If being radiated by 280－300nm UV light, the skin will release chemical substances, which make blood vessels expand and induce inflammation. If the time of radiation is over 24 hours, the skin will turn red, thick, and hard, and then become dry, rough, and dehydrated, etc. Under serious condition, it will lead to sunburn or even skin cancer and also cause cataracts, denaturation and degeneration of the retina, and destructive effects on the immune system (Snustad, D.P., Simmons, M.J., 2010, page 361).

Ultraviolet light is a potent mutagen to the human body. The maximum absorption of UV by DNA is at a wavelength of 254 nm. Maximum mutagenicity also occurs at 254 nm, suggesting that the UV-induced mutation process is mediated directly by the absorption of UV by purines and pyrimidines. In vitro studies show that the pyrimidines absorb strongly at 254 nm and, as a result, become very reactive. Two major products of UV absorption by pyrimidines (thymine and cytosine) are pyrimidine hydrates and pyrimidine dimers. Pyrimidine dimers cause mutations in two ways. (1) Dimers perturb the structure of DNA double helices and interfere with accurate DNA replication. (2) Errors occur during the cellular processes that repair defects in DNA, such as UV-induced thymine dimmers (Snustad, D.P., Simmons, M.J., 2010, page 361).

The human body lacks in one kind of photolyases present in many animals and plants that can repair serious damage caused by exposure to solar radiation. For many photosynthetic organisms, photolyases can directly break the thymine pyrimidine dimmer and finish repairing the damage. Nevertheless, this photolyase mechanism doesn’t work in humans and other placental mammals, and thus make them fail to cope with the frequently-occurring DNA damage.

The skin cells of the New Human Line have the capacity to resist the damage caused by solar radiation. He can utilize the newly-discovered Absolutely Constant Energy Source and the new biological engineering techniques to convert photo-energy to chemical energy, break down the cyclobutane ring in the cyclobutane pyrimidine dimmer, reverse it back to normal bases, and prevent UV-induced mutation and danger. This capacity is therefore called proton reactivation, which can recognize UV-induced dimmers formed by neighboring pyrimidines covalently bonded at the nucleic acid chain, combine with them and start to absorb photons while emitting electrons and protons to the damaged DNA chain, which then break the dimmers into two normal monomers of pyrimidines and reverse them back to original bases.