PARP-1 Is a Potential Marker of Retinal Photooxidation and a Key Signal Regulator in Retinal Light Injury

Abstract

Advancements in technology have resulted in increasing concerns over the safety of eye exposure to light illumination, since prolonged exposure to intensive visible light, especially to short-wavelength light in the visible spectrum, can cause photochemical damage to the retina through a photooxidation-triggered cascade reaction. Poly(ADP-ribose) polymerase-1 (PARP-1) is the ribozyme responsible for repairing DNA damage. When damage to DNA occurs, including nicks and breaks, PARP-1 is rapidly activated, synthesizing a large amount of PAR and recruiting other nuclear factors to repair the damaged DNA. However, retinal photochemical damage may lead to the overactivation of PARP-1, triggering PARP-dependent cell death, including parthanatos, necroptosis, and autophagy. In this review, we retrieved targeted articles with the keywords such as “PARP-1,” “photoreceptor,” “retinal light damage,” and “photooxidation” from databases and summarized the molecular mechanisms involved in retinal photooxidation, PARP activation, and DNA repair to clarify the key regulatory role of PARP-1 in retinal light injury and to determine whether PARP-1 may be a potential marker in response to retinal photooxidation. The highly sensitive detection of PARP-1 activity may facilitate early evaluation of the effects of light on the retina, which will provide an evidentiary basis for the future assessment of the safety of light illumination from optoelectronic products and medical devices.

Types of Cell Death That Occurred Due to the Influence of Active Forms of Oxygen and Damage to Dna

“…Полімер PAR, який в основному утворюється в ядрі, здатний переміщатися в цитозоль, а потім і в мітохондрії, де зв'язується з апоптозініціюючим фактором (AIF) і сприяє його транслокації в ядро. Фактор, потрапляючи в ядро, викликає конденсацію хроматину і активує ендонуклеази, які також беруть участь у фрагментації ДНК, таким чином настає клітинна загибель [39,40]. Партанатос як варіант програмованої клітинної загибелі, ініційованої гіперактивацією PARP-1, котра реалізується у вигляді енергетичної катастрофи, пов'язаної з пошкодженням ДНК, вдалося виявити при таких станах, як гіпоксія, оксидативний стрес, запалення, гіпоглікемія.…”

Roles of DNA damage repair and precise targeted therapy in renal cancer (Review)

“…PARP is associated with necroptosis, autophagy and other types of cell death (53). PARP is cleaved by activated caspases both in vitro and in vivo, resulting into two fragments of 24 and 89 kDa, which is deemed to be a hallmark of the apoptosis (54).…”