Cadmium Chloride Induces Memory Deficits and Hippocampal Damage by Activating the JNK/p66Shc/NADPH Oxidase Axis

2020 ◽  
Vol 39 (5) ◽  
pp. 477-490
Author(s):  
Attalla Farag El-kott ◽  
Ali S. Alshehri ◽  
Heba S. Khalifa ◽  
Abd-El-karim M. Abd-Lateif ◽  
Mohammad Ali Alshehri ◽  
...  
Keyword(s):  
Nadph Oxidase ◽  
Cadmium Chloride ◽  
Nicotinamide Adenine Dinucleotide Phosphate ◽  
Male Rats ◽  
Hippocampal Damage ◽  
Vitro Experiment ◽  
In Vitro Experiment ◽  
In Vivo Experiment

This study investigated whether the mechanism underlying the neurotoxic effects of cadmium chloride (CdCl2) in rats involves p66Shc. This study comprised an initial in vivo experiment followed by an in vitro experiment. For the in vivo experiment, male rats were orally administered saline (vehicle) or CdCl2 (0.05 mg/kg) for 30 days. Thereafter, spatial and retention memory of rats were tested and their hippocampi were used for biochemical and molecular analyses. For the in vitro experiment, control or p66Shc-deficient hippocampal cells were treated with CdCl2 (25 µM) in the presence or absence of SP600125, a c-Jun N-terminal kinase (JNK) inhibitor. Cadmium chloride impaired the spatial learning and retention memory of rats; depleted levels of glutathione and manganese superoxide dismutase; increased reactive oxygen species (ROS), tumor necrosis factor α, and interleukin 6; and induced nuclear factor kappa B activation. Cadmium chloride also decreased the number of pyramidal cells in the CA1 region and induced severe damage to the mitochondria and endoplasmic reticulum of cells in the hippocampi of rats. Moreover, CdCl2 increased the total unphosphorylated p66Shc, phosphorylated (Ser36) p66Shc, phosphorylated JNK, nicotinamide adenine dinucleotide phosphate (NADPH) oxidase, cytochrome c, and cleaved caspase-3. A dose–response increase in cell death, ROS, DNA damage, p66Shc, and NADPH oxidase was also observed in cultured hippocampal cells treated with CdCl2. Of note, all of these biochemical changes were attenuated by silencing p66Shc or inhibiting JNK with SP600125. In conclusion, CdCl2 induces hippocampal ROS generation and apoptosis by promoting the JNK-mediated activation of p66Shc.

Influence of Neuroleptics on Cytotoxic Activity of Rat Natural Killer Cells

1998 ◽  
Vol 11 (2) ◽  
pp. 57-62
Author(s):  
A.J. Madej ◽  
J. Kowalski ◽  
D. Belowski ◽  
Z. S. Herman
Keyword(s):  
Cytotoxic Activity ◽  
Nk Cells ◽  
Nk Cell ◽  
Cell Activity ◽  
Nk Cell Activity ◽  
Vitro Experiment ◽  
In Vitro Experiment ◽  
In Vivo Experiment

The aim of the study was to evaluate the in vivo and in vitro effects of three neuroleptics (chlorpromazine, haloperidol, and sulpiride) on the activity of rat spleen NK cells. In the in vivo experiment, rats were injected with different intraperitoneal doses of neuroleptics given once, for 14 or 28 days. In the in vitro experiment rat spleen NK cells were cultured in medium containing two different concentrations of neuroleptics for three days. The cytotoxic activity of NK cells was evaluated by measuring 51Cr release from YAC-1 target cells after 4-hour incubation. We also measured, using fluorescein-labelled anti-NK monoclonal antibody, the percentage of NK cells in the splenocyte population before and after single intraperitoneal injections of neuroleptics. In the in vitro experiment, both haloperidol (1×10−5 M and 1×10−6 M) and sulpiride (1.5×10−3 M and 1.5×10−4 M) induced a statistically significant decrease in the cytotoxic activity of NK cells. The lower dose of chlorpromazine (6×10−6 M) decreased the cytotoxic activity of NK cells, while the higher dose (6×10−5 M) did not. In the in vivo experiment, both single and repeated doses of chlorpromazine (2 mg /kg /day), haloperidol (0.5 mg/kg/day) and sulpiride (50 mg/kg/day) increased NK cell activity. That effect reflected an increase in NK cell activity but not in the number of NK cells. The study has shown that the immunomodulatory effect of neuroleptics on NK cell activity depends mainly on drug concentrations and experimental conditions.

In Vitro Experimental Investigation of the Integrity of the Stem–Cement Interface

2013 ◽  
Vol 647 ◽  
pp. 53-56
Author(s):  
Hong Yu Zhang ◽  
Leigh Fleming ◽  
Liam Blunt
Keyword(s):  
Experimental Investigation ◽  
Fluid Flow ◽  
Hip Replacement ◽  
Hip Prosthesis ◽  
Vitro Experiment ◽  
Cement Interface ◽  
In Vitro Experiment ◽  
Mechanical Bonding

The rationale behind failure of cemented total hip replacement is still far from being well understood in a mechanical and molecular perspective. In the present study, the integrity of the stem–cement interface was investigated through an in vitro experiment monitoring fluid flow along this interface. The results indicated that a good mechanical bonding formed at the stem–cement interface before debonding of this interface was induced by physiological loadings during the in vivo service of the hip prosthesis.

