Riboflavin deficiency effect

Esophageal cancer can also be influenced by other nutrients. Riboflavin (B ) deficiency results in severe changes in the epithelium of the oral tissues and esophagus in rats and primates. The effects of riboflavin deficiency in human populations are well known (29,30) but animal models for investigation of consequences of the deficiency have been used very little. 

Dr. Henry Foy (personal communication) has drawn attention to the severe effects of riboflavin deficiency in the baboon, with particular attention to the dysplasia of the epithelium of the oral cavity and esophagus. Dr. Foy has pursued these studies for many years at the Wellcome Research Laboratories in Nairobi. We have observed similar lesions in the Rhesus monkey, and have further pursued the effects of riboflavin deficiency in the rat. We have superimposed an esophageal carcinogen (MBN) on the deprived, damaged oral cavity and esophageal epithelium. Table IX lists results of a five month study, emphasizing the profound enhancement the deficiency can have on the esophagus (31). 

In conclusion, we have found that the presently set Recommended Dietary Allowances for riboflavin for women are inadequate even when they are not exercising, and that their riboflavin requirements are Increased by exercise. Weight reduction per se does not have an effect on riboflavin requirements. However, women who are exercising and on a weight reduction diet may get an inadequate amount of the vitamin because of their restricted food intake. We have no evidence, at least in the U.S., that athletes are at risk for clinical riboflavin deficiency. We do not think that it is necessary for those engaged in exercise to take megadoses of this B vitamin or of other B vitamins. 

The main effect of riboflavin deficiency is on lipid metabolism. In experimental animals on a riboflavin-free diet, feeding a high-fat diet leads to more marked impairment of growth, and a higher requirement for riboflavin to restore growth. There are also changes in the patterns of long-chain polyunsaturated fatty acids in membrane phospholipids. 

Duerden JM and Bates CJ (1985) Effect of riboflavin deficiency on lipid metabolism of liver and brown adipose tissue of sucking rat pups. British Journal of Nutrition 53, 107-15. 

Dutta P, Pinto J, and Rivlin R (1985) Antimalarial effects of riboflavin deficiency. Lancet 2,1040-3. 

Powers HJ, Weaver LT, Austin S, Wright AJ, and Eairweather-Tait SJ (1991) Riboflavin deficiency in the rat effects on iron utilization and loss. British Journal of Nutrition 65,487-96. 

Veitch K, Draye JP, Van Hoof F, and Sherratt HS (1988) Effects of riboflavin deficiency and clofibrate treatment on the five acyl-CoA dehydrogenases in rat liver mitochondria. 

Burch HB, Combs AM, Lowry OH, Padilla AM. Effects of riboflavin deficiency and realimentation on flavin enzymes of tissues. J Biol Chem 1956 223 29-45. 

Terroine (1954) has examined the effect of ascorbic acid on biotin deficiency in rats. She used lower levels than in her later experiments on thiamine and riboflavin deficiencies. She found that 0.1-0.5% ascorbic acid only slightly improved growth and appetite but considerably reduced the incidence of signs of biotin deficiency. Thus, in 92 days, all the deficient animals had developed alopecia, but only 30% of those receiving ascorbic acid. Similarly, 90% of the deficient group had spectacle eyes, but none... 

In the first part of this book devoted to cellular metabolism, it was pointed out that riboflavin is converted to monophosphate and diphosphate, yielding the active coenzymes of a large number of enzymes involved in the cellular oxidation-reduction reaction. As can be expected, the enzyme activity for which these flavoproteins are responsible is decreased in riboflavin deficiency. This has been clearly demonstrated for amino acid oxidase. Extensive studies on the effect of riboflavin deficiency on a large number of proteins have not been carried out but it seems logical to assume that the clinicopathological changes that develop in riboflavin deficiency result from the reduced activity of the flavoprotein enzyme. Yet, many... 

The clinical implications of a low riboflavin status in patients on AEDs are largely unknown. There may be an inhibitory effect on C677T MTHFR function and homocysteine metabolism. Importantly, riboflavin deficiency may be related to the elevated risk of foetal malformations in women on AEDs. 

Chloro-7-methyl-9-(i -D-ribityl)isoalloxazine (6-chloro-7-methylflavin), stimulates the growth of the riboflavin-deficient rat at any quantity administered from 3 /ig to 2 mg per day. When small quantities are given for limited periods of time the growth response is equal to that produced by one-half the quantity of riboflavin. All quantities lead to the death of the animal in spite of this growth but the animal can be protected against the lethal effects of this flavin by the administration of adequate amounts of riboflavin. This material does not antagonize riboflavin in the classical or expected manner . 

As mentioned earlier, Moore suggested that riboflavin deficiency was, in part, responsible for the occurrence of the syndrome, and certainly riboflavin intake tends to be low because of the limited intake of animal protein. The clinical signs of riboflavin deficiency—angular stomatitis and flexural dermatitis—are almost certainly non-specific effects of depressed tissue oxidation, and could be a direct or an indirect effect of cyanide itself. Although one report [39] suggested that riboflavin deficiency was slight in this area, more refined studies are required to decide whether or not coexisting riboflavin deficiency and delayed cyanide detoxication may not potentiate their adverse effect on neuronal metabolism. 

Many tissues are affected by riboflavin deficiency (aribofla-vinosis). Riboflavin deficiency requires 3-4 months of deprivation to manifest and symptoms include lesions on the lips, inflammation of the tongue, lowered levels of white and red blood cells, excessive sensitivity to pain and vascu-larisation of the cornea. Deficiency also results in decreased conversion of tryptophan into niacin. A test for deficiency is to measure glutathione reductase levels, which are depressed when riboflavin levels are low as are xanthine oxidase levels. There is a link between riboflavin deficiency in pregnancy and the development of pre-eclampsia. However, supplementation with riboflavin in a trial indicated that there was no effect on the prevention of pre-eclampsia. Alcoholics are at increased risk of riboflavin deficiency as... 

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