Selenium deficiency — Which clinical consequence is most classically linked to inadequate selenium status in biological systems?

Introduction / Context:
Selenium, incorporated as selenocysteine in antioxidant enzymes, protects against oxidative damage. Deficiency syndromes vary by species and context but share themes of impaired antioxidant defense. This question focuses on the classical association widely cited in nutrition and pathology texts.

Given Data / Assumptions:

• Selenium-dependent enzymes include glutathione peroxidases and thioredoxin reductases.
• Deficiency increases vulnerability to oxidative injury.
• Outcomes differ between humans and animal models but have overlap.

Concept / Approach:
In animal studies, selenium deficiency produces hepatic necrosis and muscular degeneration due to unchecked lipid peroxidation. In humans, low selenium is associated with Keshan disease (cardiomyopathy) and potential immune dysfunction; nonetheless, the classic exam answer among the given choices is liver necrosis as a hallmark pathologic lesion reflecting oxidative damage in deficiency states.

Step-by-Step Solution:

Verification / Alternative check:
Experimental depletion of selenium diminishes glutathione peroxidase activity, with subsequent hepatic and muscular lesions; repletion prevents or reverses damage, supporting causality.

Why Other Options Are Wrong:

• Diarrhea: nonspecific and not a hallmark lesion of selenium deficiency.
• Multiple sclerosis/Crohn's disease: complex etiologies not defined by selenium deficiency.
• G6PD deficiency: X-linked enzyme defect unrelated to selenium status.

Common Pitfalls:
Assuming all antioxidant-related deficiencies present identically. Selenium deficiency has characteristic organ targets and differs from, for example, vitamin E deficiency, though they can interact.

Final Answer:
liver necrosis.