Does the trace element manganese have a role in glaucoma and is it beneficial or harmful?
For those new to this discussion, let's be sure we don't confuse manganese and magnesium. We discussed magnesium in another thread recently. Despite their similar-sounding names, they are very different minerals. Magnesium, the most abundant divalent cation in the human body, is a major essential mineral, while manganese is a trace mineral, required only in small amounts.
Considerations on the role of manganese in glaucoma are primarily linked to mitochondrial health. Mitochondrial dysfunction or compromise is potentially one of the most significant aspects of glaucoma pathology.
Manganese is a trace element critical for cellular processes, particularly in the mitochondria. It's a required cofactor for the mitochondrial version of superoxide dismutase (MnSOD or SOD2), an antioxidant enzyme within the mitochondrial matrix.
MnSOD has a crucial role in cellular antioxidant defense, converting superoxide radicals, a byproduct of oxidative phosphorylation, into less reactive molecules like hydrogen peroxide (H2O2) and molecular oxygen (O2). By doing so, it prevents oxidative stress, a condition that could lead to cellular damage and contribute to glaucoma's pathology. The lethal nature of MnSOD knockout in mice highlights this function's importance.
Furthermore, MnSOD is suggested to regulate mitochondrial function and signaling, thus impacting processes like apoptosis and cellular growth regulation. Therefore, manganese, through its role as a cofactor for MnSOD, is integral to mitochondrial health and function.
However, it's crucial to regulate manganese homeostasis, as both its deficiency and excess can lead to pathological conditions. This perspective is supported by contrasting findings in the following study:
Influence of Trace Elements on Neurodegenerative Diseases of The Eye—The Glaucoma Model - PMC
NOTE: PEX is an acronym for pseudoexfoliation (PEX) syndrome and PEG is an acronym for pseudoexfoliation glaucoma (PEG).
Ceylan et al. found that manganese concentration was significantly increased in patients with PEX [69]. The authors suggested that [higher] Mn levels had a strong association with PEX and that the increased levels of serum Mn may have a possible role in the pathobiology of PEX. When the three groups (PEX, PEG, and control) were analyzed together, Mn concentration was significantly different.
On the other hand, as reported by Lin et al., blood manganese level was negatively associated with glaucoma diagnosis in a population-based study on 2680 South Korean individuals [124]. These findings suggest that a low blood manganese level could be associated with greater susceptibility to glaucoma. This element may have some, as yet undetermined, relationship with the occurrence of this disease.
The reference 124 refers to the following article:
in the Korean study, measurements of blood manganese, mercury, lead, and cadmium and urinary Arsenic to investigate associations between body levels of trace metals and the prevalence of glaucoma in a cross-sectional population-based study.
Conclusions and Relevance These findings in a cross-sectional study of the South Korean population suggest that a lower blood manganese level and a higher blood mercury level are associated with greater odds of glaucoma. For more confidence that trace metals may have a role in the pathogenesis of glaucoma, prospective studies would need to confirm that the presence of such trace metals increases the chance of developing glaucoma.
The role of manganese in glaucoma is a complex topic, with both low and high levels being associated with the disease, depending on the study. Manganese's critical role in mitochondrial health, primarily through its function as a cofactor for MnSOD, is well-documented. However, research presents conflicting evidence regarding the association of manganese levels with glaucoma. As such, it would be premature and potentially unsafe to recommend manganese supplementation for those with glaucoma without a thorough understanding of an individual's nutritional status and medical condition, and without further conclusive evidence from large-scale, prospective studies. As always, such decisions should be made in consultation with a healthcare provider.
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