Antioxidants Aleviate Nicotine-Induced Platelet Aggregation in Cerebral Arterioles of Mice in Vivo

Physiological Research ◽

10.33549/physiolres.932114 ◽

2011 ◽

pp. 695-700 ◽

Cited By ~ 5

Author(s):

M. A. FAHIM ◽

A. NEMMAR ◽

S. SINGH ◽

M. Y. HASSAN

Keyword(s):

Experimental Data ◽

Vitamin E ◽

Platelet Aggregation ◽

Vitamin C ◽

Total Blood ◽

Cerebral Microvessels ◽

Cerebral Arterioles ◽

Total Blood Flow ◽

Cerebral Microvessel

Experimental data on the effect of nicotine on cerebral microvessel thrombosis is lacking. Therefore, this study was carried out to elucidate the effects of nicotine on platelet aggregation in cerebral (pial) microcirculation of the mouse, and the possible protective effect of vitamins C and E. Male TO mice were divided into six groups, and injected i.p. with saline as a control, nicotine (1 mg/kg), vitamin C alone (100 mg/kg), vitamin E alone (100 mg/kg), nicotine plus vitamin C or nicotine plus vitamin E, all for one week before the experiment. After one week, platelet aggregation in cerebral microvessels of these groups of mice were studied in vivo. The appearance of the first platelet aggregation and total blood flow stop in arterioles and venules were timed in seconds. In the animals treated with nicotine, venules did not show any alteration in the platelet aggregation time in comparison to the control animals. However, in arterioles platelet aggregation time was significantly accelerated (p<0.001) in nicotine-treated animals as compared to controls. Both vitamins C and E prevented the shortening of arteriolar platelet aggregation time significantly (p<0.001) when applied with nicotine but not alone. It can be concluded that nicotine enhances the susceptibility to thrombosis in the cerebral arterioles in vivo and that vitamins C and E have alleviating effect on nicotine-induced thrombotic events in mice pial microvessels.

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Effectiveness of Vitamin C and Vitamin E Antioxidant Combination on Caspase-3 Expression in Wistar White Rat Pulmonum Contusion

Sriwijaya Journal of Surgery ◽

10.37275/sjs.v3i1.26 ◽

2020 ◽

Vol 3 (1) ◽

pp. 31-44

Author(s):

Bermansyah ◽

Gama Satria ◽

Ahmad Umar

Keyword(s):

Cell Death ◽

Vitamin E ◽

Vitamin C ◽

Wistar Rats ◽

Caspase 3 ◽

Cell Function ◽

Pulmonary Contusion ◽

Tnf Α ◽

Male Wistar Rats

Introduction.Pulmonary contusions can cause a progressive inflammatory response. Activation of TNF-α cytokines and reactive oxygen species (ROS) can cause pulmonary cell death. Antioxidants can have the potential to neutralize ROS. The purpose of this study is to determine the effectiveness of antioxidant administration in maintaining pulmonary cell function in wistar rats that have been induced to experience pulmonary contusions through caspase-3 levels. Methods.This study was an in vivo experimental study conducted on thirty male wistar rats and divided into five groups (n = 6): control, pulmonary contusion + asthaxanthine 5 mg/kgBW, pulmonary contusion + vitamin C and E 50 mg/kgBW, pulmonary contusion + vitamin C and E 100 mg/kgBW, pulmonary contusion + vitamin C and E 200 mg/kgBW. The value of Caspase-3 is evaluated by the IHC. All data analyzes used SPSS 18. Results. Low doses of antioxidants have the potential to reduce pulmonary cell death in wistar rats induced by pulmonary contusions.Conclussion. Vitamin C and E effective to reduce polmonary cell death in pulmonary contusion.Keywords: antioxidants, vitamin C, vitamin E, pulmonary contusions animal model, apoptosis, caspase-3

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In vivo changes in antioxidant systems and protective role of melatonin and a combination of vitamin C and vitamin E on oxidative damage in erythrocytes induced by chlorpyrifos-ethyl in rats

Archives of Toxicology ◽

10.1007/s002040100219 ◽

2001 ◽

Vol 75 (2) ◽

pp. 88-96 ◽

Cited By ~ 183

Author(s):

Fatih Gultekin ◽

Namik Delibas ◽

Sulhattin Yasar ◽

Ibrahim Kilinc

Keyword(s):

