University of Hertfordshire

NADPH oxidase is the source of ROS in STZ rat aorta: use of the novel highly selective NOX inhibitor VAS2870

Research output: Chapter in Book/Report/Conference proceedingConference contribution

Standard

NADPH oxidase is the source of ROS in STZ rat aorta : use of the novel highly selective NOX inhibitor VAS2870. / Dugic, Elma; Shamsaldeen, Yousif; Benham, Christopher David; MacKenzie, Louise.

Young Life Scientists Symposium 2013. 2013.

Research output: Chapter in Book/Report/Conference proceedingConference contribution

Harvard

Dugic, E, Shamsaldeen, Y, Benham, CD & MacKenzie, L 2013, NADPH oxidase is the source of ROS in STZ rat aorta: use of the novel highly selective NOX inhibitor VAS2870. in Young Life Scientists Symposium 2013. YSL2013: Young Life Scientists Symposium: Cardiovascular Medicine, London, United Kingdom, 6/09/13.

APA

Dugic, E., Shamsaldeen, Y., Benham, C. D., & MacKenzie, L. (2013). NADPH oxidase is the source of ROS in STZ rat aorta: use of the novel highly selective NOX inhibitor VAS2870. In Young Life Scientists Symposium 2013

Vancouver

Dugic E, Shamsaldeen Y, Benham CD, MacKenzie L. NADPH oxidase is the source of ROS in STZ rat aorta: use of the novel highly selective NOX inhibitor VAS2870. In Young Life Scientists Symposium 2013. 2013

Author

Dugic, Elma ; Shamsaldeen, Yousif ; Benham, Christopher David ; MacKenzie, Louise. / NADPH oxidase is the source of ROS in STZ rat aorta : use of the novel highly selective NOX inhibitor VAS2870. Young Life Scientists Symposium 2013. 2013.

Bibtex

@inproceedings{373d822068a8474b8b597534aa325d2f,
title = "NADPH oxidase is the source of ROS in STZ rat aorta: use of the novel highly selective NOX inhibitor VAS2870",
abstract = "Abnormal vascular responsiveness in diabetes has been attributed to a number of changes in contractile and dilatory pathways, affected in part by the overproduction of reactive oxygen species (ROS). It has been reported that NADPH oxidase (NOX) is increased in endothelial cells of streptozotocin (STZ) treated rats, a model of diabetes. However pharmacological tools used in NOX studies are of limited use; the NOX inhibitor apocynin is non-selective and has off-target effects1 and may inhibit nitric oxide synthase. Here we use the novel, highly selective NOX inhibitor VAS28702 to confirm the source of ROS in aorta of STZ rats. Male Wistar rats (250 to 350g) were injected with 65mg/kg STZ; development of diabetes was confirmed after 5 days by testing blood glucose levels. Rats were killed by CO2 asphyxiation, and the thoracic aorta removed and cleaned for mounting in a 20ml organ bath. Aorta were tensioned to 1g, equilibrated and incubated with 10-5M VAS2870, 10-5M apocynin, 150U/ml superoxide dismutase (SOD) or vehicle control (0.1{\%} DMSO) in Kreb’s buffer for 30 minutes, followed by an increasing concentration of phenylephrine (PE).",
author = "Elma Dugic and Yousif Shamsaldeen and Benham, {Christopher David} and Louise MacKenzie",
year = "2013",
month = "9",
language = "English",
booktitle = "Young Life Scientists Symposium 2013",

}

RIS

TY - GEN

T1 - NADPH oxidase is the source of ROS in STZ rat aorta

T2 - use of the novel highly selective NOX inhibitor VAS2870

AU - Dugic, Elma

AU - Shamsaldeen, Yousif

AU - Benham, Christopher David

AU - MacKenzie, Louise

PY - 2013/9

Y1 - 2013/9

N2 - Abnormal vascular responsiveness in diabetes has been attributed to a number of changes in contractile and dilatory pathways, affected in part by the overproduction of reactive oxygen species (ROS). It has been reported that NADPH oxidase (NOX) is increased in endothelial cells of streptozotocin (STZ) treated rats, a model of diabetes. However pharmacological tools used in NOX studies are of limited use; the NOX inhibitor apocynin is non-selective and has off-target effects1 and may inhibit nitric oxide synthase. Here we use the novel, highly selective NOX inhibitor VAS28702 to confirm the source of ROS in aorta of STZ rats. Male Wistar rats (250 to 350g) were injected with 65mg/kg STZ; development of diabetes was confirmed after 5 days by testing blood glucose levels. Rats were killed by CO2 asphyxiation, and the thoracic aorta removed and cleaned for mounting in a 20ml organ bath. Aorta were tensioned to 1g, equilibrated and incubated with 10-5M VAS2870, 10-5M apocynin, 150U/ml superoxide dismutase (SOD) or vehicle control (0.1% DMSO) in Kreb’s buffer for 30 minutes, followed by an increasing concentration of phenylephrine (PE).

AB - Abnormal vascular responsiveness in diabetes has been attributed to a number of changes in contractile and dilatory pathways, affected in part by the overproduction of reactive oxygen species (ROS). It has been reported that NADPH oxidase (NOX) is increased in endothelial cells of streptozotocin (STZ) treated rats, a model of diabetes. However pharmacological tools used in NOX studies are of limited use; the NOX inhibitor apocynin is non-selective and has off-target effects1 and may inhibit nitric oxide synthase. Here we use the novel, highly selective NOX inhibitor VAS28702 to confirm the source of ROS in aorta of STZ rats. Male Wistar rats (250 to 350g) were injected with 65mg/kg STZ; development of diabetes was confirmed after 5 days by testing blood glucose levels. Rats were killed by CO2 asphyxiation, and the thoracic aorta removed and cleaned for mounting in a 20ml organ bath. Aorta were tensioned to 1g, equilibrated and incubated with 10-5M VAS2870, 10-5M apocynin, 150U/ml superoxide dismutase (SOD) or vehicle control (0.1% DMSO) in Kreb’s buffer for 30 minutes, followed by an increasing concentration of phenylephrine (PE).

M3 - Conference contribution

BT - Young Life Scientists Symposium 2013

ER -