Posted: Jun 23, 2014 10:20 pm
Meanwhile, a thought has just crossed my mind.
The idea that photo-oxidative damage to opsins could be a factor here, omits one key feature. Namely, that opsins are replaced over time. We don't just start off with one collection of opsin molecules, which have to serve us for the rest of our lives. Replacement opsins are manufactured metabolically. Otherwise, why would Vitamin A be an essential part of our diet?
Plus, vertebrate opsins are different from those of invertebrates. According to here, vertebrates use Go and Gs family opsins, whilst arthropods and molluscs (including cephalopods) use Gq family opsins.
Furthermore, according to this page on the Visual Cycle, recharging of "spent" opsins is performed by at least one reducingenzyme. Which would seem to be a factor mitigating against oxidative damage, if the same reducing process is found in organisms other than vertebrates. Metabolic replacement of opsins damaged oxidatively in ways unrecoverable by those enzymes would solve the problem in any case.
EDIT: A far more comprehensive treatment can be found here, a page devoted to comprehensive physiology and molecular biology of the eye.
The idea that photo-oxidative damage to opsins could be a factor here, omits one key feature. Namely, that opsins are replaced over time. We don't just start off with one collection of opsin molecules, which have to serve us for the rest of our lives. Replacement opsins are manufactured metabolically. Otherwise, why would Vitamin A be an essential part of our diet?
Plus, vertebrate opsins are different from those of invertebrates. According to here, vertebrates use Go and Gs family opsins, whilst arthropods and molluscs (including cephalopods) use Gq family opsins.
Furthermore, according to this page on the Visual Cycle, recharging of "spent" opsins is performed by at least one reducingenzyme. Which would seem to be a factor mitigating against oxidative damage, if the same reducing process is found in organisms other than vertebrates. Metabolic replacement of opsins damaged oxidatively in ways unrecoverable by those enzymes would solve the problem in any case.
EDIT: A far more comprehensive treatment can be found here, a page devoted to comprehensive physiology and molecular biology of the eye.