Vitamin E ◽

Vitamin C ◽

Oxidative Damage ◽

Protective Role ◽

Antioxidant Systems ◽

Chlorpyrifos Ethyl

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Chronic Lead Treatment Accelerates Photochemically Induced Platelet Aggregation in Cerebral Microvessels of Mice, in Vivo

Environmental Research ◽

10.1006/enrs.1995.1024 ◽

1995 ◽

Vol 69 (1) ◽

pp. 51-58 ◽

Cited By ~ 3

Author(s):

A.H. Aldhaheri ◽

F. Elsabban ◽

M.A. Fahim

Keyword(s):

Platelet Aggregation ◽

Cerebral Microvessels

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Determination of tissue-specific interaction between vitamin C and vitamin E in vivo using senescence marker protein-30 knockout mice as a vitamin C synthesis deficiency model

British Journal Of Nutrition ◽

10.1017/s0007114521004384 ◽

2021 ◽

pp. 1-33

Author(s):

Ayami Sato ◽

Yuka Takino ◽

Tomohiro Yano ◽

Koji Fukui ◽

Akihito Ishigami

Keyword(s):

Gene Expression ◽

Vitamin E ◽

Vitamin C ◽

Specific Interaction ◽

Marker Protein ◽

Tissue Specific ◽

Transfer Protein

Abstract Vitamin E (α-tocopherol; VE) is known to be regenerated from VE radicals by vitamin C (L-ascorbic acid; VC) in vitro. However, their in vivo interaction in various tissues is still unclear. Therefore, we alternatively examined the in vivo interaction of VC and VE by measurement of their concentrations in various tissues of senescence marker protein-30 (SMP30) knockout (KO) mice as a VC synthesis deficiency model. Male SMP30-KO mice were divided into four groups (VC+/VE+, VC+/VE-, VC-/VE+, and VC-/VE-), fed diets with or without 500 mg/kg VE and given water with or without 1.5 g/L VC ad libitum. Then, VC and VE concentrations in the plasma and various tissues were determined. Further, gene expression levels of transporters associated with VC and VE, such as α-tocopherol transfer protein (α-TTP) and sodium-dependent vitamin C transporters (SVCTs), were examined. These results showed that the VE levels in the VC-depleted (VC-/VE+) group were significantly lower than those in the VC+/VE+ group in the liver and heart; the VC levels in the VE-depleted (VC+/VE-) group were significantly lower than those in the VC+/VE+ group in the kidneys. The α-TTP gene expression in the liver and kidneys were decreased by VC and/or VE depletion. Moreover, SVCT1 gene expression in the liver was decreased by both VC and VE depletion. In conclusion, these results indicate that VC spares VE mainly in the liver and heart, and that VE spares VC in the kidneys of SMP30-KO mice. Thus, interaction between VC and VE is likely to be tissue specific.

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Inhibiting NOS blocks microvascular recruitment and blunts muscle glucose uptake in response to insulin

AJP Endocrinology and Metabolism ◽

10.1152/ajpendo.00021.2003 ◽

2003 ◽

Vol 285 (1) ◽

pp. E123-E129 ◽

Cited By ~ 180

Author(s):

M. A. Vincent ◽

E. J. Barrett ◽

J. R. Lindner ◽

M. G. Clark ◽

S. Rattigan

Keyword(s):