Surface Changes of Fluoride-Releasing Composites: a Comparison of in Vivo and in Vitro Results

1995 ◽  
Vol 9 (4) ◽  
pp. 348-354 ◽  
Author(s):  
G.E.H.M. Dijkman ◽  
J. De Vries ◽  
W.L. Jongebloed ◽  
J. Arends
Keyword(s):  
Mechanical Properties ◽  
Outer Surface ◽  
Tap Water ◽  
Surface Microhardness ◽  
Vitro Experiment ◽  
In Vitro Experiment ◽  
Over Time ◽  
Surface Changes

Fluoride-releasing composites lose fluoride very slowly over time. An interesting question is the possible change in mechanical properties related to the F release. If this happens, it might be expected that the mechanical properties of the outer surface of a fluoridating composite are affected first. The purpose of this study was to investigate in vivo and in vitro the changes in surface microhardness and surface structure of three fluoride-releasing composites and a non-F-containing control after 28 days. In the in vitro experiment, the composites were stored in tap water at 37°C. The results show that all composites stored in water were significantly softened after 28 days. In vivo, however, a very different picture emerged: The surface microhardness of the fluoride-releasing composites did not change significantly. In vitro, the data indicate that the amount of softening of the fluoridating composites is related to the amount of fluoride released. No relation was found between the amount of F released in one month in vitro and the microhardness changes in vivo. SEM micrographs of fluoridating composites do not reflect the microhardness changes mentioned.

scholarly journals Dextromethorphan Reduces Oxidative Stress and Inhibits Uremic Artery Calcification

2021 ◽  
Vol 22 (22) ◽  
pp. 12277
Author(s):  
En-Shao Liu ◽  
Nai-Ching Chen ◽  
Tzu-Ming Jao ◽  
Chien-Liang Chen
Keyword(s):  
Oxidative Stress ◽  
Nadph Oxidase ◽  
Vascular Calcification ◽  
Wistar Rats ◽  
Nicotinamide Adenine Dinucleotide Phosphate ◽  
Oxidase Inhibitor ◽  
In Vivo Studies ◽  
Ros Production

Medial vascular calcification has emerged as a key factor contributing to cardiovascular mortality in patients with chronic kidney disease (CKD). Vascular smooth muscle cells (VSMCs) with osteogenic transdifferentiation play a role in vascular calcification. Nicotinamide adenine dinucleotide phosphate (NADPH) oxidase inhibitors reduce reactive oxygen species (ROS) production and calcified-medium–induced calcification of VSMCs. This study investigates the effects of dextromethorphan (DXM), an NADPH oxidase inhibitor, on vascular calcification. We used in vitro and in vivo studies to evaluate the effect of DXM on artery changes in the presence of hyperphosphatemia. The anti-vascular calcification effect of DXM was tested in adenine-fed Wistar rats. High-phosphate medium induced ROS production and calcification of VSMCs. DXM significantly attenuated the increase in ROS production, the decrease in ATP, and mitochondria membrane potential during the calcified-medium–induced VSMC calcification process (p < 0.05). The protective effect of DXM in calcified-medium–induced VSMC calcification was not further increased by NADPH oxidase inhibitors, indicating that NADPH oxidase mediates the effect of DXM. Furthermore, DXM decreased aortic calcification in Wistar rats with CKD. Our results suggest that treatment with DXM can attenuate vascular oxidative stress and ameliorate vascular calcification.

scholarly journals A novel pathway spatiotemporally activates Rac1 and redox signaling in response to fluid shear stress

2013 ◽  
Vol 201 (6) ◽  
pp. 863-873 ◽  
Author(s):  
Yunhao Liu ◽  
Caitlin Collins ◽  
William B. Kiosses ◽  
Ann M. Murray ◽  
Monika Joshi ◽  
...  
Keyword(s):  
Nadph Oxidase ◽  
Molecular Mechanisms ◽  
Fluid Shear Stress ◽  
Nicotinamide Adenine Dinucleotide Phosphate ◽  
Redox Signaling ◽  
Hemodynamic Forces ◽  
Rac1 Gtpase ◽  
Embryonic Organ

Hemodynamic forces regulate embryonic organ development, hematopoiesis, vascular remodeling, and atherogenesis. The mechanosensory stimulus of blood flow initiates a complex network of intracellular pathways, including activation of Rac1 GTPase, establishment of endothelial cell (EC) polarity, and redox signaling. The activity of the nicotinamide adenine dinucleotide phosphate (NADPH) oxidase can be modulated by the GTP/GDP state of Rac1; however, the molecular mechanisms of Rac1 activation by flow are poorly understood. Here, we identify a novel polarity complex that directs localized Rac1 activation required for downstream reactive oxygen species (ROS) production. Vav2 is required for Rac1 GTP loading, whereas, surprisingly, Tiam1 functions as an adaptor in a VE-cadherin–p67phox–Par3 polarity complex that directs localized activation of Rac1. Furthermore, loss of Tiam1 led to the disruption of redox signaling both in vitro and in vivo. Our results describe a novel molecular cascade that regulates redox signaling by the coordinated regulation of Rac1 and by linking components of the polarity complex to the NADPH oxidase.

