flavin-adenine-dinucleotide and Liver-Cirrhosis

When our liver does not work well, it can induce damage to other organs causing their dysfunction. With this background, we aim to study the effect of liver fibrosis on other organs such as heart, lungs, kidney and spleen by assessing the variations in the inherent emission property of the tissue, using fluorescence spectroscopy. Fluorescence emission spectra from excised organs of liver fibrosis induced rats were collected at excitation wavelengths 320 and 410 nm. Optical redox ratio derived from the spectral data supported by multivariate statistical analysis, principal component analysis followed by linear discriminant analysis (PCA-LDA) distinguished between control and fibrosis induced groups. The two different excitation wavelength provided variations in the endogenous flurophores collagen, nicotinamide adenine dinucleotide (NADH), flavin adenine dinucleotide (FAD), lipopigments and porphyrins. Additionally, evaluation of redox ratio provided variations in tissue metabolic activity of different organs. The PCA-LDA modelling yielded a sensitivity of 85 to 97% and specificity of 80 to 96% on 320 nm excitation and a sensitivity of 72 to 100% and specificity of 59 to 100% on 410 nm excitation. Fluorescence emission spectral study along with multivariate analysis paved way to identify the biochemical alterations caused to other organs due to the development of liver fibrosis, which could lead to their damage and dysfunction.

Topics: Animals; Flavin-Adenine Dinucleotide; Liver Cirrhosis; Multivariate Analysis; NAD; Rats; Spectrometry, Fluorescence

The metabolism of vitamin B2 was studied in five female patients with liver cirrhosis of varying etiology. Following the oral administration of 40 mg (106.3 mumol) riboflavin, plasma concentrations of riboflavin and flavo-coenzymes as well as urinary riboflavin excretion were analyzed over a period of 48 h. Results were compared to data obtained for healthy controls (Zempleni J. et al, Am. J. Clin. Nutr., 1996 [15]). About 18% of the administered vitamin was recovered from patients' urine, indicating an absorption similar to healthy subjects (p > 0.05). The area under the riboflavin plasma concentration vs time curve was 1.2-fold larger among patients than controls, but the difference was not significant (p > 0.05). Riboflavin peak concentrations in plasma (315.6 nmol/l) and times when those concentrations were achieved (3.0 h) were similar to those found for healthy subjects (p > 0.05). Flavocoenzyme peak plasma concentrations were increased 1.4-fold above their baseline levels in cirrhotics which was equal to controls (p > 0.05). 7 alpha-Hydroxyriboflavin was detected in the plasma of patients. Distribution and elimination kinetics of riboflavin were analyzed by using a two-compartment open model; the riboflavin plasma disposition rate constants of the patients (k alpha = 0.7232 h-1; k beta = 0.0627 h-1) were not different from controls (p > 0.05). No differences between both groups were found regarding renal excretion (renal clearance, first-order rate constants for renal excretion; p > 0.05). In conclusion, patients with liver cirrhosis of varying etiology and varying medical treatment did not show alterations of riboflavin turnover.

Topics: Adult; Female; Flavin Mononucleotide; Flavin-Adenine Dinucleotide; Humans; Kinetics; Liver Cirrhosis; Liver Cirrhosis, Alcoholic; Middle Aged; Riboflavin

An investigation on vitamin B2 (V.B2) metabolism was undertaken, using perfused livers isolated from 1. normal rats, 2. riboflavin deficient rats, 3. choline deficient rats with fatty cirrhtic livers, and 4. alloxan diabetic rats, without the effect of extrahepatic factors. From the results, it was concluded that phosphorylation of V.B2 was performed in the liver, and was remarkably reduced in fatty cirrhosis. Moreover, in alloxan diabetic liver, the affected phosphorylation of V.B2 was improved by the infusion of insulin. The important role that liver performs on V.B2 metabolism, can be emphasized from these findings.

Topics: Animals; Choline Deficiency; Diabetes Mellitus, Experimental; Female; Flavin Mononucleotide; Flavin-Adenine Dinucleotide; In Vitro Techniques; Liver; Liver Cirrhosis; Male; Perfusion; Rats; Riboflavin; Riboflavin Deficiency

Topics: Ascorbic Acid; Blood; Carbon Radioisotopes; Enzyme Activation; Erythrocytes; Flavin-Adenine Dinucleotide; Flavins; Glucosephosphate Dehydrogenase Deficiency; Glutathione Reductase; Hemolysis; Humans; Liver Cirrhosis; Methylene Blue; Riboflavin; Umbilical Cord; Uremia

Topics: Female; Flavin Mononucleotide; Flavin-Adenine Dinucleotide; Flavins; Humans; Kidney; Kidney Diseases; Liver; Liver Cirrhosis; Liver Diseases; Male; Nutrition Surveys; Proteins; Riboflavin; Vitamins

Topics: Adult; Erythrocytes; Flavin-Adenine Dinucleotide; Glucosephosphate Dehydrogenase Deficiency; Glutathione Reductase; Humans; Liver Cirrhosis; Protein Binding; Uremia