RT Journal Article
T1 Melatonin counteracts oxidative damage in lens by regulation of Nrf2 and NLRP3 inflammasome activity
A1 Lledó Mayans, Victoria Eugenia
A1 Alkozi, Hanan Awad
A1 Sánchez Naves, Juan
A1 Fernández Torres, Miguel Ángel
A1 Guzmán Aránguez, Ana Isabel
AB Oxidative stress, generated because of an imbalance between reactive oxygen species (ROS) generation and elimination, is associated with lens damage and cataract progression. ROS generation is known to activate NLRP3(nucleotide-binding oligomerization domain-like receptor family, pyrin domain-cointaining 3) inflammasome, and is believed to be an important link between oxidative stress and inflammation, that is also related to cataract development. Potential oxidative hazard to the lens by white light-emitting diode (LED) light, a source of illu-mination commonly used nowadays, has been suggested, although available information is limited. In this work,we evaluated the cytotoxicity induced by hydrogen peroxide (an oxidative stressor agent) and white LED light in lens epithelial cells as well as melatonin ability to counteract the effects induced by them. Melatonin is a neurohormone secreted by different ocular structures that could be useful to alleviate oxidative damage induced by different oxidative stressors in lens. Particularly, the modulation of Nrf2 (nuclear erythroid 2-related factor)/Keap 1 (Kelch-like ECH-associated protein 1), an essential oxidative stress regulator, and NLRP3 activity by melatonin was evaluated in lens epithelial cells. ROS levels rose after white LED light exposure and cell viability was reduced after challenge with oxidative stressor agents. Melatonin prevented cell death triggered by hydrogen peroxide and white LED light, precluded ROS generation induced by white LED light and promoted antioxidant lens capacity through upregulation of Nrf2 protein levels and SOD activity. NLRP3, caspase-1 and IL1-β expression significantly increased in human lens cells exposed to H2O2 or irradiated with white LED light.Activation of NLRP3 inflammasome triggered by oxidative stressors was also abrogated by melatonin. Attenuation of inflammatory and cytotoxic effects induced by oxidative stressors provided by melatonin in lens indicate the interest of this molecule as a potential therapeutic agent for cataract prevention/management
PB Elsevier
SN 0014-4835
YR 2021
FD 2021-12-30
LK https://hdl.handle.net/20.500.14352/72453
UL https://hdl.handle.net/20.500.14352/72453
LA eng
NO Lledó Mayans, V. E., Alkozi, H. A., Sánchez Naves, J. et al. «Melatonin Counteracts Oxidative Damage in Lens by Regulation of Nrf2 and NLRP3 Inflammasome Activity». Experimental Eye Research, vol. 215, febrero de 2022, p. 108912. DOI.org (Crossref), https://doi.org/10.1016/j.exer.2021.108912.
NO Universidad Complutense de Madrid
NO Ministerio de Sanidad (España)
NO Comunidad de Madrid
DS Docta Complutense
RD 26 dic 2025