Give the role of vitamin C in scurvy and cholesterol metabolism.

Vitamin C and Scurvy

Scurvy is a disease resulting from prolonged deficiency of Vitamin C. The primary biochemical defect in scurvy relates to the synthesis of collagen, a vital structural protein found in connective tissues throughout the body.

Collagen Synthesis and Vitamin C

• Proline and Lysine Hydroxylation: Vitamin C acts as a crucial cofactor for the enzymes prolyl hydroxylase and lysyl hydroxylase. These enzymes catalyze the post-translational hydroxylation of proline and lysine residues within procollagen molecules. Hydroxylation is essential for the proper folding and stability of the collagen triple helix.
• Cross-linking: Vitamin C is also required for the enzyme ascorbyl oxidase, which participates in the cross-linking of collagen fibers, providing tensile strength to tissues.
• Pathophysiology of Scurvy: Without sufficient Vitamin C, hydroxylation is impaired, leading to the production of unstable collagen. This results in weakened connective tissues, manifesting as symptoms like bleeding gums, loose teeth, impaired wound healing, joint pain, and petechiae (small, pinpoint hemorrhages).

Historically, James Lind’s experiment in 1747 demonstrated the efficacy of citrus fruits in preventing and treating scurvy, laying the foundation for understanding Vitamin C’s role.

Vitamin C and Cholesterol Metabolism

While not directly involved in cholesterol synthesis, Vitamin C plays a significant role in cholesterol metabolism through several mechanisms.

Bile Acid Synthesis

• Cholesterol to Bile Acids: Vitamin C is essential for the conversion of cholesterol into bile acids in the liver. Bile acids are crucial for the emulsification and absorption of dietary fats, including cholesterol.
• Increased Bile Acid Excretion: Adequate Vitamin C levels promote increased bile acid excretion, reducing the cholesterol pool in the body.

Antioxidant Protection and LDL Oxidation

• LDL Oxidation: Low-density lipoprotein (LDL) cholesterol is susceptible to oxidation, a process that contributes to the development of atherosclerosis. Oxidized LDL is more readily taken up by macrophages, forming foam cells, a hallmark of atherosclerotic plaques.
• Vitamin C as an Antioxidant: Vitamin C is a potent water-soluble antioxidant. It scavenges free radicals, protecting LDL cholesterol from oxidation.
• Increased HDL Cholesterol: Some studies suggest that Vitamin C supplementation may increase levels of high-density lipoprotein (HDL) cholesterol, often referred to as "good" cholesterol, further contributing to cardiovascular health.

Vitamin C and Endothelial Function

Vitamin C enhances the production of nitric oxide (NO) by endothelial cells. NO is a vasodilator, improving blood flow and reducing blood pressure, thereby contributing to cardiovascular health. Impaired endothelial function is a key early event in atherosclerosis.

The relationship between Vitamin C and cholesterol metabolism is complex and still under investigation, but evidence suggests a protective role against cardiovascular disease.