*6.1. Chemical Chelators*

Whether iron dysmetabolism in the retina is a cause or a consequence of various retinal diseases, iron accumulation is pathogenic, and its neutralization was shown to protect the retina from oxidative damage and retinal cell death in various models using di fferent neutralizing strategies [133] (Table 2). As early as in the 1970s, an iron chelator, Deferroxamine, was used in humans to reduce the amount of "rust" deposited on the eye with satisfactory results. Used in many other models of retinal degeneration (retinitis pigmentosa [166] or light-induced retinal damage models [167]), this chelator reduces the iron load and preserves the retina. Other chelators, such as Deferriprone, have shown significant protection of the retina in mice with impaired mechanisms of iron homeostasis [168–171]. These chemical chelators are mainly used clinically to treat hemosiderosis induced by frequent transfusions. Administered orally, subcutaneously or intramuscularly, they could led to several eye side e ffects, including vision loss [172,173]. These side e ffects could be explained because chemical iron chelators also bind the iron necessary for RPE and PR function [133,174].

As highlighted in a recent review [175], the clinical use of chemical chelators is complex because they should (1) target only the organ or tissue which is a ffected by the iron excess; (2) have a su fficient half-life; (3) cross the di fferent barriers that surround the tissue; and (4) have a rapid elimination route.


**Table 2.** Comparation between chemical iron chelators and transferrin in clinical use.

**Legend Table 2:** Tid: 3 times a day; q.d: once a day.
