Toxic alcohol metabolism: In human retinal tissue, the immediate product formed by oxidation of methanol (wood alcohol) is

Introduction / Context:
Methanol poisoning is clinically important due to severe visual toxicity. Understanding the metabolic sequence helps explain symptoms and guides therapy (e.g., fomepizole or ethanol to inhibit alcohol dehydrogenase).

Given Data / Assumptions:

• Methanol is oxidized by alcohol dehydrogenase (ADH).
• Subsequent oxidation involves aldehyde dehydrogenase (ALDH).
• Retinal and optic nerve tissues are highly susceptible to downstream metabolites.

Concept / Approach:
The primary (direct) oxidation of methanol by ADH produces formaldehyde. Formaldehyde is then rapidly oxidized by ALDH to formic acid, which accumulates and causes metabolic acidosis and optic nerve damage. CO2 is produced later after formate is further oxidized, a slower pathway in humans.

Step-by-Step Solution:
Methanol --(ADH)→ formaldehyde.Formaldehyde --(ALDH)→ formic acid (formate).Formate → CO2 + H2O (slow in humans), leading to accumulation of formate and toxicity.Immediate (direct) product after methanol is formaldehyde, not CO2 or sugars.

Verification / Alternative check:
Clinical management targets ADH to prevent formation of formaldehyde/formate; elevated anion gap acidosis with visual symptoms is characteristic of formate accumulation.

Why Other Options Are Wrong:

• Sugars: Methanol is not converted to sugars.
• CO2: A later product; not immediate.
• Formic acid: Formed after formaldehyde; therefore not the direct first product.

Common Pitfalls:
Skipping the aldehyde intermediate; both formaldehyde and formate are toxic, but formaldehyde is the immediate product of ADH.

Final Answer:
Formaldehyde.