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The Chemistry of Sight
In his book Darwin's Black Box, the prominent American biochemist Dr. Michael J. Behe stresses that the structure of the living cell and all other biochemical systems were unknown "black boxes" for Darwin and his contemporaries. Darwin assumed that these black boxes possessed very simple structures and could have come about by chance. Now, however, modern biochemistry has opened up these black boxes and revealed the irreducibly complex structure of life. Behe states that Darwin's comments on the emergence of the eye seemed convincing because of the primitive level of nineteenth-century science:  Darwin persuaded much of the world that a modern eye evolved gradually from a simpler structure, but he did not even try to explain where his starting point—the relatively simple light-sensitive spot—came from. On the contrary, Darwin dismissed the question of the eye's ultimate origin… He had an excellent reason for declining the question: it was completely beyond nineteenth-century science. How the eye works—that is, what happens when a photon of light first hits the retina—simply could not be answered at that time.1
So, how does this system, which Darwin glossed over as a simple structure, actually work? How do the cells in the eye's retinal layer perceive the light rays that fall on them? The answer to that question is rather complicated. When photons hit the cells of the retina they activate a chain action, rather like a domino effect. The first of these domino pieces is a molecule called "11-cis-retinal" that is sensitive to photons. When struck by a photon, this molecule changes shape, which in turn changes the shape of a protein called "rhodopsin" to which it is tightly bound. Rhodopsin then takes a form that enables it to stick to another resident protein in the cell called "transducin." Prior to reacting with rhodopsin, transducin is bound to another molecule called GDP. When it connects with rhodopsin, transducin releases the GDP molecule and is linked to a new molecule called GTP. That is why the new complex consisting of the two proteins (rhodopsin and transducin) and a smaller molecule (GTP) is called "GTP-transducin-rhodopsin." But the process has only just begun. The new GTP-transducin-rhodopsin complex can now very quickly bind to another protein resident in the cell called "phosphodiesterase." This enables the phosphodiesterase protein to cut yet another molecule resident in the cell, called cGMP. Since this process takes place in the millions of proteins in the cell, the cGMP concentration is suddenly decreased. How does all this help with sight? The last element of this chain reaction supplies the answer. The fall in the cGMP amount affects the ion channels in the cell. The so-called ion channel is a structure composed of proteins that regulate the number of sodium ions within the cell. Under normal conditions, the ion channel allows sodium ions to flow into the cell while another molecule disposes of the excess ions to maintain a balance. When the number of cGMP molecules falls, so does the number of sodium ions. This leads to an imbalance of charge across the membrane, which stimulates the nerve cells connected to these cells, forming what we refer to as an "electrical impulse." Nerves carry the impulses to the brain and "seeing" happens there.2 In brief, a single photon hits a single cell, and through a series of chain reactions the cell produces an electrical impulse. This stimulus is modulated by the energy of the photon—that is, the brightness of the light. Another fascinating fact is that all of the processes described so far happen in no more than one thousandth of a second. As soon as this chain reaction is completed, other specialized proteins within the cells convert elements such as 11-cis-retinal, rhodopsin and transducin back to their original states. The eye is under a constant shower of photons, and the chain reactions within the eye's sensitive cells enable it to perceive each one of these. The process of sight is actually a great deal more complicated than the outline presented here would indicate. However, even this brief overview is sufficient to demonstrate the extraordinary nature of the system. The eye is so complicated, and finely calculated that it is nonsensical to claim that this system could have come about by chance. The system possesses a totally irreducibly complex structure. If even one of the many molecular parts that enter into a chain reaction with each other were missing, or did not possess a suitable structure, then the system would not function at all. It is clear that this system deals a heavy blow to Darwin's explanation of life by "chance." Michael Behe makes this comment on the chemistry of the eye and the theory of evolution: Now that the black box of vision has been opened, it is no longer enough for an evolutionary explanation of that power to consider only the anatomical structures of whole eyes, as Darwin did in the nineteenth century (and as popularizers of evolution continue to do today). Each of the anatomical steps and structures that Darwin thought were so simple actually involves staggeringly complicated biochemical processes that cannot be papered over with rhetoric.3 The irreducibly complex structure of the eye not only definitively disproves the Darwinist theory, but also shows that life was created. 1. Michael J. Behe, Darwin's Black Box, The Free Press, New York, 1996, p. 18.
2. Michael J. Behe, Darwin's Black Box, The Free Press, New York, 1996, pp. 18-21.
3. Michael J. Behe, Darwin's Black Box, The Free Press, New York, 1996, p. 22. (emphasis added)
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At first glance, bird feathers seem to have a very simple structure. When we study them closer, however, we come across the very complex structure of feathers that are light yet extremely strong and waterproof. 
