Hostname: page-component-7479d7b7d-767nl Total loading time: 0 Render date: 2024-07-10T10:26:06.713Z Has data issue: false hasContentIssue false

A Cytochemical Study of NADH Oxidase and H2O2 in Developing Atheromas

Published online by Cambridge University Press:  02 July 2020

E. Ann Ellis
Affiliation:
Department of Medicine, University of Florida, Gainesville, FL32610
David M. Bush
Affiliation:
Department of Medicine, University of Florida, Gainesville, FL32610
Thomas J. Wargovich
Affiliation:
Department of Medicine, University of Florida, Gainesville, FL32610
Maria B. Grant
Affiliation:
Department of Medicine, University of Florida, Gainesville, FL32610
Get access

Extract

Recent data suggests that reactive oxygen species (ROS) play a role in the progression of atherosclerosis. Superoxide (O2˙−) and its free radical metabolites can participate in the oxidation of LDLs, activation of proto-oncogenes and promotion of cellular growth. Endothelial and vascular smooth muscle cells are capable of producing O2˙− and other ROS. A major source of O2˙- and other reactive ROS in vascular tissues is a membrane associated NADH oxidase. This paper presents a study of NADH oxidase by cytochemical localization in developing atheromas in a rabbit model of diet-induced atherosclerosis.

NADH oxidase generates O2˙− which dismutates to hydrogen peroxide (H2O2). Cerium perhydroxide, an electron dense precipitate of cerium and H2O2, is the reaction product of NADH oxidase. Cytochemical localization of NADH oxidase was done by the cerium method in developing atheromas in abdominal aorta and iliac arteries of New Zealand rabbits made atherosclerotic by feeding a diet of 0.2% cholesterol/5% peanut oil over four months.

Type
From Scanning Probe Microscopy to High Resolution Ultrasound: New Versions of the Vasculature
Copyright
Copyright © Microscopy Society of America 1997

Access options

Get access to the full version of this content by using one of the access options below. (Log in options will check for institutional or personal access. Content may require purchase if you do not have access.)

References

1.Mohazzab, H. K. M.et al., Amer. J. Physiol., 266(1994)H2568.Google Scholar
2.Briggs, R. T.et al., J. Cell Biol., 67(1975)566.10.1083/jcb.67.3.566CrossRefGoogle Scholar
3.Rosenfeld, M. E.et al., Arteriosclerosis, 7(1987)9.10.1161/01.ATV.7.1.9CrossRefGoogle Scholar
4.Ellis, E. A.et al., Proc. 51st Ann. MSA Meeting, (1993)318.10.1017/S0424820100147430Google Scholar
5.Schubert, J. and Wilmer, J. W., Free Rad. Biol. Med., 11(1991)545.10.1016/0891-5849(91)90135-PCrossRefGoogle Scholar
6.Baas, A. S. and Berk, B. C., Circ. Res., 77(1995)29.10.1161/01.RES.77.1.29CrossRefGoogle Scholar