Our aim is to further delineate the relationship between UV exposure, lens aging and cataractogenesis at the molecular level and correlate these data with our other methods of evaluation (optical spectroscopy, morphology, and the CCRG photographic classification system) and with the in vivo methods we have developed (UV slit lamp densitography and surface scanning NMR spectroscopy). We have further refined the UV slit lamp densitographic technique to permit widespread clinical application. An automated program has now been developed which can measure both corneal and lenticular fluorescence levels and provide biometric data as well. This program will be further tested on at least 100 patients during the coming year. In addition to the foregoing biophysical techniques, we are expanding our efforts to perform multiprobe NMR spectroscopy on whole eyes (fresh donor specimens) and on live monkeys and rabbits. We are currently performing 23Na as well as 31P analyses and proton imaging in order to develop specific parameters for in vivo NMR spectroscopy. These two in vivo biophysical approaches will enable us to correlate changes in the living lens with our ongoing multifaceted in vitro spectroscopic analyses. We have also expanded our program in which we perform the Schiempflug photos (with the UV-visible slit lamp apparatus) on patients prior to cataract surgery, and correlate these data with our laboratory analyses on the extracted lens or lens matter from these patients. A similar pilot study involving NMR spectroscopy will be instituted this year. Aside from our ongoing studies on the effects of direct UV radiation exposure on the ocular lens, we are continuing our investigations on (UV) photosensitized damage as exemplified by our work on the Psoralens and Allopurinol. The biophysical (fluorescence) in vivo approach is being applied to such patients, and our in vitro spectroscopic analysis (involving fluorescence, phosphorescence, and NMR spectroscopy) are being utilized to further delineate the types of mechanisms involved in such damage (Type I or Type II reaction).

Agency
National Institute of Health (NIH)
Institute
National Eye Institute (NEI)
Type
Research Project (R01)
Project #
5R01EY001575-13
Application #
3256017
Study Section
Visual Sciences A Study Section (VISA)
Project Start
1978-06-01
Project End
1988-09-29
Budget Start
1987-09-30
Budget End
1988-09-29
Support Year
13
Fiscal Year
1987
Total Cost
Indirect Cost
Name
Emory University
Department
Type
Schools of Medicine
DUNS #
042250712
City
Atlanta
State
GA
Country
United States
Zip Code
30322
Lerman, S (1992) Free radical damage and defense mechanisms in the ocular lens. Lens Eye Toxic Res 9:9-24
Lerman, S (1991) NMR & fluorescence studies on human and animal lenses. Lens Eye Toxic Res 8:121-54
Lerman, S; Mandal, K (1991) Fluorescence polarization and circular dichroism studies on aging human lens proteins. Ophthalmic Res 23:147-53
Lerman, S; Mandal, K; Misra, B et al. (1991) Phototoxicity involving the ocular lens: in vivo and in vitro studies. Photochem Photobiol 53:243-7
Lerman, S; Wandel, T; Schechter, A et al. (1991) In vivo non-invasive studies on the human lens. Magn Reson Imaging 9:525-32
Lerman, S (1991) Evaluation of risk factors in human cataractogenesis. Dev Ophthalmol 21:120-8
Lerman, S (1990) Biophysical methods to monitor lens aging and pre-cataractous changes in vivo. Lens Eye Toxic Res 7:243-9
Lerman, S (1989) In vivo evaluation of lenticular phototoxicity. Lens Eye Toxic Res 6:301-8
Lerman, S; Moran, M (1989) NMR pulse relaxation studies on the normal aging and cataractous lens. Exp Eye Res 48:451-9
Lerman, S (1989) In vivo lens fluorescence as a cataract marker. Dev Ophthalmol 17:60-4

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