What is the primary mechanism of mercury-induced neurotoxicity?

Question

BlackTom AI · Accepted Answer

Mercury neurotoxicity primarily stems from its high affinity for sulfhydryl (thiol) groups in proteins, including tubulin, which interferes with the normal polymerization of microtubules in neurons. This disruption impairs axonal transport and structural integrity of dendrites, contributing to neurotoxic effects.

Option 1: 'Mercury disrupts GTP binding to microtubules, leading to impaired axonal transport and synaptic transmission.' While microtubule dynamics involve GTP binding and hydrolysis, the dominant mechanism of mercury toxicity is through binding to sulfhydryl groups on tubulin and associated proteins, not specifically by blocking GTP binding. Thus this statement misstates the primary biochemical target.

Option 2: 'Mercury prevents the assembly of beta tubulin subunits, leading to destabilization of microtubules and dendritic atrophy.' This aligns with the established mechanism: mercury interacts with thiol groups on tubulin, inhibiting its polymerization into microtubules, causing destabilization and structural neuronal damage such as dendritic atrophy.

Option 3: 'Mercury enhances GTP binding to microtubules, resulting in hyperactive axonal growth and excessive synaptic signalling.' There is no evidence that mercury increases GTP binding or promotes hyperactive growth; in fact, mercury tends to disrupt cytoskeletal dynamics, not enhance them.

Option 4: 'Mercury promotes the assembly of beta tubulin subunits, causing microtubule hyperstability and increased neuronal excitability.' This statement contradicts the known effect of mercury on the cytoskeleton; mercury does not promote assembly or hyperstability of microtubules, and increased excitability is not the typical outcome described for mercury-induced microtubule disruption.

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What is the primary mechanism of mercury-induced neurotoxicity?

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