrupt the bone formation activity of osteoblasts which can lead to osteoporosis. This study was conducted to investigate the effects ofγ-tocotrienol on lipid peroxidation, antioxidant enzymes activities, and apoptosis of osteoblast exposed to hydrogen peroxide (H2O2). Osteoblasts were treated with 1, 10, and 100 μM ofγ-tocotrienol for 24 hours before being exposed to 490 μM (IC50) H2O2for 2 hours. Results showed thatγ-tocotrienol prevented the malondialdehyde (MDA) elevation induced by H2O2in a dose-dependent manner. As for the antioxidant enzymes assays, all doses ofγ-tocotrienol were able to prevent the reduction in SOD and CAT activities, but only the dose of 1 μM of GTT was able to prevent the reduction in GPx. As for the apoptosis assays,γ-tocotrienol was able to reduce apoptosis at the dose of 1 and 10 μM. However, the dose of 100 μM ofγ-tocotrienol induced an even higher apoptosis than H2O2. In conclusion, low doses ofγ-tocotrienol offered protection for osteoblasts against H2O2toxicity, but itself caused toxicity at the high doses.

scholarly journals Regenerative Effects of CDP-Choline: A Dose-Dependent Study in the Toxic Cuprizone Model of De- and Remyelination

2021 ◽  
Vol 14 (11) ◽  
pp. 1156
Author(s):  
Viktoria Gudi ◽  
Nora Schäfer ◽  
Stefan Gingele ◽  
Martin Stangel ◽  
Thomas Skripuletz
Keyword(s):  
Multiple Sclerosis ◽  
Clinical Trial ◽  
Central Nervous System ◽  
Nervous System ◽  
Animal Studies ◽  
Low Doses ◽  
Key Factors ◽  
Beneficial Effects ◽  
The Central Nervous System ◽  
Dose Dependent

Inflammatory attacks and demyelination in the central nervous system (CNS) are the key factors responsible for the damage of neurons in multiple sclerosis (MS). Remyelination is the natural regenerating process after demyelination that also provides neuroprotection but is often incomplete or fails in MS. Currently available therapeutics are affecting the immune system, but there is no substance that might enhance remyelination. Cytidine-S-diphosphate choline (CDP-choline), a precursor of the biomembrane component phospholipid phosphatidylcholine was shown to improve remyelination in two animal models of demyelination. However, the doses used in previous animal studies were high (500 mg/kg), and it is not clear if lower doses, which could be applied in human trials, might exert the same beneficial effect on remyelination. The aim of this study was to confirm previous results and to determine the potential regenerative effects of lower doses of CDP-choline (100 and 50 mg/kg). The effects of CDP-choline were investigated in the toxic cuprizone-induced mouse model of de- and remyelination. We found that even low doses of CDP-choline effectively enhanced early remyelination. The beneficial effects on myelin regeneration were accompanied by higher numbers of oligodendrocytes. In conclusion, CDP-choline could become a promising regenerative substance for patients with multiple sclerosis and should be tested in a clinical trial.

scholarly journals Vascular endothelial growth factor stimulates dephosphorylation of the catenins p120 and p100 in endothelial cells

2000 ◽  
Vol 346 (1) ◽  
pp. 209-216 ◽  
Author(s):  
Elaine Y. M. WONG ◽  
Louise MORGAN ◽  
Caroline SMALES ◽  
Paul LANG ◽  
Sharon E. GUBBY ◽  
...  
Keyword(s):  
Vascular Endothelial Growth Factor ◽  
Endothelial Cells ◽  
Growth Factor ◽  
Molecular Mechanisms ◽  
Vegf Receptor ◽  
Vascular Endothelial ◽  
Extracellular Signal ◽  
Dose Dependent Decrease ◽  
Endothelial Growth Factor ◽  
Dose Dependent

Vascular endothelial growth factor (VEGF) is an endothelium-specific mitogen that induces angiogenesis and increases vascular permeability. These processes involve regulation of cell-cell adhesion, but molecular mechanisms have yet to be fully established. p120, also termed p120ctn, and its variant p100 are catenins which associate with cadherins and localize to adherens junctions. VEGF was reported to stimulate tyrosine phosphorylation of catenins in endothelial cells. In contrast, we have found that VEGF potently stimulated a rapid and dose-dependent decrease in serine/threonine phosphorylation of p120 and p100. VEGF acted via VEGF receptor 2 to achieve this effect which was independent of activation of the extracellular-signal-regulated kinase pathway. Histamine and activators of protein kinase C had a very similar effect to that of VEGF on phosphorylation of p120 and p100, suggesting that these diverse stimuli may converge on a common signalling element regulating p120/p100 serine/threonine phosphorylation. These data raise the possibility that the dephosphorylation of p120 and p100 triggered by VEGF may contribute to mechanisms regulating permeability and/or motility through modulation of cadherin adhesiveness.

