13 research outputs found
Electroanalysis may be used in the Vanillin Biotechnological Production
This study shows that electroanalysis may be used in vanillin biotechnological production. As a matter of fact, vanillin and some molecules implicated in the process like eugenol, ferulic acid, and vanillic acid may be oxidized on electrodes made of different materials (gold, platinum, glassy carbon). By a judicious choice of the electrochemical method and the experimental conditions the current intensity is directly proportional to the molecule concentrations in a range suitable for the biotechnological process. So, it is possible to imagine some analytical strategies to control some steps in the vanillin biotechnological production: by sampling in the batch reactor during the process, it is possible to determine out of line the concentration of vanillin, eugenol, ferulic acid, and vanillic acid with a gold rotating disk electrode, and low concentration of vanillin with addition of hydrazine at an amalgamated electrode. Two other possibilities consist in the introduction of electrodes directly in the batch during the process; the first one with a gold rotating disk electrode using linear sweep voltammetry and the second one requires three gold rotating disk electrodes held at different potentials for chronoamperometry. The last proposal is the use of ultramicroelectrodes in the case when stirring is not possible
Metabolism of homovanillamine to homovanillic acid in guinea pig liver slices
Background/ Aims: Homovanillamine is a biogenic amine that it is
catalyzed to homovanillyl aldehyde by monoamine oxidase A and B, but the
oxidation of its aldehyde to the acid derivative is usually ascribed to
aldehyde dehydrogenase and a potential contribution of aldehyde oxidase
and xanthine oxidase is usually ignored. Methods: The present
investigation examines the metabolism of homovanillamine to its acid
derivative by concurrent incubation with monoamine oxidase and aldehyde
oxidase. In addition, the metabolism of homovanillamine in freshly
prepared and cryopreserved liver slices is examined and the relative
contribution of aldehyde oxidase, xanthine oxidase and aldehyde
dehydrogenase activity by using specific inhibitors of each oxidizing
enzyme is compared. Results: Homovanillamine was rapidly converted
mainly to homovanillic acid when incubated with both momoamine oxidase
and aldehyde oxidase. Homovanillic acid was also the main metabolite in
the incubations of homovanillamine with freshly prepared or
cryopreserved liver slices, via the intermediate homovanillyl aldehyde.
The acid formation was 70-75% inhibited by disulfiram ( specific
inhibitor of aldehyde dehydrogenase), whereas isovanillin ( specific
inhibitor of aldehyde oxidase) inhibited acid formation to a lesser
extent (50-55%) and allopurinol ( specific inhibitor of xanthine
oxidase) had almost no effect. Conclusions: Homovanillamine is rapidly
oxidized to its acid, via homovanillyl aldehyde, by aldehyde
dehydrogenase and aldehyde oxidase with little or no contribution from
xanthine oxidase. Copyright (C) 2005 S. Karger AG, Basel
Effect of hepatic stimulator substance (HSS) on cadmium-induced acute hepatotoxicity in the rat liver
The hepatoprotective effect of HSS against cadmium-induced liver injury
was investigated. Rats were intoxicated with a dose of cadmium (3.5
mg/kg b.w.). The rats were treated with normal saline (group I) or HSS
(100 mg protein/kg b.w.; group II) 2 hr later and killed at different
time points. Hematoxylin-eosin (HE) sections were assessed for necrosis,
apoptosis, peliosis, mitoses, and inflammatory infiltration. Serum
enzyme activities were assayed. Apoptosis was quantified by the Tunel
technique. Thymidine kinase activity and the rate of [H-3] thymidine
incorporation into DNA were also assayed. Necrosis, hepatocyte
apoptosis, and peliosis were minimized in HSS-treated rats (group II).
Nonparenchymal cell apoptosis and liver regeneration were not
quantitively altered in the HSS-treated group, though the time profile
was different. HSS protects hepatocytes against cadmium-induced
necrosis, apoptosis, and peliosis. Apoptosis was the major type of cell
death for nonparenchymal liver cells and strongly correlated with the
extent of peliosis. Interactions between hepatocytes and nonparenchymal
liver cells seem to be important for the genesis of hepatic trauma in
acute cadmium hepatotoxicity
Aldehyde oxidase-dependent species difference in hepatic metabolism of fasudil to hydroxyfasudil
Enzymatic oxidation of vanillin, isovanillin and protocatechuic aldehyde with freshly prepared Guinea pig liver slices.
