https://faculty.missouri.edu/~glaserr/3700s14/Antioxidant_Carotenoids_2005.pdf

Carotenoid actions and their relation to health and disease.

Evidence for protection against age-related macular degeneration by carotenoids and antioxidant vitamins

Proton therapy treatments are based on a proton RBE (relative biological effectiveness) relative to high-energy photons of 1.1. The use of this generic, spatially invariant RBE within tumors and normal tissues disregards the evidence that proton RBE varies with linear energy transfer (LET), physiological and biological factors, and clinical endpoint.Based on the available experimental data from published literature, this review analyzes relationships of RBE with dose, biological endpoint and physical properties of proton beams. The review distinguishes between endpoints relevant for tumor control probability and those potentially relevant for normal tissue complication. Numerous endpoints and experiments on sub-cellular damage and repair effects are discussed.Despite the large amount of data, considerable uncertainties in proton RBE values remain. As an average RBE for cell survival in the center of a typical spread-out Bragg peak (SOBP), the data support a value of ~1.15 at 2 Gy/fraction. The proton RBE increases with increasing LETd and thus with depth in an SOBP from ~1.1 in the entrance region, to ~1.15 in the center, ~1.35 at the distal edge and ~1.7 in the distal fall-off (when averaged over all cell lines, which may not be clinically representative). For small modulation widths the values could be increased. Furthermore, there is a trend of an increase in RBE as (α/β)x decreases. In most cases the RBE also increases with decreasing dose, specifically for systems with low (α/β)x. Data on RBE for endpoints other than clonogenic cell survival are too diverse to allow general statements other than that the RBE is, on average, in line with a value of ~1.1.This review can serve as a source for defining input parameters for applying or refining biophysical models and to identify endpoints where additional radiobiological data are needed in order to reduce the uncertainties to clinically acceptable levels.

https://iopscience.iop.org/article/10.1088/0031-9155/59/22/R419/pdf

Relative biological effectiveness (RBE) values for proton beam therapy. Variations as a function of biological endpoint, dose, and linear energy transfer

The macular region of the primate retina is yellow in color due to the presence of the macular pigment, composed of two dietary xanthophylls, lutein and zeaxanthin, and another xanthophyll, meso-zeaxanthin. The latter is presumably formed from either lutein or zeaxanthin in the retina. By absorbing blue-light, the macular pigment protects the underlying photoreceptor cell layer from light damage, possibly initiated by the formation of reactive oxygen species during a photosensitized reaction. There is ample epidemiological evidence that the amount of macular pigment is inversely associated with the incidence of age-related macular degeneration, an irreversible process that is the major cause of blindness in the elderly. The macular pigment can be increased in primates by either increasing the intake of foods that are rich in lutein and zeaxanthin, such as dark-green leafy vegetables, or by supplementation with lutein or zeaxanthin. Although increasing the intake of lutein or zeaxanthin might prove to be protective against the development of age-related macular degeneration, a causative relationship has yet to be experimentally demonstrated.

Biologic mechanisms of the protective role of lutein and zeaxanthin in the eye.

A GROWING body of literature attests to the deleterious effects of long term exposure to light1–8. To define more critically the differences between thermal and photochemical effects, we have exposed the retinae of rhesus monkeys to eight monochromatic laser lines from 1,064–441.6 nm. Thermal damage to the retina is to be expected for the 1,064-nm line since the photopigments are not involved and energy absorption takes place predominantly in the melanin granules of the pigment epithelium and the choroid. Although data on pathogenesis are not yet available, we found some interesting differences in retinal sensitivity in going from the near infrared to the blue wavelengths in the visible spectrum.

Retinal sensitivity to damage from short wavelength light

—Exposure of the retina of the rhesus monkey to visible and infrared radiation from CW optical sources like the Sun, xenon lamps, etc. produces small lesions or scotomata which may be classified as thermal or photochemical, depending on the wavelength and duration of exposure. The action spectrum for the production of retinal lesions has been determined for eight monochromatic laser wavelengths extending from 1064 to 441 nm. The corneal power required to produce a lesion decreases by three orders of magnitude in going from 1064 to 441 nm. Exposure to 1064 nm radiation for 1000 s produces a typical thermal lesion at elevated retinal temperatures. whereas a 1000 s exposure to 441 nm light produces a photochemical lesion at power levels too low to raise the retinal temperature by an appreciable amount (<0.1°). The two types of lesion have entirely different characteristics as will be discussed in some detail. The photopathology of thc photochemical lesion has been studied at postexposure times ranging from 1 h to 90 days and will be demonstrated in a number of histological slides. Moreover, this photopathology correlates well with monocular visual acuity tests in the rhesus monkey as defined by the Landolt ring technique.

To further elucidate the differential effects on the retina of short vs long wavelength CW radiation, we have divided a simulated solar spectrum at sea level into two spectral bands. 400–800 nm and 700–1400 nm, and determined the radiant exposures required to produce very mild lcsions on the rhesus retina for exposure times of 1, 10, 100 and 1000 s. To correlate our data with solar retinitis and eclipse blindness the image diameter or spot size on the retina was 159 μm, corresponding to the image size of the Sun on the human retina. Exposure to the 400–800 nm spectrum for durations of 10 s or greater required approximately 400 J/cm2 to produce a mild photochemical lesion. Reciprocity is maintained over the exposure range 10–1000 s. Radiant exposure to the 700–1400 nm spectrum, on the other hand, required roughly 69,100 J/cm2 for a 1000 s exposure. This was a mild thermal lesion. We were unable to produce a lesion for exposure times less than 1000 s. We interpret these data to mean that solar retinitis and eclipse blindness are primarily photochemical events produced by the short wavelength component of the solar spectrum, and that the infrared component of the solar spectrum plays only a minor role in these retinal pathologies.

Sensitivity of the retina to radiation damage as a function of wavelength

The nature of retinal radiation damage: Dependence on wavelength, power level and exposure time

An optical source simulating the sun at the top of the atmosphere has been constructed and used to obtain retinal burn thresholds in the rhesus monkey for image diameters corresponding to that of the solar disk on the human retina. Powers incident on the cornea and retinal irradiances required to produce threshold lesions are given for exposure times ranging from 1 s to 3 min. The ocular hazards associated with viewing the sun through aircraft window systems are assessed in terms of these data. Also, radiation in the near infrared is shown to be less dangerous than visible light in producing thermal injury to the retina.

Ocular hazard from viewing the sun unprotected and through various windows and filters.

The transmission of light; through the ocular media of the rabbit eye.

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