Difficulty: Easy
Correct Answer: Copper
Explanation:
Introduction / Context:Copper is a critical trace element in iron metabolism. Multiple cuproenzymes support iron transport and hemoglobin synthesis, and copper deficiency can present with anemia resembling iron deficiency that is unresponsive to iron alone. This question targets recognition of copper’s enabling role in iron utilization.
Given Data / Assumptions:
Concept / Approach:Identify the mineral that functions through ferroxidases and transport proteins to mobilize iron. Copper deficiency impairs iron export from enterocytes and delivery to transferrin, reducing availability for erythropoiesis. Hence, copper is the correct choice.
Step-by-Step Solution:
Determine minerals tied to iron trafficking → copper via ceruloplasmin/hephaestin.Link mechanism → Fe2+ to Fe3+ oxidation for transferrin binding.Predict outcome → improved iron utilization and hemoglobin synthesis requires adequate copper.Verification / Alternative check:Clinical copper deficiency (e.g., in malabsorption) causes microcytic, hypochromic anemia that corrects with copper repletion.
Why Other Options Are Wrong:
a) Calcium can inhibit non-heme iron absorption when co-ingested in large amounts.b) Phosphorus is central to energy metabolism, not iron trafficking.c) Cobalt is part of vitamin B12, relevant to megaloblastic anemia, not iron utilization.e) Zinc has broad enzymatic roles but no specific ferroxidase function.Common Pitfalls:Assuming all trace metals enhance iron absorption; copper is uniquely essential via ferroxidase activity.
Final Answer:Copper.
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