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Biomedical subjects

J F Kuck

Publications and source records attributed to J F Kuck.

48 records · Page 3Linked to original sources

Red fluorescence in older and brunescent human lenses.

Brunescent lenses and normal human lenses more than 70 years old exhibit red fluorescence due to a fluorophor with emission maximum at 672 nm under excitation by the 647.1 nm line of krypton ion laser. The properties and mode of occurrence of this fluorophor suggest that its formation is highly pertinent to senile nuclear pathology.

Adolescent↗

Effect of long-wave ultraviolet light on the lens. I. Model systems for detecting and measuring effect on the lens in vitro.

Rat mouse, and chick lenses incubated with 3-aminotriazole under long-wave ultraviolet (UV) show reduced accumulation and incorporation of leucine and a loss of glutathione. The effect on leucine incorporation is strikingly enhanced when capsule-epithelium pools are incubated. The procedure may identify photosensitizers or metabolic inhibitors which are cataractogenic when acting in conjunction with UV.

Amitrole↗

Laser raman spectroscopy of the lens in situ, measured in an anesthetized rabbit.

We have obtained the first Raman spectrum from the lens of a live animal. A laser beam (514.5 nm; 15 mW) was directed into the eye of an anesthetized rabbit at 60 degrees from the visual axis and Raman emission was collected at 90 degrees from the incident beam. The power density at the retina was estimated at 0.5 W/cm2. The entire scattering column in the lens can be imaged on the entrance slit of a spectrometer with so little distortion that Raman "optical dissection" analysis (Askren, Yu and Kuck (1979) Exp. Eye Res. 29, 647) can be performed on the in situ lens. The advantages of multichannel detectors over photomultiplier tubes with respect to in situ measurements are discussed.

Animals↗

The Emory mouse cataract: an animal model for human senile cataract.

The Emory mouse cataract is a late-appearing lens opacity which may serve as an animal model for some human senile cataracts. It is inherited as an autosomal dominant trait and has a typical course of development. Lens opacities may become readily apparent as early as 6-8 months in mice having a familial history of early cataracto-genesis. Many gross morphologic and microscopic features resemble findings in human senile cataract. As an animal model it has many desirable characteristics. Its slow development permits studies of the lens at the pre-cataractous stage and makes it a good assay system for drugs or other factors affecting cataractogenesis. In this paper are given some morphologic and histologic aspects of the developing cataract.

Age Factors↗

Increased lipid peroxidation and altered membrane functions in Emory mouse cataract.

Lipid peroxidation has been shown to be involved in the pathogenesis of some types of cataract. The possibility of such a mechanism was investigated in Emory mouse cataract. Malondialdehyde, a breakdown product of lipid peroxides, increased 4-fold in advanced cataract. Studies on cation transport revealed that in early cataract there was no alteration in permeability and active transport of cations. However, these functions were significantly altered in advanced cataract as evidenced by about 300% increase in cellular influx of 22Na+ (140 mM) and 50% fall in cellular uptake of 86Rb+ (5 mM). At this stage of cataract, the ouabain- inhibitable component of uptake of Rb+ was drastically decreased, whereas the ouabain-resistant component was unchanged. The mannitol-space increased markedly with progression of cataract. Altered transport of cations in cataract was indicative of damaged membranes which may be due to peroxidation of unsaturated fatty acids in the lipid bilayers concomitant with oxidation of sulfhydryl groups of proteins of the plasma membrane. Superoxide dismutase, catalase and glutathione peroxidase, the defensive enzymes against reactive species of oxygen, were decreased 54%, 57% and 62% respectively in cataract, exposing the lens to oxidants such as 02(-), H202, 0H. and 1 delta 02, which can initiate lipid peroxidation and/or oxidation of protein.

Animals↗