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Eye Damage from Blue Light
Quote by Ray Peat, PhD:
“By the 1960s, several studies had been published showing the inhibition of respiratory enzymes by blue light, and their activation by red light.”
“Old observations such as Warburg’s, that visible light can restore the activity of the “respiratory pigments,” showed without doubt that visible light is biochemically active. By the 1960s, several studies had been published showing the inhibition of respiratory enzymes by blue light, and their activation by red light. The problem to be explained is why the science culture simply couldn’t accept crucial facts of that sort.”
“Red and orange wavelengths penetrate tissue very effectively, because of their tissues because of their weaker absorption of water, allowing them to react with pigments in the cell, such as cytochrome oxidase, which is activated (or re-activated) by red light, increasing production of ATP. This effect counteracts the toxic effects of ultraviolet light, but there are probably other mechanism involved in the many beneficial effects of red light.”
“Blue light is now known to be toxic to the eye, by activating the oxidation of polyunsaturated fatty acids; it has been known to be toxic to various cells, including plant cells, for more than 50 years. In the eye, blue light creates free radicals in melanin, which catalyze the oxidations.”
“Cytochrome oxidase is one of the enzymes damaged by stress and by blue light, and activated or restored by red light, thyroid, and progesterone. It’s a copper enzyme, so it’s likely to be damaged by excess iron. It is most active when it is associated with a mitochondrial lipid, cardiolipin, that contains saturated palmitic acid; the substitution of polyunsaturated fats lowers its activity. Mitochonrial function in general is poisoned by the unsaturated fats, especially arachidonic acid and DHA.”
“Red light is protective, blue light (or u.v.) is harmful, so wearing orange lenses would be helpful. Progesterone and pregnenolone, by reducing the stress reactions, should be helpful–in the eye diseases of infancy and old age, as they are in the respiratory distress syndromes.”
Graefes Arch Clin Exp Ophthalmol. 1993 Jul;231(7):416-23.
Inhibition of cytochrome oxidase and blue-light damage in rat retina.
Chen E.
The activity of cytochrome oxidase, outer nuclear layer thickness, and edema were quantitatively evaluated in the blue-light exposed rat retina. Dark-adapted or cyclic-light reared rats were exposed to blue light with a retinal dose of 380 kJ/m2. Immediately, 1, 2, and 3 day(s) after exposure, the retinas of six rats from each adaptation group were examined. There was no difference between the dark-adapted and cyclic-light reared rats. Immediately after light exposure, cytochrome oxidase activity decreased. The activity in the inner segments remained low at day 1, while severe edema was observed in the inner and outer segments. The outer nuclear layer thickness decreased 1-3 days after exposure. The blue-light exposure inhibited cytochrome oxidase activity and caused retinal injury. Similarity of the injury process in the dark-adapted and cyclic-light reared retinas suggests that rhodopsin was not involved. The inhibition of cytochrome oxidase could be a cause of retinal damage.
Acta Ophthalmol Suppl. 1993;(208):1-50.
Inhibition of enzymes by short-wave optical radiation and its effect on the retina.
Chen E.
Exposure to short-wave optical radiation is a potential hazard for vision. In the present study, blue-light damage is studied in rat retina. It was hypothesized that the absorption of blue light by cytochrome oxidase in rat retina inhibits this enzyme, and may reduce the retinal oxidative metabolism. Irreversible inhibition of the oxidative metabolism may decrease the activity of the Na/K-ATPase, hence redistribute ions, increase intracellular osmotic pressure and cause cellular edema. Severe retinal edema may be the cause of retinal degeneration…Blue light inhibited cytochrome oxidase at a retinal dose of about 110 kJ/m2. This inhibition was reversible, and is probably related to the light regulation of retinal metabolism. At a retinal dose of about 380 kJ/m2, the inhibition of cytochrome oxidase was followed consecutively by a probable redistribution of chlorine and potassium in the inner and outer segments, damage to the mitochondria in the inner segments, edema in the inner and outer segments, and progressive degeneration of photoreceptor cells. Dark adaptation did not increase the blue-light retinal injury. These findings support the hypothesis that inhibition of cytochrome oxidase is one of the causes of blue-light retinal damage. The alteration of enzyme kinetics after in vitro exposure to short-wave optical radiation was estimated using lactate dehydrogenase as a model. The ultraviolet-radiation exposure inhibited lactate dehydrogenase with a significant decrease in maximal velocity, while Michaelis constant remained unchanged.
Curr Eye Res. 1992 Sep;11(9):825-31.
Cytochrome oxidase activity in rat retina after exposure to 404 nm blue light.
Chen E, Söderberg PG, Lindström B.
Cytochrome oxidase (CYO), a key enzyme in the respiratory chain, was observed as an indicator of retinal metabolism after an in vivo blue light exposure. Thirty Sprague-Dawley rats were exposed to optic radiation of 404 nm with a retinal dose of 110kJ/m2. Immediately after exposure, the CYO activity in the pigment epithelium, in the outer and inner segments of photoreceptors, and in the outer plexiform layer of the exposed retina, was reduced to one-third-to-half of the control level. However, there was an increase in CYO activity in the exposed retina one day after exposure. One week after exposure, the CYO activity in the inner segment and the outer plexiform layer was higher, while the activity in the other two layers was lower, than that at one day, although still higher than in the control. Two weeks after exposure, the CYO activity in the four retinal layers returned to the level of the control retina, as did the activity four weeks after. After exposure, no ophthalmoscopically visible retinal change and no light-microscopically evident morphological alterations were found. There was no retinal edema or loss of photoreceptor cells. The observed alteration in CYO activity after blue light exposure may represent an inhibition of retinal metabolism. The inhibition was reversible. If this compensation mechanism is overwhelmed, retinal damage may occur.
