Toxic and Nutritional Optic Neuropathies—An Updated Mini-Review

Baj, Jacek; Forma, Alicja; Kobak, Joanna; Tyczyńska, Magdalena; Dudek, Iga; Maani, Amr; Teresiński, Grzegorz; Buszewicz, Grzegorz; Januszewski, Jacek; Flieger, Jolanta

doi:10.3390/ijerph19053092

Cited by 23 publications

(17 citation statements)

References 140 publications

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“…As patients overrepresent some human leukocyte antigens, genetic predisposition to optic neuritis seems to be of importance [ 32 , 33 , 34 , 35 , 36 ]. Studies have shown that chronic exposure to heavy metals may also contribute to optic neuropathy [ 37 ]. So far, cobalt (Co) neurotoxicity, leading to visual impairment and loss of vision, has been confirmed [ 38 ].…”

Section: Introductionmentioning

confidence: 99%

Multi-Elemental Analysis of Human Optic Chiasm—A New Perspective to Reveal the Pathomechanism of Nerve Fibers’ Degeneration

Baj

Forma

Kowalska

et al. 2022

IJERPH

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The effect of metals on the functioning of the human eye is multifactorial and includes enzyme activity modulation, trace metal metabolic pathways changes, and cytotoxic activity. Functional dysfunctions appear mostly as a result of the accumulation of toxic xenobiotic metals or disturbances of micronutrients’ homeostasis. So far, the affinity of selected metals to eye tissues, i.e., the cornea, choroid, lens, and anterior chamber fluid, has been most studied. However, it is known that many eye symptoms are related to damage to the optic nerve. In order to fill this gap, the aim of the study is to perform a multi-element analysis of tissue collected postmortem from optic chiasm and optic nerves. A total of 178 samples from 107 subjects were tested. The concentrations of 51 elements were quantified by inductively coupled plasma mass spectrometry (ICP-MS) after the wet-mineralization step. In terms of elemental composition, the optic chiasm is dominated by two trace elements, i.e., iron (Fe) and zinc (Zn), besides macro-elements Ca, K, Na, P, and Mg. The subjects formed a homogeneous cluster (over 70% subjects) with the highest accumulation of aluminum (Al). The remaining two departing clusters were characterized by an increased content of most of the elements, including toxic elements such as bismuth (Bi), uranium (U), lead (Pb), chromium (Cr), and cadmium (Cd). Changes in elemental composition with age were analyzed statistically for the selected groups, i.e., females, males, and subjects with alcohol use disorder (AUD) and without AUD. A tendency of women to lose Se, Cu, Zn, Fe with age was observed, and a disturbed Ca/Mg, Na/K ratio in subjects with AUD. Although the observed trends were not statistically significant, they shed new light on the risks and possible pathologies associated with metal neurotoxicity in the visual tract.

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Section: Introductionmentioning

confidence: 99%

Multi-Elemental Analysis of Human Optic Chiasm—A New Perspective to Reveal the Pathomechanism of Nerve Fibers’ Degeneration

Baj

Forma

Kowalska

et al. 2022

IJERPH

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“…The increasing incidence of nutritional optic neuropathy may be related to the widespread of gastric bypass surgeries and vegan diets. 9,24 However, the causal connection remains unproven and very few unequivocally confirmed cases of optic neuropathy are described to be caused by a identified single toxin or nutrient deficiency. 25 The pathophysiology in both forms involve in biochemical pathways of cell energy metabolism, oxidative stress and free radicals, triggering dysfunction of the ON.…”

Section: Toxic/nutritional Optic Neuropathymentioning

confidence: 99%

Optic nerve diseases and regeneration: How far are we from the promised land?

Cen

Park

2023

Clinical Exper Ophthalmology

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The retinal ganglion cells (RGCs) are the sole output neurons that connect information from the retina to the brain. Optic neuropathies such as glaucoma, trauma, inflammation, ischemia and hereditary optic neuropathy can cause RGC loss and axon damage, and lead to partial or total loss of vision, which is an irreversible process in mammals. The accurate diagnoses of optic neuropathies are crucial for timely treatments to prevent irrevocable RGCs loss. After severe ON damage in optic neuropathies, promoting RGC axon regeneration is vital for restoring vision. Clearance of neuronal debris, decreased intrinsic growth capacity, and the presence of inhibitory factors have been shown to contribute to the failure of post‐traumatic CNS regeneration. Here, we review the current understanding of manifestations and treatments of various common optic neuropathies. We also summarise the current known mechanisms of RGC survival and axon regeneration in mammals, including specific intrinsic signalling pathways, key transcription factors, reprogramming genes, inflammation‐related regeneration factors, stem cell therapy, and combination therapies. Significant differences in RGC subtypes in survival and regenerative capacity after injury have also been found. Finally, we highlight the developmental states and non‐mammalian species that are capable of regenerating RGC axons after injury, and cellular state reprogramming for neural repair.

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“…Therefore, cells like neurons that acquire their energy mostly from aerobic reactions are more vulnerable to hypoxia. [1][2][3] So, methanol can lead to optic neuropathy through this mechanism.…”

Section: Introductionmentioning

confidence: 99%

“…Formic acid has an inhibitory effect on cytochrome C oxidase, an enzyme in the aerobic respiration pathway, and causes cell hypoxia. Therefore, cells like neurons that acquire their energy mostly from aerobic reactions are more vulnerable to hypoxia 1–3 . So, methanol can lead to optic neuropathy through this mechanism.…”

Section: Introductionmentioning

confidence: 99%