Blue light phototoxicity toward human corneal and conjunctival epithelial cells in basal and hyperosmolar conditions

Abstract

Blue light induced cell death and significant ROS production, and altered the expression of inflammatory genes and operation of the cellular defensive system. We established for the first time that hyperosmolar stress impacted phototoxicity, further suggesting that DED patients might be more sensitive to blue light ocular toxicity.

Blue light exposure in vitro causes toxicity to trigeminal neurons and glia through increased superoxide and hydrogen peroxide generation

“…Oxidative stress and excessive ROS generation are the key factors in the pathogenesis of various ocular surface diseases [36,37]. In the retina and cornea, the phototoxicity of blue light is mostly reported as inducing an oxidative stress [17,18,28,38]. As expected, in our experiments, exposure to 410 nm light increased the rates of hydrogen peroxidase and of mitochondrial superoxide anion.…”

“…However, to the best of our knowledge, no thorough study about the phototoxicity in trigeminal neural cells has been published so far. We previously reported the blue light phototoxicity onto the ocular surface in an in vitro model of dry eye disease (DED) [17] and in vivo, the implication of trigeminal pain-related pathways in ocular inflammation [27]. In the present work, we demonstrate in vitro the major cell death and oxidative stress related cytotoxic impact of blue light on primary cultured neural cells from mouse trigeminal ganglia.…”

“…TGFβ2, one of the major ligands involved in the modulation of cell behavior in ocular tissues [47] and in neural inflammatory responses [48], showed a trend for down-regulation at 410 and 440 nm exposures. We may ascribe this fact to a probable negative loop regulation that turned on when highly stressed cells produced TGFβ2 in excess amount as we have previously proposed for the phototoxically-stressed cells of ocular surface [17]. Moreover, TGFβ2 was reported to have an antiinflammatory role [49], meaning that TGFβ2 underproduction may be partially responsible for an enhanced phototoxicity.…”

“…So far a lot of studies have already investigated the UV and blue-light photodamage related to ocular diseases such as keratitis, cataract, and retinal degeneration [12][13][14][15][16]. Similarly, the interest in dry-eye-related phototoxicity on the ocular surface is constantly growing [17][18][19][20][21][22].…”

Induction of DDIT4 Impairs Autophagy Through Oxidative Stress in Dry Eye

“…5,6 Excessive ROS can cause severe oxidative stress and induce human corneal epithelial cell (HCEC) damage by targeting DNA, proteins, and intracellular processes. [7][8][9][10] However, the ROS-related signaling pathways involved in susceptibility or resistance to cell death in DED have not been thoroughly investigated. Interestingly, one recent work suggested that oxidative stress can regulate macroautophagy (hereafter, autophagy) in the corneal epithelium.…”