NoBackground/Aims: The oxidation of xenobiotic-derived aromatic aldehydes with freshly prepared liver slices has not been previously reported. The present investigation compares the relative contribution of aldehyde oxidase, xanthine oxidase and aldehyde dehydrogenase activities in the oxidation of vanillin, isovanillin and protocatechuic aldehyde with freshly prepared liver slices. Methods: Vanillin, isovanillin or protocatechuic aldehyde was incubated with liver slices in the presence/absence of specific inhibitors of each enzyme, followed by HPLC. Results: Vanillin was rapidly converted to vanillic acid. Vanillic acid formation was completely inhibited by isovanillin (aldehyde oxidase inhibitor), whereas disulfiram (aldehyde dehydrogenase inhibitor) inhibited acid formation by 16% and allopurinol (xanthine oxidase inhibitor) had no effect. Isovanillin was rapidly converted to isovanillic acid. The formation of isovanillic acid was not altered by allopurinol, but considerably inhibited by disulfiram. Protocatechuic aldehyde was converted to protocatechuic acid at a lower rate than that of vanillin or isovanillin. Allopurinol only slightly inhibited protocatechuic aldehyde oxidation, isovanillin had little effect, whereas disulfiram inhibited protocatechuic acid formation by 50%. Conclusions: In freshly prepared liver slices, vanillin is rapidly oxidized by aldehyde oxidase with little contribution from xanthine oxidase or aldehyde dehydrogenase. Isovanillin is not a substrate for aldehyde oxidase and therefore it is metabolized to isovanillic acid predominantly by aldehyde dehydrogenase. All three enzymes contribute to the oxidation of protocatechuic aldehyde to its acid
The hepatoprotective effect of hepatic stimulator substance (HSS) against liver regeneration arrest induced by acute ethanol intoxication
Male Wistar rats were randomized to receive ethanol (2.5 ml/kg by
gastric intubation every 8 hr; group I), equal volumes of isocaloric to
ethanol sucrose solution (group II), or ethanol and HSS (100 mg/kg
intraperitoneally 10 and 16 hr after partial hepatectomy; groups III and
IV, respectively) for up to 96 hr after partial hepatectomy, with
ethanol administration starting 1 hr prior to partial hepatectomy.
Animals were killed at 8, 12, 16, 20, 24, 28, 32, 36, 40, 44, 48, 60,
and 96 hr after partial hepatectomy. The rate of liver regeneration was
evaluated by the mitotic index in H&E-stained sections, immunochemical
detection of Ki67 nuclear antigen, rate of [H-3]thymidine
incorporation into hepatic DNA, and liver thymidine kinase enzymatic
activity. The biological activity of HSS in groups I and II rats was
evaluated using a bioassay. Ethanol administration arrested liver
regeneration during the first 32 hr after partial hepatectomy and
suppressed HSS activity throughout the period examined. Liver
regeneration progressed after 32 hr despite the low levels of HSS
activity. HSS administration at 10 and 16 hr reversed liver regeneration
arrest induced by ethanol. Acute ethanol administration induces cell
cycle arrest during the first 32 hr after partial hepatectomy and
suppression of HSS biological activity seems to contribute to this
effect. HSS administration reversed the inhibitory effect of ethanol on
liver regeneration and caused synchronized entrance of hepatocytes in
the S phase of the cell cycle. HSS seems to participate in the network
of growth factors controlling the G1/S cell cycle checkpoint
The exploration of interaction studies of smaller size, mostly ignored yet intrinsically inestimable molecules towards BSA; An example of STD and DOSY NMR
Direct comparison of the four aldehyde oxidase enzymes present in mouse gives insight into their substrate specificities
Flavonoid Glycosides Isolated from Unique Legume Plant Extracts as Novel Inhibitors of Xanthine Oxidase
Legumes and the polyphenolic compounds present in them have gained a lot of interest due to their beneficial health implications. Dietary polyphenolic compounds, especially flavonoids, exert antioxidant properties and are potent inhibitors of xanthine oxidase (XO) activity. XO is the main contributor of free radicals during exercise but it is also involved in pathogenesis of several diseases such as vascular disorders, cancer and gout. In order to discover new natural, dietary XO inhibitors, some polyphenolic fractions and pure compounds isolated from two legume plant extracts were tested for their effects on XO activity. The fractions isolated from both Vicia faba and Lotus edulis plant extracts were potent inhibitors of XO with IC50 values range from 40-135 mu g/mL and 55-260 mu g/mL, respectively. All the pure polyphenolic compounds inhibited XO and their K-i values ranged from 13-767 mu M. Ten of the compounds followed the non competitive inhibitory model whereas one of them was a competitive inhibitor. These findings indicate that flavonoid isolates from legume plant extracts are novel, natural XO inhibitors. Their mode of action is under investigation in order to examine their potential in drug design for diseases related to overwhelming XO action