Bókkon István, Vimal Ram Lakhan Pandey
Doctoral School of Pharmaceutical and Pharmacological Sciences, Semmelweis University, H-1085 Ulloi út 26, Budapest, Hungary.
J Photochem Photobiol B. 2009 Sep 4;96(3):255-9. doi: 10.1016/j.jphotobiol.2009.07.002. Epub 2009 Jul 7.
Spontaneous rhodopsin activation produces discrete noises indistinguishable from single-photon responses. However, there is a serious discrepancy between the apparent energy barrier of thermal events compared with that of the photon-driven process. Current estimates of the activation energies of discrete dark noises in vertebrate rod and cone pigments are approximately 40-50 cal/mol for activation by photon and approximately 20-25 kcal/mol for activation by heat. To reconcile this discrepancy, it was assumed that thermal activation and photon activation of rhodopsin follow different molecular mechanisms. The most convincing hypothesis for a separate low-energy thermal pathway is that the discrete dark noises of rods arise in a small subpopulation of rhodopsins, where the Schiff base linking the chromophore to the protein part has been deprotonated. According to Narici et al.' experiments (2009, Radiation Measurements), phosphene perception in space travel is due to the ionizing radiation-induced free radicals that generate chemiluminescent photons from lipid peroxidation. These photons are absorbed by the photoreceptors chromophores, which modify the rhodopsin molecules (bleaching) and start the photo-transduction cascade resulting in the perception of phosphenes. Here, we point out that not only retinal phosphenes but also the discrete dark noise of rods can be due to the natural redox related (free radical) bioluminescent photons in the retina. In other words, under regulated conditions, lipid peroxidation is a natural process in cells and also in retinal membranes. Since the natural lipid peroxidation is one of the main sources of bioluminescent photons and the photoreceptors have the highest oxygen demand and polyunsaturated fatty acid (PUFA) concentration, there is a continuous, low level bioluminescent photon emission in the retina without any external photonic stimulation. During photopic or scotopic vision, evanescent bioluminescent photon emission is negligible. In contrast, in dark-adapted retinal cells this evanescent bioluminescent photon emission is not negligible. Therefore, our hypothesis is that the discrete dark noise of rods can be due to these bioluminescent photons.
视紫红质的自发激活会产生与单光子响应无法区分的离散噪声。然而，热事件的表观能垒与光子驱动过程的能垒之间存在严重差异。目前对脊椎动物视杆和视锥色素中离散暗噪声激活能的估计，光子激活约为40 - 50卡/摩尔，热激活约为20 - 25千卡/摩尔。为了调和这种差异，人们假定视紫红质的热激活和光子激活遵循不同的分子机制。对于单独的低能热途径，最有说服力的假设是视杆的离散暗噪声出现在一小部分视紫红质中，其中连接发色团与蛋白质部分的席夫碱已经去质子化。根据纳里西等人（2009年，《辐射测量》）的实验，太空旅行中的光幻视是由于电离辐射诱导的自由基从脂质过氧化中产生化学发光光子。这些光子被光感受器发色团吸收，从而改变视紫红质分子（漂白）并启动光转导级联反应，导致光幻视的感知。在此，我们指出，不仅视网膜光幻视，视杆的离散暗噪声也可能归因于视网膜中与自然氧化还原相关（自由基）的生物发光光子。换句话说，在受调控的条件下，脂质过氧化是细胞以及视网膜膜中的一个自然过程。由于自然脂质过氧化是生物发光光子的主要来源之一，且光感受器具有最高的氧需求和多不饱和脂肪酸（PUFA）浓度，因此在没有任何外部光子刺激的情况下，视网膜中存在持续的低水平生物发光光子发射。在明视觉或暗视觉期间，瞬逝的生物发光光子发射可以忽略不计。相比之下，在暗适应的视网膜细胞中，这种瞬逝的生物发光光子发射不可忽略。因此，我们的假设是视杆的离散暗噪声可能归因于这些生物发光光子。
