What is glaucoma?

Glaucoma is a group of eye conditions that damage the optic nerve, which is vital for good vision. This damage is often caused by abnormally high pressure in the eye, known as intraocular pressure (IOP). Glaucoma is a leading cause of irreversible blindness worldwide, and it typically progresses slowly over time, often without symptoms until significant vision loss has occurred.


There are several types of glaucoma, but the two most common forms are:


  • Primary Open-Angle Glaucoma (POAG): This is the most common type of glaucoma. It occurs when the drainage angle within the eye becomes less efficient over time, leading to a gradual increase in IOP. In POAG, the peripheral vision is typically affected first, and the condition progresses slowly without noticeable symptoms until later stages.


  • Angle-Closure Glaucoma: This type of glaucoma occurs when the drainage angle within the eye becomes blocked or narrowed suddenly, causing a rapid increase in IOP. Angle-closure glaucoma can lead to severe symptoms such as eye pain, headache, nausea, and sudden vision loss. It is considered a medical emergency and requires immediate treatment to prevent permanent vision loss.


Other types of glaucoma include secondary glaucoma (caused by other eye conditions or systemic diseases), congenital glaucoma (present at birth), and normal-tension glaucoma (damage to the optic nerve despite normal IOP).


What is the relationship between glaucoma and oxidative stress?

The relationship between glaucoma and oxidative stress involves complex interactions between oxidative damage, impaired antioxidant defenses, and the pathophysiology of glaucomatous optic neuropathy. Oxidative stress refers to an imbalance between the production of reactive oxygen species (ROS) and the body’s antioxidant defense mechanisms, leading to cellular damage and dysfunction. Several lines of evidence suggest that oxidative stress plays a significant role in the development and progression of glaucoma:


  • Increased Oxidative Damage: Studies have shown that patients with glaucoma have elevated levels of oxidative stress markers, such as lipid peroxidation products, protein carbonyls, and DNA damage, in the aqueous humor (fluid in the eye), retinal tissues, and optic nerve head. This suggests that oxidative damage to ocular tissues may contribute to the pathogenesis of glaucoma.


  • Impaired Antioxidant Defenses: Glaucomatous eyes may have reduced levels of antioxidants and antioxidant enzymes, such as superoxide dismutase (SOD), catalase, and glutathione peroxidase, which normally protect against oxidative damage. Decreased antioxidant capacity and impaired antioxidant defenses may render ocular tissues more susceptible to oxidative stress and damage in glaucoma.


  • Mitochondrial Dysfunction: Mitochondrial dysfunction and oxidative stress have been implicated in the pathogenesis of glaucomatous optic neuropathy. Mitochondria are essential for cellular energy production and play a critical role in maintaining cellular function and survival. Dysfunctional mitochondria produce increased levels of ROS and contribute to oxidative stress, which can damage retinal ganglion cells (RGCs) and optic nerve fibers, leading to apoptosis (cell death) and optic nerve degeneration in glaucoma.


  • Retinal Ganglion Cell Damage: Retinal ganglion cells (RGCs) are the primary target of damage in glaucoma, and oxidative stress may contribute to RGC apoptosis and loss. Increased ROS levels can activate apoptotic pathways, induce DNA damage, and disrupt cellular signaling mechanisms, leading to RGC dysfunction and death in glaucoma.


  • Vascular Dysfunction: Oxidative stress can impair vascular function and disrupt ocular blood flow regulation, which may contribute to optic nerve ischemia and damage in glaucoma. Reduced ocular perfusion and microvascular dysfunction have been observed in glaucomatous eyes, and oxidative stress may play a role in vascular abnormalities associated with glaucoma.


Overall, oxidative stress appears to be involved in multiple aspects of glaucoma pathophysiology, including retinal ganglion cell damage, mitochondrial dysfunction, vascular impairment, and optic nerve degeneration.