Harm H
Mutat Res. 1980 Jan;69(1):157-65. doi: 10.1016/0027-5107(80)90185-2.
Photoreactivation (PR) of ultraviolet (254 nm)-inactivated cornea cells of the potoroo (or rat kangaroo; Potorous tridacylus) has been studied at wavelengths greater than 375 nm from either fluorescent "white" light or sunlight. In both cases the PR kinetics curves pass through maxima, which most likely result from the superposition of concomitant inactivation by the photoreactivating light. The inactivating effect of light was directly demonstrated for non-UV-irradiated cells, permitting correction of the PR curves. Wavelengths greater than 475 nm, and even greater than 560 nm, which do not noticeably damage cells, still photoreactivate, though less effectively than shorter wavelengths. Light treatment of UV-inactivated Herpes simplex Virus-1 (HSV-1) after infection leads to PR effects resembling those observed for cells, while light treatment of unirradiated virus after infection likewise causes inactivation. The "fluence-reduction factor" of PR, which is greater than 3 for the virus, exceeds that for the cells, where it decreases with increasing UV fluence. In vitro tests have indicated that sunlight greater than 375 nm causes photorepairable DNA lesions which are virtually fully repaired by the same light. Thus cell inactivation resulting from these solar wavelengths must be due to non-photorepairable damage.
已对长吻袋貂（或鼠袋鼠；长吻袋貂）经紫外线（254纳米）灭活的角膜细胞在波长大于375纳米的荧光“白光”或日光下的光复活（PR）进行了研究。在这两种情况下，PR动力学曲线都经过最大值，这很可能是由于光复活光伴随的灭活作用叠加所致。对于未受紫外线照射的细胞，直接证明了光的灭活作用，从而可以对PR曲线进行校正。波长大于475纳米，甚至大于560纳米的光，虽然对细胞的损伤不明显，但仍能进行光复活，不过其效果不如较短波长的光。感染后对紫外线灭活的单纯疱疹病毒1型（HSV-1）进行光处理会导致类似于细胞所观察到的PR效应，而感染后对未照射的病毒进行光处理同样会导致灭活。PR的“通量降低因子”在病毒中大于3，超过了细胞中的该因子，在细胞中它会随着紫外线通量的增加而降低。体外试验表明，波长大于375纳米的日光会导致可光修复的DNA损伤，而同样的光几乎可以将其完全修复。因此，这些太阳波长导致的细胞灭活必定是由于不可光修复的损伤。
