Abstract
Purpose: :
Data indicate that Coenzyme Q10 (CoQ10), an essential cofactor of the electron transport chain, protects against ischemia/reperfusion damage in the heart and produces neuroprotective effects in neurodegenerative disorders (Matthews RT. 1998). The anti–apoptotic activity of CoQ10 has been related not only to its free radial scavenger ability but also to a specific regulation of the mitochondrial permeability transition pore (Papucci L. 2003). In our study, we evaluated the neuroprotective effects of CoQ10 in an in vivo model of retinal ganglion cell (RGC) death.
Methods: :
In Sprague–Dawley rats, IOP was raised unilaterally to 120 mmHg for 45 minutes by elevating a saline reservoir connected to the eye. Study group (n=4) received topical treatment with a solution containing CoQ10 0.1% (50 µl, 4 times, 1 hour before ischemia and further 4 times in the first hour of the reperfusion phase). As controls, eyes for which the saline flask was not lifted up were used. After 24 hours of reperfusion, animals were sacrificed and retinal coronal sections (n=5 per eye) passing through the optic nerve head were stained with haematoxylin and eosin and processed for RGC counting. In particular, the number of RGC was counted in 6 areas of each section at 300 µm from the optic nerve on the superior and inferior hemisphere using light microscopy (40X) (see Nucci C. 2005).
Results: :
High IOP–induced ischemia caused a reduction in the number of RGC per counted area by approximately 25% compared to controls (n=9). Topical treatment with CoQ10 significantly prevented RGC loss (ANOVA followed by Tukey–Kramer’s Test).
Conclusions: :
Our data indicate that topical administration of CoQ10 is associated with neuroprotective effects in the RGC layer, thus suggesting a potential use of this agent in the treatment of diseases affecting retinal ganglion cells.
Keywords: neuroprotection • antioxidants • retina: proximal (bipolar, amacrine, and ganglion cells)