Natural visible light is an electromagnetic wave composed of a spectrum of monochromatic wavelengths, each with a characteristic color. Photons are the basic units of light, and their wavelength correlates to the energy of light; short-wavelength photons carry high energy. The retina is a fragile neuronal tissue that senses light and generates visual signals conducted to the brain. However, excessive and intensive light exposure will cause retinal light damage. Within the visible spectrum, short-wavelength light, such as blue light, carries higher energy, and thus the retinal injury, is more significant when exposed to these wavelengths. The damage mechanism triggered by different short-wavelength light varies due to photons carrying different energy and being absorbed by different photosensitive molecules in the retinal neurons. However, photooxidation might be a common molecular step to initiate cell death. Herein, we summarize the historical understanding of light, the key molecular steps related to retinal light injury, and the death pathways of photoreceptors to further decipher the molecular mechanism of retinal light injury and explore potential neuroprotective strategies.

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.