May 1995
Volume 36, Issue 6
Free
Articles  |   May 1995
Hyperthermia accelerates retinal light damage in rats.
Author Affiliations
  • D T Organisciak
    Department of Biochemistry and Molecular Biology, Wright State University, Dayton, Ohio 45435, USA.
  • R M Darrow
    Department of Biochemistry and Molecular Biology, Wright State University, Dayton, Ohio 45435, USA.
  • W K Noell
    Department of Biochemistry and Molecular Biology, Wright State University, Dayton, Ohio 45435, USA.
  • J C Blanks
    Department of Biochemistry and Molecular Biology, Wright State University, Dayton, Ohio 45435, USA.
Investigative Ophthalmology & Visual Science May 1995, Vol.36, 997-1008. doi:
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    • Get Citation

      D T Organisciak, R M Darrow, W K Noell, J C Blanks; Hyperthermia accelerates retinal light damage in rats.. Invest. Ophthalmol. Vis. Sci. 1995;36(6):997-1008.

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      © ARVO (1962-2015); The Authors (2016-present)

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Abstract

PURPOSE: To study the time course of visual cell damage resulting from hyperthermic light exposure and the possible involvement of rod outer segment (ROS) lipids in the process. METHODS: Rats were acclimated in darkness for 2 hours in a hyperthermic chamber to elevate core body temperature and then exposed to intense green light for up to 4 hours during hyperthermia. After light exposure, the animals were either sacrificed immediately for biochemical or morphologic analysis of retinal light damage or returned to darkness for up to 2 weeks at ambient temperature before analysis. Rod outer segment lipid profiles were characterized, and visual cell loss was determined by rhodopsin and visual cell DNA measurements. Morphology was performed at the light and electron microscopic level. RESULTS: Retinal damage resulting from hyperthermic light exposure was found to be temperature, time, and light intensity dependent. At an elevated environmental temperature of 34.5 degrees, 50% visual cell loss was found after 1.5 hours of 1100 lux light exposure; the same degree of visual cell loss occurred after only 1 hour when rats were maintained at 37 degrees C. At ambient temperatures, 4 hours of light exposure had no effect on visual cell loss. Irrespective of environmental temperature, when rats were maintained in darkness no visual cell loss occurred. Whereas docosahexaenoic acid (22:6) was unchanged in the purest fraction of ROS isolated immediately after light treatment, a 5 mol% loss of the polyunsaturated fatty acid was found in ROS isolated 2 or 24 hours after light exposure. Rod outer segment lipid composition was largely unaffected by hyperthermic light exposure, but the density of some ROS increased. Morphologically, the ROS appeared to be nearly normal immediately after hyperthermic light exposure and structurally more abnormal 2 and 24 hours later. The retinal pigment epithelium exhibited damage immediately after exposure, which also increased 2 and 24 hours later. CONCLUSIONS: Hyperthermia in rats dramatically accelerates retinal light damage compared with light exposure under euthermic conditions. Over loss of ROS 22:6 does not occur during hyperthermic light exposure, but it is apparent during the 24-hour period after light treatment. This suggests that the disappearance of 22:6 from ROS occurs in tandem with the process of visual cell death resulting from retinal light damage.

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