Research Institute for Advanced Studies, 1450 South Rolling Road, Baltimore, Maryland.
Plant Physiol. 1966 Jun;41(6):1044-9. doi: 10.1104/pp.41.6.1044.
Ultraviolet light inhibits the photoreduction of 2,6-dichlorophenolindo-phenol or nicotinamide adenine dinucleotide phosphate with water as the electron donor (evolution of oxygen) but not the photoreduction of nicotinamide adenine dinucleotide phosphate with ascorbate as the electron donor. It inhibits photophosphorylation associated with either system. Experiments undertaken to test whether plastoquinone is the site of UV inhibition yielded inconclusive results.Visible light (> 420 mmu) causes the loss of all chloroplast activities, photosystem I being more sensitive than system II. The data suggests 2 modes of action for visible light. The one sensitized by system II results in damage resembling that of UV light. The other, sensitized by system I, results in the destruction of the reaction center of this system.
紫外线抑制 2,6-二氯苯酚靛酚或烟酰胺腺嘌呤二核苷酸磷酸与水作为电子供体的光还原（氧气的进化），但不抑制以抗坏血酸作为电子供体的烟酰胺腺嘌呤二核苷酸磷酸的光还原。它抑制与任一系统相关的光合磷酸化。为了测试质体醌是否是紫外线抑制的部位而进行的实验得出的结果并不明确。可见光（>420nm）会导致所有叶绿体活性的丧失，光系统 I 比光系统 II 更敏感。这些数据表明可见光有两种作用模式。一种由系统 II 敏化，导致类似于紫外线的损伤。另一种由系统 I 敏化，导致该系统反应中心的破坏。