scholarly journals Alternative control of post-harvest diseases in Tainung 1 papaya

2018 ◽  
Vol 48 (1) ◽  
pp. 29-35 ◽  
Author(s):  
Andréa Mirne de Macêdo Dantas ◽  
Selma Rogéria de Carvalho Nascimento ◽  
Beatriz Letícia Silva da Cruz ◽  
Fernando Henrique Alves da Silva ◽  
Márcia Michelle de Queiroz Ambrósio ◽  
...  
Keyword(s):  
Essential Oil ◽  
Mycelial Growth ◽  
Vitro Experiment ◽  
In Vitro Experiment ◽  
Post Harvest ◽  
Randomized Design ◽  
Clove Essential Oil

ABSTRACT Controlling post-harvest papaya diseases without using agrochemicals is a challenge for producers. This study aimed at evaluating the effect of clove essential oil, biological fungicide (Trichodermil®), resistance inducer (Cob Sistem®) and chemical fungicide (Imazacure®) on the in vitro control of phytopathogenic fungi isolates from papaya as well as on the post-harvest quality of Tainung 1 papaya. The in vitro experiment was conducted in a complete randomized design, with five fungal species x five treatments and five replications. The in vivo experiment was conducted in a complete randomized design, with five treatments x five storage times, five replications and three fruits per replication. The fruits were stored under refrigeration at 10 ± 2 ºC and 90 ± 5 % of relative humidity and evaluated at 0, 7, 14, 21 and 28 days of storage, plus two shelf life days at 25 ± 2 ºC, to simulate marketing conditions. The inhibition of mycelial growth was evaluated in the in vitro experiment, while the diseases occurrence and post-harvest quality of the fruits were evaluated in the in vivo experiment. The clove essential oil and Trichodermil® were as efficient as Imazacure® in inhibiting the mycelial growth of Alternaria sp., Colletotrichum gloeosporioides and Rhizopus sp. The treatments with clove essential oil, Trichodermil® and Imazacure® were similar in controlling the pathogens up to 21 days of storage. The treatments had no effect on the fruits soluble solid contents.

scholarly journals Study the effect of the mixture of alcoholic extract of Peganum harmala seeds & Pericarp of Punica granutum on viability of protoscolices of Echinococcus granulosus in vitro and in vivo

2013 ◽  
Vol 7 (2) ◽  
pp. 39-46
Author(s):  
Fawzia Ahmed AL-Shanawi ◽  
Noor Nihad Baker
Keyword(s):  
Echinococcus Granulosus ◽  
Infected Group ◽  
Alcoholic Extract ◽  
Peganum Harmala ◽  
Vitro Experiment ◽  
In Vitro Experiment ◽  
Complete Inactivation

This study included the preparation of the mixture of alcoholic extracts of Peganum harmala seeds and Pericarp of Punica granutum at concentration (1+40), (1.5+45), (2+50) mgml. To study the influence of the mixture of alcoholic extracts of P. harmala and P. granutum on viability of the protoscolices of Echinococcus granulosus In vitro (In tubes), and In vivo (In albaino white mice injected intraperitoneal with protoscolices). In vitro experiment revealed complete inactivation of protoscolices (death) with concentration (2+ 50) mg/ ml after 30 minute. In vivo a significant reduction in weight of liver and spleen occurred in treated groups in comparison to control (untreated) infected group.

An In-Vitro Experiment to Study Sustained Torque on the Spine

2009 ◽  
Author(s):  
Robert Rizza ◽  
Xue-Cheng Liu ◽  
Mohammad Mahinfalah ◽  
Yu Wang ◽  
John Thometz ◽  
...  
Keyword(s):  
Shear Force ◽  
Bone Growth ◽  
Axial Loading ◽  
Spinal Curvature ◽  
Vitro Experiment ◽  
In Vitro Experiment ◽  
Immature Spine ◽  
Tension Loading

In adolescent scoliosis patients, as the vicious cycle hypothesis proposed by Dr. Stokes suggests [1], a lateral spinal curvature produces asymmetrical loading of the skeletally immature spine, which in turn causes asymmetrical growth and therefore progressive wedging deformity. Numerous studies have been done to evaluate the effect of sustained compression or tension loading on the spinal bone growth [2,3]. However, in scoliosis patients, there is not only the asymmetrical axial loading which will worsen the curve progression, but also constant shear force in the transverse plane that may affect the bone growth. So far, no in vivo experiment has been done to study the effect of shear force on the spine. The goal of this study is to design an in vitro experiment that will provide incessant torques in the calves’ tails, and determine the relationship between the magnitude of the torque and change of stress between tail segments.

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