scholarly journals Influence of cadmium contamination on brain glial cells: consequences and bioindication possibilities

2020 ◽  
Vol 49 ◽  
pp. 67-83
Author(s):  
V. S. Nedzvetsky ◽  
V. Ya. Gasso ◽  
A. M. Hahut ◽  
I. A. Hasso
Keyword(s):  
Oxidative Stress ◽  
Glial Cells ◽  
Functional Activity ◽  
Molecular Mechanisms ◽  
Glucose Utilization ◽  
Animal Health ◽  
Toxic Effects ◽  
Low Doses ◽  
Cellular Models ◽  
The Brain

Cadmium (Cd) is a heavy metal that currently presents in almost all components of the environment. Cd is a ubiquitous pollutant that is constantly entering the environment from industry and agriculture, mining, forest fires and many more sources. Some occupational diseases have aftereffects associated with Cd cytotoxicity. Despite long-term studies of the toxic effects of Cd, its cytotoxicity of low doses and the chronic effects on the nerve tissue cells remain undiscovered. The results of determining the Cd neurotoxicity indicate a disturbance of the permeability of the blood-brain barrier, the accumulation of Cd in the brain and the deterioration of the functional activity of the central nervous system. One of the main cellular targets for Cd in the brain are astrocytes. Astrocytes provide nutrition and functional activity of neurons, as well as recovery of physical and metabolic damage. The cytoskeleton of astrocytes is built of glial fibrillary acidic protein (GFAP). GFAP participates in important functions of astrocytes and its condition reflects the astrocytes reactivity. The molecular mechanisms of the neurotoxic effects of Cd on the glial cytoskeleton remain unknown. Glioblastomas are widely used to study the cytotoxic mechanisms of various compounds, including heavy metals, as cellular models of astrocytes. Taking into account the role of oxidative stress in a cell damage, as well as the reactive response of glial cells, we study the influence of low doses of Cd on oxidative stress and expression of GFAP and glucose-6-phosphate dehydrogenase (G6PD) in U373GM cells. Doses of 2-10 μM Cd induced a dose-dependent increase in reactive oxygen species and lipid peroxidation products. The same doses inhibited the expression of the cytoskeletal marker of astrocytes (GFAP) and metabolic marker of glucose utilization (G6PD). The obtained results indicate a pronounced cytotoxic effect of low doses of Cd in the astrocytic cell model U373GM. In addition, the astroglial cytotoxicity of Cd may be mediated by oxidative damage, inhibition of glial intermediate filament expression, and glucose utilization disorders. These parameters can be promising biomarkers of toxic effects both for the assessment of human and animal health and for determining the state of the environment as a whole.

scholarly journals The Pathophysiological Aspects of Cerebral Diseases

2022 ◽  
Author(s):  
Henrique Coelho Silva ◽  
Rafael Costa Lima Maia ◽  
Paulo Roberto Leitao de Vasconcelos ◽  
Orleancio Gomes Ripardo de Azevedo
Keyword(s):  
Oxidative Stress ◽  
Nervous Tissue ◽  
Molecular Mechanisms ◽  
Cerebrovascular Disorders ◽  
Neuron Specific Enolase ◽  
Cerebrovascular Diseases ◽  
Negative Effects ◽  
Cerebral Diseases ◽  
Negative Impacts ◽  
And Oxidative Stress

Introduction. Cerebrovascular disorders are the main causes of heavy burden health worldwide, also, it is critical to understand the pathophysiological mechanism and then trying to prevent the neurological sequels. Objective. To discuss the inflammatory and oxidative stress aspects associated to the cerebrovascular diseases, focusing on biomarkers, also the role of omega oils, and the intracellular molecular network associated to the tissue burden on those conditions. Results. One of the most promising biomarkers it is Neuron-Specific Enolase (NSE). Serum NSE levels were elevated in stroke-patients compared to the non-stroke controls. Also, studies have demonstrated that in specific ratio omega oils 3, 6 and 9 can ameliorate the inflammatory and oxidative stress in nervous tissue and could be useful to the inflammatory and oxidative stress negative effects of cerebrovascular diseases. In addition, the study of the molecular mechanisms is essential to understand which molecules could be addressed in cascade of events preventing the permanent damage on the nervous tissue. Final considerations. The studies on cerebrovascular disorders must precisely identify the mechanisms and key molecules involved and improve the time of diagnostics and prognostics reducing the negative impacts of those conditions.

scholarly journals Cytokine-mediated regulation of expression of Gfi1 and U2afll4 genes activated by T-cells with different differentiation status in vitro

