Vitamin B12: Name, Function, and Sources to Vitamin C: Excess and Toxicity

Vitamin B12

Also called cobalamin.

Function

Cofactor for methionine synthase (transfers CH₃ groups as methylcobalamin) and methylmalonyl-CoA mutase. Important for DNA synthesis.

Found in animal products. Synthesized only by intestinal microbiota. Site of synthesis in humans is distal to site of absorption; thus B12 must be consumed via animal products.

Deficiency

Macrocytic, megaloblastic anemia, hypersegmented PMNs; paresthesias and subacute combined degeneration (degeneration of dorsal columns, lateral corticospinal tracts, and spinocerebellar tracts) due to abnormal myelin. Associated with ↑ serum homocysteine and methylmalonic acid levels, along with 2° folate deficiency. Prolonged deficiency → irreversible nerve damage.

Very large reserve pool (several years) stored primarily in the liver. Deficiency caused by malabsorption (eg, sprue, enteritis, Diphyllobothrium latum, achlorhydria, bacterial overgrowth, alcohol overuse), lack of intrinsic factor (eg, pernicious anemia, gastric bypass surgery), absence of terminal ileum (surgical resection, eg, for Crohn disease), certain drugs (eg, metformin), or insufficient intake (eg, veganism).

B12 (folate) supplementation can mask the hematologic symptoms of B12 deficiency, but not the neurologic symptoms.

Vitamin B12 Metabolic Pathways

#boundingbox

This diagram illustrates the two main metabolic pathways involving Vitamin B12. On the left, we see the methionine synthase pathway where homocysteine is converted to methionine, with Vitamin B12 acting as a cofactor. On the right, the methylmalonyl-CoA mutase pathway shows methylmalonyl-CoA being converted to succinyl-CoA, also requiring Vitamin B12. This pathway is linked to the TCA cycle and heme synthesis. The diagram also shows the input of protein and fatty acids with odd number of carbons and branched-chain amino acids into these pathways.

Vitamin C

Also called ascorbic acid.

Function

Antioxidant; also facilitates iron absorption by reducing it to Fe²⁺ state. Necessary for hydroxylation of proline and lysine in collagen synthesis. Necessary for dopamine β-hydroxylase (converts dopamine to NE).

Found in fruits and vegetables. Pronounce “ascorbic” acid. Ancillary treatment for methemoglobinemia by reducing Fe³⁺ to Fe²⁺.

Deficiency

Scurvy—swollen gums, easy bruising, petechiae, hemarthrosis, anemia, poor wound healing, perifollicular and subperiosteal hemorrhages, “corkscrew” hair. Weakened immune response.

Deficiency may be precipitated by tea and toast diet. Vitamin C deficiency causes scurvy due to a Collagen hydroxylation defect.

Excess

Nausea, vomiting, diarrhea, fatigue, calcium oxalate nephrolithiasis (excess oxalate from vitamin C metabolism). Can ↑ iron toxicity in predisposed individuals by increasing dietary iron absorption (ie, can worsen hemochromatosis or transfusion-related iron overload).

Topics Covered:

• Vitamin B12: Name, Function, and Sources
• Vitamin B12 Deficiency: Symptoms
• Vitamin B12 Deficiency: Causes and Treatment Considerations
• Vitamin B12: Key Metabolic Pathways
• Vitamin C: Name, Function, and Sources
• Vitamin C Deficiency: Scurvy
• Vitamin C: Excess and Toxicity