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Oxidative Stress in the Protection and Injury of the Lacrimal Gland and the Ocular Surface: are There Perspectives for Therapeutics PY2022 IR95 Glutathione 教材
資訊來源：
https://pmc.ncbi.nlm.nih.gov/articles/PMC8963457/
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lacrimal functional unit (LFU)
The LFU is defined as a system that integrates the ocular surface, the central nervous system (CNS) and the exocrine glands responsible for the tear film. The ocular surface is composed of the cornea, the conjunctiva, and the lids that send sensorial neural inputs to the CNS, and throughout the autonomic nervous system, they provide feedback with stimuli to the exocrine glands, modulating the volume and content of the tear film that wets and nourishes the ocular surface. Among these exocrine glands are the lacrimal gland (LG), Meibomian glands (MG), accessory glands and the epithelial layer of the ocular surface, with their constitutive and regulated secretory and paracrine capacity (Bron and Seal 1986; Halliwell and Gutteridge 1990; Crouch et al., 1991; Droge 2002; Stern et al., 2004; Rocha et al., 2008).
OS is ubiquitous and has been implicated in the protective and pathogenic mechanisms of dry eye (DE) and ocular surface diseases. Therefore, any proposal of therapeutic modulation of those reactions must consider its dual effect (Morrison and Allen 1966; Fridovich 2013; Forman 2016).
As a protector, OS works against microorganisms and other sources of free radicals, maintaining homeostasis and triggering the response to protect against other harmful events that challenge the LFU. In a recent study on tear proteomics, the comparison between healthy and DE individuals revealed that lactoperoxidase (LPO) is the most downregulated enzyme in the DE group (Soria et al., 2017). In parallel, the increase in various proinflammatory proteins in their tears was confirmed in previous studies that used LPO as a biomarker of dysfunction for DE and LFU, as detailed below (Bromberg et al., 1989; Soria et al., 2017).
Throughout evolution, heme peroxidases, similar to myeloperoxidase (MPO), LPO, salivary peroxidase (SPO), and thyroid peroxidase (TPO), were found to be key enzymes for modulating the OS process in the cytoplasmic and secretory fluids (Davies et al., 2008). Antioxidants or free radical scavengers are incorporated into the innate immune arsenal, hormone synthesis and exocrine secretions, generating ROS with antimicrobial actions and counterbalancing the actions of other OS-related enzymes, including the glutathione peroxidases (GPx) family (Morrison and Allen 1966; Petrides and Nauseef 2000; Ihalin et al., 2006; Davies et al., 2008). Recently, a family of six protein isoforms called peroxiredoxins was described, and their structure and function associated with OS were further detailed (Rhee et al., 2012).
As a disease mediator, GPx levels and ROS accumulation have been identified as biomarkers and implicated in the protective mechanisms and damage triggered by the LFU (Wakamatsu et al., 2008). The expression and activity of these markers were associated with DE caused by hormone deficits, systemic autoimmune diseases, microelement deficiency, pollution, and ocular surface disease not necessarily related to systemic conditions (Bakker et al., 2005; Davies et al., 2008; Wakamatsu et al., 2008; Kawashima et al., 2010; Kojima et al., 2012; Uchino et al., 2012; Cejkova and Cejka 2015; Jung et al., 2018).
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