Disease relevance of Riboflavin Deficiency

• Development of deficiencies was monitored by growth rate, food intake, ratio of liver weight to body weight and the biochemical parameters (thiamin diphosphate effects for thiamin deficiency, glutathione reductase activity coefficient for riboflavin deficiency and erythrocyte glutamate-oxaloacetate transaminase activity for pyridoxine deficiency) [1].
• Two possible mechanisms by which riboflavin deficiency might influence the growth and multiplication of P. berghei are discussed, namely, a depression of reticulocytosis and an effect on the synthesis of reduced glutathione in the parasite or red blood cell [2].

High impact information on Riboflavin Deficiency

• The effects of riboflavin deficiency on the metabolism of N-nitrosodimethylamine [(DMN) CAS: 62-75-9] and other nitrosamines were examined in rats [3].
• For the first time, a significant riboflavin deficiency has been found to be related to CTS [4].
• In certain cases, such as thiamin deficiency and mild riboflavin deficiency, however, enhanced rates of metabolism of xenobiotics were observed [5].
• These results suggest that in some patients with multiple acyl-CoA dehydrogenase deficiency riboflavin supplementation may be effective in restoring the activity of SCAD, and possibly of other mitochondrial flavin-dependent enzymes [6].
• The most prominent biochemical consequence of riboflavin deficiency in rats is a drastic decrease in various acyl-CoA dehydrogenase activities, especially that of short chain and isovaleryl-CoA dehydrogenase (IVD) [7].

Chemical compound and disease context of Riboflavin Deficiency

• Less than 10% of patients showed evidence of vitamin B12, nicotinic acid, thiamin, or riboflavin deficiency, and 17% had evidence of folic acid deficiency [8].
• Prevalence of riboflavin deficiency was significantly lower in SCD (42.5%) than in control subjects (83%) and there was less pyridoxine deficiency in SCD (10.3%) than control subjects (54.5%) [9].
• Riboflavin deficiency may exert some of its effects by reducing the metabolism of other B vitamins, notably folate and vitamin B-6 [10].
• Folic acid given as a 400 microg/day supplement appeared to exacerbate a tendency toward riboflavin deficiency, as suggested by an increase in the proportion of individuals with EGRAC > or =1.4 from 52% to 65% after supplementation (P <0.05) [11].
• The effects of riboflavin deficiency on hepatic peroxisomal and mitochondrial palmitoyl-CoA oxidation were examined in weanling Wistar-strain male rats [12].

Biological context of Riboflavin Deficiency

• 5. It is concluded that acute riboflavin deficiency affects lipid metabolism in a characteristic manner, probably by interfering with beta-oxidation of fatty acids, but that diets of high lipid content do not significantly increase the extent of flavin depletion [13].
• Since acute ethanol consumption and riboflavin deficiency each induces oxidative stress within tissues, we examined whether their combined effects compromise the major antioxidative system in liver, namely, reduced glutathione (GSH) metabolism [14].

Anatomical context of Riboflavin Deficiency

• A test on glutathione reductase activity in erythrocytes revealed a stronger riboflavin deficiency among patients than among control subjects (p less than 0.005) [15].
• Effects of riboflavin deficiency and clofibrate treatment on the five acyl-CoA dehydrogenases in rat liver mitochondria [16].
• The oxidation of palmitoyl-CoA and palmitoylcarnitine, and to a lesser extent, glutamate, pyruvate and succinate, by hepatic mitochondria isolated from the young rats was depressed with riboflavin deficiency [17].
• Whereas riboflavin deficiency reduces in vitro iron-mobilising activity at the gastro-intestinal mucosa, this has no impact on body iron stores in these animals [18].
• Effects of riboflavin deficiency upon age-related changes in beta-adrenergic and adenosine receptor binding in rat adipocytes [19].

Gene context of Riboflavin Deficiency

• 3. There was no statistical difference in the activation coefficient (AC) of reductase (+FAD/-FAD) between groups, which seems to indicate that the lower activity of glutathione reductase observed in the aged group was not due to riboflavin deficiency [20].
• Biochemical riboflavin deficiency was identified in 41% controls and 33% patients with active rheumatoid arthritis but was significantly less frequent (9%) in patients with inactive compared to active disease (P = 0.02) or healthy controls (P = 0.0006) [21].
• The influence of G-6-PD activity on the response of erythrocyte glutathione reductase to riboflavin deficiency [22].
• The specific activities of peroxisomal catalase and palmitoyl-CoA-dependent NAD+ reduction were not affected by up to 10 weeks of riboflavin deficiency [12].
• Red cell transketolase (for thiamine deficiency), glutathione reductase (for riboflavin deficiency) and aspartate transaminase (for pyridoxine deficiency) were measured [23].

Analytical, diagnostic and therapeutic context of Riboflavin Deficiency

• A reduced activity of glutathione reductase, indicating a riboflavin deficiency, was observed only when the low protein diet was additionally deprived of a vitamin-mineral premix containing a fodder B2 preparation [24].

References