Tadasuke Kondo

Serum glycoproteins in the liver diseases. III. Desialylated glycoproteins in the acute hepatitis.

SummaryCirculating desialylated glycoprotein level in acute hepatitis was studied by using the competitive binding assay reported by us. Statistically significant differences of the level among acute hepatitis in the peak of illness, fulminating hepatitis and normal subjects were observed. The desialylated glycoprotein level in acute hepatitis was elevated associating with S-GPT and serum bilirubin levels, and it returned to the normal range before S-GPT and serum bilirubin were normalized. The desialylated glycoprotein in a fulminant hepatitis was increasing associated with bilirubin even when S-GPT was decreasing.

Serum glycoproteins in the liver diseases. V. Desialylated glycoproteins in chronic hepatitis.

SummarySerum desialylated glycoprotein level was tested for chronic hepatitic patients. The level was significantly elevated in patients with chronic aggressive hepatitis but not in chronic persistent hepatitis comparing to normal subjects. In chronic aggressive hepatitis, severe type (2B), serum desialylated glycoprotein levels were significantly enhanced but not in moderate type (2A) when compared to chronic persistent hepatitis. Sera taken serially from patients with chronic aggressive hepatitis, severe type (2B), demonstreated a slight correlation between circulating desialylated glycoprotein level and serum glutamic-pyruvic transaminase activity.

Serum glycoproteins in the liver diseases IV. Alpha-1 acid glycoprotein level in liver cirrhosis

SummaryCirculating alpha-1 acid glycoprotein level in cirrhotic patients was determined by radioimmunoassay, and was compared to the ones in normal subjects and chronic active hepatitis with sublobular necrosis.Serum alpha-1 acid glycoprotein levels in liver cirrhosis (p< 0.001) and chronic active hepatitis with sublobular necrosis (p< 0.02) were significantly reduced comparing to the normal subjects, although any statistically significant difference was not observed between the formers.In liver cirrhosis, the serum alpha-1 acid glycoprotein level correlated negatively with serum albumin concentration but neither with serum alpha-1 globulin fraction nor with Indocyanine green clearance rate.

Characterization of the ester form bilirubin fraction showing positive phosphate ester reaction

SummaryPositive phosphate-ester fraction of the ester-form bilirubin was prepared from the rat bile after intravenous injection of32P-sodium phosphate and also from the jaundiced urine of various liver diseases. The administered32P-radioactivity was mainly recovered in the third spot of ester-form bilirubin on the radioautogram and the radiochromatogram. The maxium absorption of the aqueous solution was 410-420mµ, and that of its azo-pigment and acid azo-pigment was 550-560 mµ and 555-565 mµ, respectively. Photochemical and chemical properties were the same as we have previously reported on the ester-form bilirubin. Molar ratios of phosphate and bilirubin in this fraction were from 1.22 to 1.90 and ratios of Pigment A and Pigment B were from 0.10 to 0.41. These results suggest the existence of bilirubin diphosphate-ester.

Serum glycoproteins in the liver diseases

SummaryThe human liver as well as rat liver particulate fraction was determined to have an ability to bind desialylated a1-acid glycoprotein. The binding activity of human liver was the same order of the rat one. A more increased amount of binding of desialylated glycoprotein was found in a new born liver than an adult one.Serum obtained from a cirrhotic patient inhibited the binding. The sucrose density gradient centrifugation revealed that the activity located partly in fractions in which a membrane enzyme, alkaline phosphatase, was detected. The binding activity was a linear function of concentration of human liver particulate fraction added to incubation mixture.

Proceedings of the 19th autumn meeting from October 18 to 20, 1977-Nara, Japan

The first step in the formation of bile acids is 7uhydroxylation of cholesterol. Subsequently 7ahydroxycholest-4-en-3-one is formed, which is a common precursor of the two primary bile acids, cholic acid and chenodeoxycholic acid. 5,BCholestane-3~t , 7a -d io l , a p recursor of chenodeoxycholic acid is formed from the A4-3-keto intermediate by a pathway which involves the reduction of the keto group and the saturation of the double bond but not a hydroxylation at C-12, while a pathway involving the 12a-hydroxylation of the A4-3-keto intermediate leads to the formation of 5flcholestane-3~, 7a, 12a-triol, which is a precursor of cholic acid. The C2~-bile alcohol intermediates , 5flcholestane-3a, 7t~-diol and 5,g-cholestane-3tz, 7t~, 1 2 ~ t r i o l , a r e t h e n t r a n s f o r m e d i n t o chenodeoxycholic acid and cholic acid by the degradation of the side chain which entails an moxidation followed by fl-oxidation. Chenodeoxycholic acid is also formed by a number of different pathways differing only with respect to the stage of nuclear transformation at which oxidation of the side chain is initiated. A number of cholestanepolyols such as 5flcholestane-3ct, 70t, 12ct, 25-tetrol are accumulated in the bile and feces of patients with cerebrotendinous xanthomatosis. No 26-hydroxylated bile alcohols are accumulated. The results suggest that there exists an alternative pathway of cholic acid biosynthesis involving the 25-hydroxylated bile alcohol as an intermediate. (2) Analytical methods of bile acids in biological materials

A simple method for the quantitative determination of urinary hippuric acid excreted after administration of sodium benzoate for use as a liver function test

Improved and simpler method for the quantitative determination of hippuric acid in urine for the use as a liver function test has been presented. The acid was extracted from urine three times with mixture of ether and iso-propanol respectively, and hippuric acid was determined at 230 mμ. The results agree with the crystallization method of Krause, the colorimetric method using p-dimethylaminobenzaldehyde in acetic anhydrate, as well as with our colorimetric method using benzene sulfonyl chloride. It is also indicated that the colorimetric method using benzene sulfonyl chloride may be used as a more specific method for urinary hippuric acid assay.

Studies on bilirubin phosphate by P32

Conclusions1)P32 loaded on the duodenum was excreated into bile after 10–15 minutes (The peak; 6–7 hours after injection). The excreation was continued still after 24 hours.2)P32 loaded on the duodenum was excreated into bile 1.7% after 8 hours and 4.7% after 24 hours.3)The radioactivity of P32 on paperchromatogram was detected on the spot corresponding to ester-form bilirubin and could not be observed in other bilirubin fractions.4)Only the ester-form bilirubin fraction, separated by Kosaka-Hara’s method showed P32-radioactivity. These results suggest that bilirubin phosphate is one part of ester-form bilirubin.