Nitric Oxide ◽

Skeletal Muscle ◽

Blood Flow ◽

Glucose Uptake ◽

Glucose Disposal ◽

Total Blood ◽

Artery Flow ◽

Microvascular Recruitment ◽

Total Blood Flow

We examined the effects of inhibiting nitric oxide synthase with Nω-nitro-l-arginine-methyl ester (l-NAME) on total hindlimb blood flow, muscle microvascular recruitment, and hindlimb glucose uptake during euglycemic hyperinsulinemia in vivo in the rat. We used two independent methods to measure microvascular perfusion. In one group of animals, microvascular recruitment was measured using the metabolism of exogenously infused 1-methylxanthine (1-MX), and in a second group contrast-enhanced ultrasound (CEU) was used. Limb glucose uptake was measured by arterial-venous concentration differences after 2 h of insulin infusion. Saline alone did not alter femoral artery flow, glucose uptake, or 1-MX metabolism. Insulin (10 mU·min-1·kg-1) significantly increased hindlimb total blood flow (0.69 ± 0.02 to 1.22 ± 0.11 ml/min, P < 0.05), glucose uptake (0.27 ± 0.05 to 0.95 ± 0.08 μmol/min, P < 0.05), 1-MX uptake (5.0 ± 0.5 to 8.5 ± 1.0 nmol/min, P < 0.05), and skeletal muscle microvascular volume measured by CEU (10.0 ± 1.6 to 15.0 ± 1.2 video intensity units, P < 0.05). Addition of l-NAME to insulin completely blocked the effect of insulin on both total limb flow and microvascular recruitment (measured using either 1-MX or CEU) and blunted glucose uptake by 40% ( P < 0.05). We conclude that insulin specifically recruits flow to the microvasculture in skeletal muscle via a nitric oxide-dependent pathway and that this may be important to insulin's overall action to regulate glucose disposal.

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The Therapeutic Relevance of Vitamin E

Revista de Chimie ◽

10.37358/rc.19.10.7630 ◽

2019 ◽

Vol 70 (10) ◽

pp. 3711-3713

Author(s):

Lucretia Anghel ◽

Liliana Baroiu ◽

Adrian Beznea ◽

Gabi Topor ◽

Camelia Ana Grigore

Keyword(s):

Oxidative Stress ◽

Immune System ◽

Vitamin E ◽

Platelet Aggregation ◽

Vitamin C ◽

Active Form ◽

Alpha Tocopherol ◽

Mitochondrial Activity ◽

Metabolic Function ◽

Therapeutic Relevance

Maintaining cellular homeostasis in the context of its normal metabolic function is achieved by establishing the balance between its own antioxidant capacity and the level of harmful compounds resulting from the mitochondrial activity and the immune system. One of the antioxidants involved in this process is vitamin E with its most active form - alpha-tocopherol, which exerts its functions through vitamin C. The main functions of this antioxidant are: regulation of platelet aggregation, cellular signaling, antioxidation. The therapeutic relevance of vitamin E has increased due to the incrimination of oxidative stress as a link in the pathophysiology of many chronic diseases. Respectively, the role most targeted is that of antioxidant.

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Carbon monoxide mediates vasodilator effects of glutamate in isolated pressurized cerebral arterioles of newborn pigs

AJP Heart and Circulatory Physiology ◽

10.1152/ajpheart.00881.2002 ◽

2003 ◽

Vol 284 (4) ◽

pp. H1073-H1079 ◽

Cited By ~ 42

Author(s):

Elisa Fiumana ◽

Helena Parfenova ◽

Jonathan H. Jaggar ◽

Charles W. Leffler

Keyword(s):

Carbon Monoxide ◽

Nmda Receptor ◽

Receptor Agonist ◽

Cerebral Microvessels ◽

Excitatory Neurotransmitter ◽

Dimanganese Decacarbonyl ◽

Cerebral Arterioles ◽

Newborn Pigs ◽

Adrenergic Receptor Agonist

The excitatory neurotransmitter glutamate causes dilation of newborn pig cerebral arterioles in vivo that is blocked by inhibition of carbon monoxide (CO) production. CO, a potent dilator in cerebral circulation in vivo, is produced endogenously in cerebral microvessels via heme oxygenase (HO). In isolated pressurized cerebral arterioles (∼200 μm) from newborn pigs, we investigated the involvement of CO and the endothelium in response to glutamate. A CO-releasing molecule, dimanganese decacarbonyl (10−8–10−6 M), dilated cerebral arterioles. Glutamate (10−6–10−4 M) and 1-aminocyclopentane- cis-1,3-dicarboxylic acid ( cis-ACPD; 10−6–10−5 M), a N-methyl-d-aspartate (NMDA) receptor agonist, caused cerebral vascular dilation. Dilation of cerebral arterioles to glutamate and cis-ACPD was abolished by chromium mesoporphyrin (CrMP; 10−6 M), a HO inhibitor. In contrast, CrMP did not alter dilation to isoproterenol, a β-adrenergic receptor agonist. Endothelium-denuded cerebral arterioles did not dilate to glutamate or bradykinin (endothelium-dependent dilator), whereas responses to isoproterenol were preserved. These data indicate that cerebral arterioles from newborn pigs may directly respond to glutamate and the NMDA receptor agonists by endothelium-dependent dilation that involves stimulation of CO production via the HO pathway in the endothelium.

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