Scurvy collagen affected

Scurvy affects the structure of collagen. However, it is due to a deficiency of ascorbic acid (Chapter 45) and is not a genetic disease. Its major signs are bleeding... 

In addition to collagen metabolism and scavenging ROS species to limit inflammation as noted above, ascorbate is required for the synthesis of norepinephrine from tyrosine, of carnitine from y-butyrobetaine whose immediate precursor is made by trimethylating lysine, for folinic acid production from folic acid. In the absence of ascorbate, the reduced activity of these processes slows nerve, energy and cardiac output, causingthe affected person to become exhausted and irritable. Scurvy is the old English word for ill-tempered. 

A. The patient exhibits the classic symptoms of scurvy, a deficiency in vitamin C. In addition to being an important biological antioxidant, ascorbic acid is required for the hydroxylation of proUne and lysine residues of procollagen in the synthesis of collagen. A deficiency leads to defects in collagen synthesis, which adversely affects the intercellular cement substances in connective tissue, bones, and dentin. 

Scurvy Vitamin C deficiency first affecting collagen with highest hydroxyproline content, such as that found in blood vessels. Thus, an early symptom is bleeding gums. 

Individuals who develop scurvy suffer from sore and bleeding gums and loss of teeth. This is due, in part, to the synthesis of a defective collagen molecule. The step that is affected in collagen biosynthesis attributable to scurvy is which of the following ... 

The hydroxylation of collagen is necessary for its proper functioning, which is why, in cases of scurvy, it is tissues rich in collagen that are most affected. 

Even the most ardent supporters of the belief that ascorbic acid is concerned in the synthesis of cortical hormones would probably hesitate today to suggest that this is the most important function of ascorbic acid in the body, still less its only function there are too many obvious reasons for thinking otherwise. The first is that human patients whose adrenals have been destroyed suffer from Addison s disease but do not develop scurvy. They continue to show normal levels of ascorbic acid in the blood (Jenovese el al., 1940), and there is no evidence that their collagen is affected. Though there were some initial reports (e.g., Wilkinson and Ashford, 1936) that patients with Addison s disease suffered from ascorbic acid deficiency, this idea has faded from the recent literature. Secondly, the amount of ascorbic acid in the adrenal cortices is less than 1 per cent of the total amount in the human body (Section III, 2) it would be against what we know of the economy of the body to think that all the rest of this active metabolite was simply hanging around in the other tissues, waiting for the adrenals to find a use for it. 

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