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|Title:||The Role of Reactive Oxygen Species in Near-Ultraviolet (320-400 NM) Light Inactivation of Escherichia Coli|
|Author(s):||Sammartano, Lauri Jo|
|Doctoral Committee Chair(s):||Tuveson, Robert W.,|
|Department / Program:||Biology|
|Degree Granting Institution:||University of Illinois at Urbana-Champaign|
|Abstract:||The biological effects of near-UV (320-400 nm; UV-A) radiation are still poorly understood. It has been clearly established, however, that the mechanism of inactivation by these wavelengths differ from that of far-UV (200-290 nm) radiation. The involvement of oxygen in the near-UV inactivation processes lead investigators to suggest that oxygen reactive species such as singlet oxygen and superoxide anion produced during exposure to near-UV.
The purpose of the present study was to further elucidate the mechanism of near-UV inactivation in Escherichia coli. Several genetic and biochemical techniques were employed to examine the role of oxygen reactive species in near-UV mediated damage to DNA and membrane components, and to identify endogenous photosensitizers.
The results demonstrate that the near-UV inactivation process is initiated when the radiant energy is absorbed by components of the respiratory chain, including cytochromes. The absorption of energy causes the chromophore to be electronically excited into the triplet state which leads to subsequent generation of oxygen reactive species within the membrane. The first line of cellular defense against this oxidative stress is a complex network of antioxidants and scavengers, including catalase, superoxide dismutase and glutathione reductase. E. coli cells also have a second line of defense that incorporates repair systems. In this study evidence is provided for an excision repair pathway that is unique to near-UV mediated damage. Results suggest that a unique, but as yet unidentified, DNA lesion occurs in near-UV irradiated cells. Evidence is also presented that shows near-UV mediated damage also occurs in the membrane.
It is now evident that exposure to near-UV radiation initiates a complex series of physiological processes which include photon absorption by photosensitizers; generation of oxygen radicals capable of damaging cellular lipids, proteins, and DNA; and the induction of an extensive array of protective agents.
Thesis (Ph.D.)--University of Illinois at Urbana-Champaign, 1988.
|Date Available in IDEALS:||2015-05-14|