Riboflavin metabolic intermediates

The vitamin B complex contains a number of factors which are closely associated in their distribution in nature and have related functions in intermediate metabolism. Of the eleven factors which are available in pure form, five have been shown to be constituents of coenzymes, namely, thiamine, riboflavin, niacinamide, pyridoxine, and pantothenic acid. It seems likely that other B vitamins may be found to function in a similar manner. Two members of the B complex, choline and inositol, appear to have lipotropic activity, and two others, folic acid and vitamin B12, have antianemic properties. Deficiency of vitamins of the B complex is one of the most frequently encountered syndromes of malnutrition in man. 

Goodwin and Jones (75) uang E. aahbyii found that the addition of unlabeled adenine markedly depressed the incorporation of label from serine-C into riboflavin, but had no effect on the amount of serine-C metabolized to carbon dioxide. This might indicate that a purine is an obligatory intermediate. However, the results could be explained equally well by the second scheme, if the rate of convermon of purines to rings B and C is more rapid than the rate of synthesis from the simple precursors, or if the added purine inhibits one of the steps of the de novo formation of riboflavin. 

Non- oxidative branch Pentose-5 -Phosphates Ribose-5-P 2 deoxy ribose-5-P 5 -phosphoribosyl-1 -pyrophosphate (PRPP) i) Structural components of nucleotides a. Basal structural component of RNA b. Basal structural component of DNA c. Precursor of both de novo and salvage synthesis of nucleotides ii) Intermediate products of purine metabolism and act as precursor molecules of cofactors, e g., riboflavin, flavin mononucleotide (FMN), flavin adenine di nucleotide (FAD) iii) Precursor of the amino acid. Histidine. 

Disturbances in fatty acid oxidation by isolated mitochondria, e.g., from livers of deficient animals, have been demonstrated, and one of the most characteristic metabolic changes, observed even in a mild deficiency state in experimental animals, is the appearance of abnormal dicarboxylic acids, and their derivatives, in the urine. These products seem to arise because fatty acyl intermediates become diverted away from the usual pathway of mitochondrial beta-oxidation, towards abnormal partial oxidation in the peroxisomes (which are less severely affected by the riboflavin deficiency state). 

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