Biomedical subjects

Y Kurumi

Publications and source records attributed to Y Kurumi.

21 records · Page 2Linked to original sources

PubMed1991

Bilirubin diglucuronide transport by rat liver canalicular membrane vesicles: stimulation by bicarbonate ion.

The purpose of this study was to provide further insight into the mechanism of bilirubin diglucuronide excretion through the hepatocyte canalicular membrane by investigating the uptake of (3H)bilirubin diglucuronide by purified canalicular membrane vesicles of rat liver. The uptake was analyzed by a rapid filtration technique. The difference between vesicle-associated (3H)bilirubin diglucuronide at 37 degrees C and at 0 degree C during the initial 1 min was regarded as uptake. Twenty second uptake was saturated by increasing the (3H)bilirubin diglucuronide concentration at a vesicle-inside-directed 100 mmol/L KCl gradient (Km = 75 mumol/L, Vmax = 320 pmol/mg protein.20 sec at 37 degrees C). No sodium dependency was observed. When canalicular membrane vesicles were preincubated with nonlabeled bilirubin diglucuronide, the uptake increased 1.3-fold (transstimulation). Vesicle-inside-positive potential induced by valinomycin and potassium caused a 1.4-fold increase in the uptake. When Cl- was replaced by equivalent ion concentrations of SO4(2-), HCO3-, NO3- and SCN-, the uptake was 78%, 244%, 68% and 50%, respectively, and specific stimulation by HCO3- was observed (Km = 75 mumol/L, Vmax = 700 pmol/mg protein.20 sec at a vesicle-inside-directed 100 mmol/L KHCO3 gradient at 37 degrees C). The uptake was inhibited in a dose-dependent manner by the addition of 4,4'-diisothiocyanatostilbene-2,2'-disulfonic acid. The uptake was ATP independent. From these results, it was concluded that bilirubin diglucuronide transport through the canalicular membrane is carrier mediated, electrogenic and stimulated by HCO3-.

4,4'-Diisothiocyanostilbene-2,2'-Disulfonic Acid↗

PubMed1988

Determination of individual serum bile acids in chronic liver diseases: fasting levels and results of oral chenodeoxycholic acid tolerance test.

Fifteen bile acids in serum of 5 normal subjects and 21 patients with chronic liver diseases were fractionated by high performance liquid chromatography. Fasting total bile acids (TBA), glycocholic acid, taurocholic acid, glycochenodeoxycholic acid (GCDCA), and taurochenodeoxycholic acid (TCDCA) were significantly increased in patients with liver cirrhosis as compared with normal subjects. The cholic acid (CA) level and the ratio of the sum of free and conjugated CA to the sum of free and conjugated chenodeoxycholic acid (CDCA) were significantly elevated in patients with compensated as compared with decompensated liver cirrhosis, and were useful for differentiation of the two conditions. Serum bile acid levels were determined after oral administration of 500 mg of CDCA in the 5 normal subjects and 11 patients with liver disease. The TBA level reached a peak 90 min after CDCA administration in patients with chronic hepatitis and after 120 min in those with liver cirrhosis. The increase in the TBA level was significantly greater in patients with liver disease than in normal subjects. CDCA, GCDCA, and TCDCA showed changes similar to those in TBA. In patients with decompensated liver cirrhosis, the reduction in the TBA and CDCA levels after the peaks was slow, and GCDCA and TCDCA levels continued to increase until 180 min after the administration of CDCA. The TBA and CDCA levels 180 min after CDCA administration were significantly different among normal subjects, patients with chronic hepatitis, those with compensated liver cirrhosis, and those with decompensated liver cirrhosis, suggesting the usefulness of CDCA administration in differentiation of these conditions.

Bile Acids and Salts↗

PubMed1983

Classification of compounds by cluster analysis of Ames test data.

The dose-response curves for various compounds in the Ames test were analyzed by combining the least-squares method with cluster analysis. The following theoretical equation was employed: m(x) = (B + Sx)exp(-Tx), where m(x) is the number of revertants at the dose of x; B, the background number; S, the mutagenicity rate; and T, the toxicity rate. This equation is derived from a one-hit model modified to take account of the toxicity, and the parameters B, S and T are determined by applying the least-squares method for the fitting between theoretical and experimental dose-response curves with the use of the program package SALS (statistical analysis with least-squares fitting). With the values for B, S and T thus obtained, cluster analysis can clearly separate mutagenic and non-mutagenic compounds. Moreover, when cluster analysis into six groups is carried out, each group has quite characteristic parameter values. Consequently, this procedure is very useful for the classification of compounds according to the nature of the dose-response curve, that is, according to the nature of their mutagenic activity.

Carcinogens↗