2016 ◽  
Vol 62 (2) ◽  
pp. 180-186
Author(s):  
K.A. Yurova ◽  
N.A. Sokhonevich ◽  
O.G. Khaziakhmatova ◽  
L.S. Litvinova
Keyword(s):  
Gene Expression ◽  
T Cells ◽  
Molecular Mechanisms ◽  
Splice Variants ◽  
Inhibitory Effect ◽  
Regulation Of Expression ◽  
Dose Dependent Decrease ◽  
Differentiation Status ◽  
Dose Dependent

The dose-dependent effects of cytokines (IL-2, IL-7, and IL-15), which have a common g-chain, on mRNA expression of U2afll4 and GFi1 genes involved in regulation of alternative splicing of the Ptprc gene, have been investigated in vitro using T-lymphocyte cultures with different degrees of differentiation. IL-2, IL-7, and IL-15 caused a similar unidirectional inhibitory effect of various severity on restimulated CD45RO+ T-cells exposed to an antigen-independent activation; they caused a dose-dependent decrease of the U2af1l4 gene expression, and an increase of Gfi1 gene expression. This may suggest formation of active forms of the CD45 receptor, and also limitation of the formation of low-molecular short splice variants of the CD45RO receptor. Under conditions of antigen-independent stimulation of naive CD45RA+-cells rIL-7 and IL-15 exhibited opposite effects on U2af1l4 and Gfi1 gene expression. The increase of IL-7 concentrations in the incubation medium of naive cells was accompanied by a decrease in expression of both genes. IL-15 IL-7 exhibited opposite effects. Cytokines possessing a common g-chain (IL-2, IL-7, and IL-15) prevented antigen-independent differentiation of naive T-cells, by preventing the formation of polyclonal “surrogate“ cells. In general, the study of the molecular mechanisms of genetic control determining homeostatic processes of T-cells in response to exposure to antigenic or non-antigenic treatments may be important for construction of a general model of self-maintenance and differentiation of immune cells

scholarly journals Biochemical Hallmarks of Oxidative Stress-Induced Overactivation of Xenopus Eggs

2019 ◽  
Vol 2019 ◽  
pp. 1-7 ◽  
Author(s):  
Alexander A. Tokmakov ◽  
Misaki Awamura ◽  
Ken-Ichi Sato
Keyword(s):  
Oxidative Stress ◽  
Hydrogen Peroxide ◽  
Protein Content ◽  
Molecular Mechanisms ◽  
Low Frequency ◽  
Cytoplasmic Protein ◽  
Lipofuscin Accumulation ◽  
Progressive Development ◽  
Biochemical Analyses ◽  
Dose Dependent

Egg overactivation occurs with a low frequency in the populations of naturally ovulated frog eggs. At present, its natural inducers, molecular mechanisms, and intracellular events remain unknown. Using microscopic and biochemical analyses, we demonstrate here that high levels of hydrogen peroxide-induced oxidative stress can cause time- and dose-dependent overactivation of Xenopus eggs. Lipofuscin accumulation, decrease of soluble cytoplasmic protein content, and depletion of intracellular ATP were found to take place in the overactivated eggs. Progressive development of these processes suggests that egg overactivation unfolds in a sequential and ordered fashion.

scholarly journals Molecular Mechanisms of Astaxanthin as a Potential Neurotherapeutic Agent

Marine Drugs ◽  
2021 ◽  
Vol 19 (4) ◽  
pp. 201
Author(s):  
Eshak I. Bahbah ◽  
Sherief Ghozy ◽  
Mohamed S. Attia ◽  
Ahmed Negida ◽  
Talha Bin Emran ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Drug Delivery ◽  
Clinical Trials ◽  
Nervous System ◽  
Neuropathic Pain ◽  
Cerebral Ischemia ◽  
Neurological Disorders ◽  
Molecular Mechanisms ◽  
Inflammatory Agent ◽  
And Oxidative Stress

Neurological disorders are diseases of the central and peripheral nervous system that affect millions of people, and the numbers are rising gradually. In the pathogenesis of neurodegenerative diseases, the roles of many signaling pathways were elucidated; however, the exact pathophysiology of neurological disorders and possible effective therapeutics have not yet been precisely identified. This necessitates developing multi-target treatments, which would simultaneously modulate neuroinflammation, apoptosis, and oxidative stress. The present review aims to explore the potential therapeutic use of astaxanthin (ASX) in neurological and neuroinflammatory diseases. ASX, a member of the xanthophyll group, was found to be a promising therapeutic anti-inflammatory agent for many neurological disorders, including cerebral ischemia, Parkinson’s disease, Alzheimer’s disease, autism, and neuropathic pain. An effective drug delivery system of ASX should be developed and further tested by appropriate clinical trials.

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