Riboflavin homeostasis

There is no evidence of any significant storage of riboflavin in addition to the limited absorption, any surplus intake is excreted rapidly thus, once metabolic requirements have been met, urinary excretion of riboflavin and its metabolites reflects intake until intestinal absorption is saturated. In depleted animals, the maximum growth response is achieved with intakes that give about 75% saturation of tissues, and the intake to achieve tissue saturation is that at which there is quantitative urinary excretion of the vitamin. 

Equally, there is very efficient conservation of tissue riboflavin in deficiency. There is only a four-fold difference between the minimum concentration of flavins in the liver in deficiency and the level at which saturation occurs. In the central nervous system, there is only a 35% difference between deficiency and saturation. 

Control over tissue concentrations of riboflavin coenzymes seems to be largely by control of the activity of flavokinase, and the synthesis and catabolism of flavin-dependent enzymes. Almost all the vitamin in tissues is enzyme bound, and free riboflavin phosphate and FAD are rapidly hydrolyzed to riboflavin. If this is not rephosphorylated, it rapidly diffuses out of tissues and is excreted. 

In deficiency, virtually the only loss of riboflavin from tissues will be the small amount that is covalently bound to enzymes. The 8a-linkage is not cleaved by mammalian enzymes and 8a-derivatives of riboflavin are not substrates for flavokinase and cannot be reutilized. 

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Spector, R., 1980b. Riboflavin homeostasis in the central nervous system. Journal of Neurochemistry. 35 202-209. 

Several mechanisms have been postulated to account for thallium s toxicity, including ligand formation with sulfhydryl groups of enzymes and transport proteins, inhibition of cellular respiration, interaction with riboflavin and riboflavin-based cofactors, alteration of the activity of K -dependent proteins, and disruption of intracellular calcium homeostasis. ... 

Sea lettuces are a source of vitamins from group B (MacArtain et al, 2007 McDermid and Stuercke, 2003). For instances, Ulva lactuca contain high amount of cobalamin or vitamin B12. Vitamin B12 plays a key role in homeostasis of the brain and nervous system, and for the formation of blood (Scalabrino, 2009). Daily ingestion of 1.4 g/day of Ulva lactuca will be enough to meet the daily requirements of vitamin B12 (MacArtain et al, 2007). One of the most important vitamins B occurring in Ulva reticulata is riboflavin (vitamin B2). Vitamin B2 deficiency is often endemic in human... 

For the uptake of riboflavin by brain cells, it is most important to maintain homeostasis. The concentration of riboflavin in the brain remains constant, both at times of riboflavin deficiency and after massive intravenous applications. In rat brains, more than 90% of total riboflavin is found as FAD and FMN (Ball 2004b). 

The same phenomenon was observed after injeetions of riboflavin into the ventricular cerebrospinal fluid of anaesthetized rabbits only some of the riboflavin was accumulated in the choroid plexus and most was removed (Speetor 1980b). Thus, support of brain homeostasis results from transport of riboflavin both from blood into the choroid plexus and in the opposite direction. 

Relevant in making the maintenance of brain homeostasis possible is the third identified human riboflavin transporter hRFT3 (GPR172A), which is expressed in the brain and salivary gland. It has the same substrate specificity as hRFTl and hRFT2, and functional characteristics similar to those of hRFTl (Yao et al. 2010). 

The kidneys are the organs for the elimination of riboflavin from mammalian organisms, maintaining the vitamin homeostasis. Riboflavin passes through the glomeruli and is transported by the tubules, where secretion or reabsorption takes place, depending on riboflavin plasma concentration. Finally, excretion is in the urine. 

The presented mechanism of active and passive uptake and transport of riboflavin has been suggested by various research groups (Ball et al. 2004b Foraker et al. 2003 Huang and Swaan 2000). However, the problem is still under discussion. Saturable active transport dominates the riboflavin uptake processes and is indisputably proven in every examined in vivo and in vitro systems. Passive diffusion at high concentrations also appears to be inevitable. However, it may be antidpated that some studies may also confirm involvement of a receptor-mediated mechanism and the role of riboflavinbinding protein in homeostasis maintenance in other mammalian tissues and organs. 

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